isnumm^ 


RJ45.C31HX64167437 

Diseases  of  infants 


RECAP 


— 

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Columbia  UttitterBitu.    \ 
in  tty  City  nf  N?ro  Hark 

OlnUpgp  of  ^tryairianB  ano  §>ur$? oita 


Urfmnre   library 


DISEASES 


OF 


INFANTS   AND    CHILDREN 


Digitized  by  the  Internet  Archive 

in  2010  with  funding  from 

Open  Knowledge  Commons 


http://www.archive.org/details/diseasesofinfantOOcaut 


THE 


DISEASES 


OF 


INFANTS    AND    CHILDREN. 


EDMUND   CAUTLEY,   U.D.  Cantab.,   F.R.C.P.   Lond., 

Senior  Physician  to  the  Be.lgra.vt  Hospital  for  Children; 

Physician  to  the  Metropolitan  Hospital;  formerly  Casualty  Physician  and  Assistant 

Demonstrator  of  Physiology  at  St.  Bartholomew's  Hospital. 


NEW     YORK: 

PAUL     B.     HOEBER, 

69     East      59TH     Street,     New     York. 

1912. 


^  *5 


C  s\ 


PREFACE. 


rnHIS  work  is  based  upon  many  years' practical  experience 
of  the  diseases  of  early  life,  the  examination  of  a  large 
number  of  children,  and  the  necessarily  somewhat  extensive 
study  of  the  literature  of  the  subject.  Its  object  is  to 
describe  the  ailments  of  children  in  a  form  suitable  for  the 
general  practitioner  of  medicine  and  sufficiently  detailed 
to  render  further  reference  to  other  works  unnecessary, 
except  in  the  case  of  unusually  rare  diseases. 

A  liberal  amount  of  space  is  devoted  to  surgical  affec- 
tions which  may  come  under  the  notice  of  physicians  in 
early  stages  and  under  the  care  of  practitioners  at  all 
periods  of  their  course.  The  knowledge  of  these  diseases 
must  be  extensive  enough  to  enable  the  practitioner  to 
clearly  understand  the  nature  of  the  illness,  to  appreciate 
the  best  lines  of  treatment,  and  to  recognise  the  conditions 
for  which  the  aid  of  a  surgeon  should  be  invoked.  Indeed, 
a  year's  experience  as  house  surgeon  is  almost  essential 
to  the  training  of  a  physician. 

Considerable  attention  is  given  to  maladies  which 
have  only  been  fully  recognised  in  recent  years,  for  instance, 


Preface. 
hypertrophic  stenosis  of  the  pylorus  in  infants,  acidosis, 
delayed  anaesthetic  poisoning,  and  cleido-cranial  dysostosis. 
In  connection  with  the  disorders  of  bone  formation  a  new 
system  of  nomenclature  is  suggested.  The  descriptions  of 
some  common  ailments  have  been  curtailed,  inasmuch  as 
in  a  book  for  graduates  it  is  unnecessary  to  amplify  the 
minutiae  of  symptoms,  diagnosis  and  treatment.  In  dis- 
cussing the  various  therapeutic  measures  no  special  method 
is  dogmatically  insisted  on,  for  it  is  obvious  that  remedies 
applicable  in  one  case  may  be  contra-indicated  in  another 
by  the  character  of  the  illness,  the  idiosyncrasy  of  the 
child,  or  the  social  position  and  environment.  In  children, 
even  more  than  in  adults,  we  have  to  deal  with  a  patient 
and  relatives,  often  a  nurse  as  well,  in  addition  to  treating 
the  particular  disease. 

Illustrations  and  charts  have  been  omitted.  The 
kindergarten  teaching  of  medicine  by  pictures,  diagrams 
and  models,  is  advantageous  for  the  student,  but  may  prove 
a  disadvantage  to  those  in  active  practice.  Photographs 
and  drawings,  except  of  pathological  states,  are  of  little 
value,  unless  so  typical  that  the  veriest  tyro  can  recognise 
the  disease  from  a  description.  They  are  injurious  in  that 
the   expectation   of   seeing  the   typical   cases   of   pictorial 


Preface. 
illustration    increases    the    danger    of    overlooking    those 
early  stages  in  which  disease  is  amenable  to  treatment. 

My  indebtedness  to  the  valuable  contributions  of 
other  writers  is  obviously  very  great,  and  must  be  warmly 
acknowledged.  That  continual  reference  in  the  text  to 
individuals  is  wanting  is  not  due  to  any  desire  to  claim 
undeserved  credit,  but  simply  in  order  not  to  burden  the 
work  with  innumerable  names  and  references.  Perhaps  at 
times  statements  and  opinions  have  been  put  forward  in  a 
somewhat  dogmatic  manner.  If  so,  the  excuse  is  that 
they  are  the  outcome  of  prolonged  thought  and  considerable 
experience. 

The  Society  for  the  Study  of  Disease  in  Children  was 
formed  in  1900,  and  after  eight  years'  active  work  became 
amalgamated  with  the  Royal  Society  of  Medicine.  In 
1904  the  late  Dr.  George  Carpenter  founded  the  British 
Journal  of  Children's  Diseases.  The  study  of  disease  in 
early  life  has  consequently  received  such  a  great  impetus 
in  this  country  that,  in  my  opinion,  a  new  systematic  and 
up-to-date  book  on  the  subject  is  required. 

Edmund  Cautley. 

London,  W., 
April,  1910. 


TABLE    OF   CONTENTS. 


Section  I. 


GENERAL    FACTORS. 

CHAPTER  PAGE 

I.  Introductory. — Definitions — The  Examination  of  Children — 
Special  Features  of  Disease  in  Children — Normal  Growth 
and  Development    -  -         -         -         1 

II.  Hereditary  and  Ante-natal  Conditions. — Heredity  — 
Pre-conceptional  Factors — Intra-uterine  or  Congenital 
Factors — Mental  Impressions — Direct  Transmission  of 
Disease — Immunity — Treatment      -         -         -         -         -       13 

III.  Diet  and  Nutrition.  —  The  Mother  or  Wet  Nurse  — 
Physiology  and  Chemistry — Breast-Feeding — Human 
Milk— Cow's  Milk— Bacteriology— The  Effect  of  Heat 
and  Attenuants — Subsidiary  Methods  of  Feeding — 
Proprietary  Foods — Diet  after  Weaning  ;  in  Early 
Childhood  ;    in  School  Life  ;    in  Illness  26 

IV.  Therapeutics. — Nursing — Hydrotherapy — Local  Applications 

of  Heat  —  Counter-Irritation  —  Cupping  —  Bleeding  — 
Pharmacotherapy  —  Cutaneous  Therapy  —  Rectal 
Therapy  —  Fever  —  Collapse  —  Vaccine  Therapy  — 
Anaesthesia      -         -         -         -         -         -         -         -         -       71 

V.  Premature  Infants       -  96 

VI.  Mortality.  —  Intra-uterine  Death  —  Intra-uterine 
Putrefaction  —  Rigor  Mortis  in  the  Still-born  — 
General  Mortality — Death  from  Overlaying  —  Sudden 
Death      -         -         -         -  -     100 


Section    II. 
AFFECTIONS    OF    THE    NEWBORN. 

VII.  Congenital  Deformities  and  Injuries  at  Birth. — 
Deformities — Ante-partum  Inj  uries — Caput  Succedaneum 
—  Cephal-hgematoma  —  Cranial  Depressions  —  Sterno- 
mastoid    Tumour — Diaphragmatic  Hernia       -  -     106 


Table  of  Contents. 

CHAPTER  PAGE 

VIII.     Asphyxia  Neonatorum  and  Atelectasis      -  115 

IX.  The  Umbilicus  and  Septic  Affections  op  the  New- 
born.— The  Cord  at  Birth — Abnormalities  and 
Diseases  of  the  Cord  and  Navel — Pyaemia  Neona- 
torum— Buhl's  Disease — Winckel's  Disease  — 
Erysipelas — Hemorrhagic  Disease — Suprarenal 
Apoplexy — Trismus  or  Tetanus  -  -     119 

X.  Jaundice  in  the  Newborn. — Icterus  Embryonum — 
Icterus  Neonatorum — Biliary  Concretions — Pyse- 
mic  Jaundice — Congenital  Defects  of  the  Bile 
Ducts          -  -         -  -  133 

XI.     Ophthalmia  Neonatorum  -     137 

XII.  Skin  Affections  of  the  Newborn. — Exfoliative 
Dermatitis — Pemphigus — Epidermolysis  —  Foetal 
Ichthyosis  —  Xerodermia  —  Sclerema  — 
Oedema — Pigmentation      -  -     142 


Section    III. 

DISORDERS    OF    METABOLISM,    NUTRITION    AND 
GROWTH. 

XIII.  Disorders    of    Metabolism. — Acholia — Lithaemia — 

Acidosis — Delayed  Anaesthetic  Poisoning — Recur- 
rent Vomiting — Diabetes — Scurvy      -         -         -     147 

XIV.  Infantile  Atrophy.  —  Athrepsia  —  Malnutrition — 

Marasmus — Inanition  -         -         -         -         -     170 

XV.     Rickets  -  -     178 

XVI.  Disorders  of  Bone  Formation. — Achondroplasia — 
Cleido-cranial  Dysostosis  vel  Anosteoplasia  — 
Osteogenesis  Imperfecta  vel  Periosteal  Aplasia    -     192 

XVII.  Anomalies  and  Disorders  of  Growth. — Dwarfs — 
Symptomatic  Infantilism — Ateleiosis — Precocity 
— Obesity — Gigantism — Hemihypertrophy  -         -     198 

XVIII.  The  Thyroid  Gland. — Congenital  Goitre — Acute 
Thyroiditis  —  Cretinism  —  Myxcedema  —  Exoph- 
thalmic Goitre  —  Parathyroids  —  Thyroglossal 
Fistula — Hygroma      -         -  -  -     203 

XIX.     The  Adrenal  Glands     -  -     210 


Table  of   Contents. 


XL 


Section    IV. 

chapter  THE   ALIMENTARY  SYSTEM.  page 

XX.  The  Mouth  and  Jaws. — Structural  Defects — The 
Tongue  —  Stomatitis  —  Uvula  —  The  Teeth  and 
Dentition — The  Salivary  Glands          -         -         -     2 IS 

XXI.  The  Throat,  Pharynx  and  Oesophagus. — Tonsillar 
Affections  —  Pharyngitis  —  Adenoids  —  Retro- 
pharyngeal and  Retro-cesophageal  Abscess— 
The  Oesophagus          ------     230 

XXII. — The  Stomach. —  Malformations  —  Dilatation  —  Gas- 
tric Contents  —  Signs  of  Gastric  Disease  —  The 
Appetite  —  Pica  —  Vomiting  —  Regurgitation  — 
Rumination  —  Functional  and  Inflammatory 
Disorders — Gastric  and  Duodenal  Ulcer  ""-         -     248 

XXIII.  The  Pylorus. — Pyloric  Spasm — Congenital  Hyper- 

trophic Stenosis  -         -         -         -         -         -261 

XXIV.  Intestinal  Digestion. — The    Stools  —  Tympanites 

— Colic  —  Reflex      Colic      and      Diarrhoea  — 
Intestinal  Dyspepsia — Carbohydrate  Fever        -     271 

XXV.  Diarrhceal  Affections. — Simple  Diarrhoea —  In- 
fective Diarrhoea  —  Infantile  Cholera  —  Ileo- 
colitis and  Colitis ;  catarrhal,  ulcerative  and 
membranous — Tuberculous  Enteritis  and  Colitis-     281 

XXVI.     Constipation. — Simple  Constipation  —  Dilatation  of 

the  Colon — Hirschsprung's  Disease    -  303 

XXVII.     Intestinal  Parasites. — Tapeworms  —  Roundworms 

— Threadworms — Trichinae — Myiasis  -         -     311 

XXVIII.  Intestinal  Obstruction. — Malformations  —  Volvu- 
lus —  Intussusception  —  Hernia  —  Congenital 
Hydrocele  -------     317 

XXIX.  The  Rectum  and  Anus. — Malformations  —  Fsecal 
Incontinence  —  Fissure — Spasm — Polypus — Pro- 
lapse —  Proctitis  —  Haemorrhoids  —  Fistula — 
Abscess  -         -  .         _         -         -     332" 


XXX.     Appendicitis 


340 


XXXI.  The  Peritoneum. — Ascites  —  Acute  Peritonitis  — 
Chronic  and  Tuberculous  Peritonitis  —  Mesen- 
teric Cysts  —  Pancreatic  Cysts  —  New  Growths-     348 

XXXII.  The  Liver. — Jaundice  —  Acute  Yellow  Atrophy  — 
Biliary  Cirrhosis  —  Atrophic  Cirrhosis  — 
Syphilis  —  Tuberculosis  —  Active  and  Passive 
Congestion  —  Abscess  —  Fatty  Liver  —  Amyloid 
Liver  —  Hvdatids  —  Tumours  -         -         -         -     358 


xii.  Table  of  Contents. 


Section    V. 
THE    RESPIRATORY    SYSTEM. 

CHAPTER  PAGE 

XXXIII.  The    Nose    and    Accessory    Sinuses. — Congenital 

Anomalies  —  Nasal  Obstruction  —  Nasal  Dis- 
charges —  Rhinitis,  acute  and  chronic  —  Epi- 
staxis  —  Sinusitis  —  Osteomyelitis  of  the  Upper 
Jaw  ..--._-.     369 

XXXIV.  Laryngeal  Affections. — The  Larynx  —  Examina- 

tion —  Croup  —  Laryngitis  Stridulosa  —  Catar- 
rhal, Membranous  and  Chronic  Laryngitis  — 
Oedema  Glottidis  —  Congenital  Laryngeal 
Stridor  —  New    Growths    -----     379 

XXXV.  The  Respiratory  System. — The  Thorax  —  The 
Lungs  and  Respiration — Respiratory  Symptoms 
— Atelectasis  —  Hypostatic  Congestion  —  The 
Trachea  —  Foreign  Bodies  in  the  Air-passages 
— Gangrene  —  Abscess  —  New  Growths  — 
Emphysema        -----  -     389 

XXXVI.     Asthma. — Hay    Fever  —  Catarrhal    and    Spasmodic 

Asthma    "  -------     400 

XXXVII.  Bronchitis  and  Broncho-Pneumonia. — Acute  Bron- 
chitis —  Plastic  Bronchitis  —  Chronic  Bron- 
chitis —  Capillary  Bronchitis  or  Broncho- 
Pneumonia         -         -         -       .  -         -         -         -     406 

XXXVIII.  Pneumonia. — Pneumonia  or  Pneumococcal  Fever — 
Pneumococcal  Infection  of  the  Lungs — Croupous 
or  Fibrinous  Pneumonia — Pleuro-Pneumonia      -     419 

XXXIX.  The  Pleura  and  Pleural  Cavity. — Hydrothorax — 
Multiple  Serositis  —  Pleurisy  —  Pleural  Effu- 
sions —  Empyema — Pneumothorax    -  432 


Section    VI. 

THE    CIRCULATORY    SYSTEM. 

XL.  The  Heart  and  Circulation. — The  Heart  at  Birth — 
Examination  of  the  Heart — The  Pulse — Func- 
tional Heart  Murmurs — Functional  Disorders 
— Diseases  of  Blood  Vessels — Oedema  and  allied 
conditions  -------     448 

XLI.  Congenital  Heart  Disease. — Cardiac  Development 
— Foetal  Circulation — Pathogenesis — Malpositions 
— Defects  in  the  Septa — Arterial  Defects — Val- 
vular Lesions  461 


Table  of  Contents. 


CHAPTER 

XLII. 


PAGE 


Acquired  Heart  Disease. — The  Myocardium  — 
Cardiac  Dilatation  —  Endocarditis  —  Valvular 
Defects  —  Pericarditis  and  Effusion  —  Medias- 
tino-pericarditis  —  Adherent  Pericardium  -         -     480 


XLIII. 


Section    VII. 

THE    HEMOPOIETIC    SYSTEM. 

The  Blood  and  Lymphoid  Tissues. — The  Blood — 
Primary  Anaemias — The  Spleen — Anaemia  Splen- 
ica Infantum  —  Splenic  Anaemia  —  Leukaemia  — 
Chloroma  —  Glandular  Affections  —  Glandular 
Fever  —  Lymphosarcoma  —  Lymphadenoma  — 
The  Thymus  —  The  Status  Lymphaticus    - 


XLIV. 


503 


Disorders  op  the  Blood  and  Lymph. — Urticaria — 

Erythema  Nodosum  —  Purpura  —  Haemophilia —     532 


Section    VIII. 

THE    URO-GENITAL    SYSTEM. 

XLV.  The  Urinary  System. — The  Urine  —  Normal  and 
Abnormal  Constituents  —  Albuminuria  — 
Haematuria  —  Haemoglobinuria  —  Micturition  — 
Diabetes  Insipidus  —  Enuresis  —  Affections  of 
the   Bladder        -  -         -     546 

XLVI.  Diseases  of  the  Kidneys. — Malformations — Mov- 
able Kidney  —  Cystic  Disease  —  Hydrone- 
phrosis —  Nephritis,  acute  and  chronic  —  Acute 
Pyelitis  —  Calculus  —  Tuberculous  Kidney  — 
New  Growths  -         -  ...     571 

XLVII.  The  Genital  System. — Affections  of  the  Male 
Genitals  —  Malformations  —  The  Penis  —  Cir- 
cumcision —  The  Urethra  —  Testes  —  The 
Mammae  —  The  Female  Genitals  —  Vulvo- 
vaginitis —  The  Vagina,  Uterus  and  Ovaries  — 
Masturbation  —  Menstruation  —  Pubertv  -         -     591 


Section    IX. 

THE    NERVOUS    SYSTEM. 

XLVIII.  The  Nervous  System. — Peculiarities  —  Examination 
— Reflexes  and  Special  Signs  of  Disease — Cere- 
brospinal Fluid — Electricity — Classification  of 
Diseases  _______     512 


XIV. 


Table  of  Contents. 


CHAPTER 


PAGE 


XLIX.  Malformations  of  the  Nervous  System. — Cranial 
Deformities  —  Cranial  and  Cerebrospinal 
Defects  —  Spina  Bifida  —  Cerebral  Malfor- 
mations —  Macrocephalus  —  Microcephalus  — 
Hydrocephalus — Porencephalia — Syringomyelia  -     623 

L.  Meningitis.— Purulent  —  Cerebrospinal ;  epidemic 
and  sporadic  —  Post-basic  —  Tuberculous  — 
Syphilitic — Pachymeningitis        -  642 


LI.  Cerebral  and  Cerebellar  Degenerations. — 
Agenesis  Corticalis  —  Cerebral  Spastic  Paralysis 
— Infantile  Cerebral  Degeneration  —  Amaurotic 
Family  Idiocy  —  General  Paralysis  —  Cerebellar 
Ataxia  —  Auto-intoxications      - 


671 


LII.  Vascular  Affections,  Tumours  and  Abscess.— 
Concussion  —  Intracranial  Haemorrhage  — 
Thrombosis  —  Embolism  —  Cerebral  and  Cere- 
bellar  Tumours   and   Abscess     -  687 


LIU.     Polioencephalitis  and  Poliomyelitis 


697 


LIV.  The  Spinal  Cord  and  the  Nerves. — Myelitis  — 
Friedreich's  Disease  —  Tabes  Dorsalis  —  Insular 
Sclerosis  —  Paralysis  Agitans  —  Tumours  — 
Birth  Palsy  —  Pressure  Paralysis  —  Peripheral 
and  Cranial  Nerves  —  The  Sympathetic  Ner- 
vous Svstem  ------ 


713 


LV .  The  Muscular  Atrophies. — Werdnig- Hoffmann  Type 
— Peroneal  Atrophy — Pseudo-hypertrophic  Para- 
lysis— Facial  Type — Erb's  Juvenile  Type — 
Amyotonia  Congenita  -----     725 

LVL  Spasmodic  Functional  Neuroses. — Convulsions — 
Epilepsy  —  Tetany  —  Laryngospasm  —  Myo- 
clonus —  Habit  Spasm  —  Tics  —  Nodding 
Spasm  —  Head  Banging  —  Nystagmus       -         -     735 

LYII.  Non-Spasmodic  Functional  Neuroses. — Headache 
— Migraine  —  Disorders  of  Sleep  —  Nightmare 
—  Somnambulism  —  Pavor  Nocturnus  —  Pavor 
Diurnus       --------     761 


LVIII.  Disorders  of  the  Higher  Faculties. — Neurotic 
Children  —  Precocity  —  Neurasthenia  —  Psy- 
chasthenia  —  Hysteria  —  Mental  Deficiency  — 
Mongolism  —  Insanity  —  Speech  Defects  — 
Deaf-Mutism  —  Word-Deafness  —  Word-Blind- 
ness —  Idioglossia  —  Stammering      - 


772 


Table  of   Contents. 


Section    X. 
THE    SKELETAL    SYSTEM. 

CHAPTER  PAGE 

LIX.     The     Muscles,     Bones,     and     Joints. — Muscular 

Defects  —  Myositis  —  Myositis  Ossificans  — 
Torticollis  —  Lateral  Curvature  —  Sprengel's 
Deformity  —  Club-foot  —  Osteomyelitis  —  Dis- 
locations —  Pulled  Elbow  —  Arthritis  — 
Rheumatoid  Arthritis  —  Pulmonary  Osteo- 
arthropathy -  -     798 


Section    XI. 

INFECTIVE    DISORDERS. 

LX.     Rheumatic  Fever  and  Chorea       -  -     823 

LXI.  Tuberculosis. — The  Bacillus  —  Mode  of  Infection 
—  Age  Incidence  —  Varieties  — -  Miliary  or 
General  Tuberculosis  —  Tuberculous  Broncho- 
pneumonia and  Pneumonia  —  Chronic  Phthisis-     844 

LXII.  Syphilis  :   Acquired  and  Congenital  -                 -  864 

LXIII.  Diphtheria  -  884 

LXIV.  Influenza  -                 -  906 

LXV.  Typhoid  and  Paratyphoid  Fever  -  -  911 

LXVL  Scarlatina. — Fourth  Disease  -  923 

LXVII.     German     Measles — Measles — Erythema     Infec- 

tiosum  -------     941 

LXVIII.     Varicella — Vaccinia — Variola  v    -  -     951 

LXIX.     Pertussis  -     961 

LXX.     Mumps — Pancreatitis      ------     971 

Section    XII. 

THE    SPECIAL    SENSE    ORGANS. 

LXXI.  The  Eye. — Blepharitis  —  Styes  —  Conjunctivitis  — 
Phlyctenules  —  Trachoma  —  The  Lachrymal 
Apparatus  —  The  Ocular  Muscles  —  The  Eye- 
ball —  Buphthalmos  —  Keratomalacia  — 
Nyctalopia  —  Retinitis  pigmentosa  —  Glioma  — 
Amblyopia  -------     975 


xvi.  Table  of   Contents. 

CHAPTER  PAGE 

LXXII.  The  Ear. — Hearing  —  Congenital  Defects  —  Affec- 
tions of  the  External  Ear  —  Foreign  Bodies 
—  Otitis  Media  —  Earache  —  Otorrhcea  — 
Mastoiditis  -  -     987 

LXXIII.  The  Skin. — Dermatotherapy  —  Intertrigo  —  Ery- 
thema —  Seborrhcea  —  Eczema  —  Psoriasis  — 
Scleroderma  —  Corns  —  Warts  —  Molhiscum  — 
Lichen  —  Alopecia  —  Sudamina  —  Strophulus  — 
Acne  —  Boils  —  Impetigo  Contagiosa  —  Ec- 
thyma —  Pemphigus  —  Herpes  —  Tuberculous 
Affections.  Parasitic  Affections. — Ringworm — 
Tinea  Tonsurans  — ■  Favus  —  Insect  Bites  — 
Harvest  Bugs  —  Pediculosis  —  Scabies  — 
Creeping    Larvfe         ------     999 


Chapter  I. 

INTRODUCTORY. 

Definitions — The  Examination  of  Children — Special  Features  of   Disease 
in  Children — Growth  and  Development. 

The  field  of  study  of  disease  in  children  covers  in  some  respects  a  more 
extensive  area  than  in  the  case  of  adults,  while  in  others  its  boundaries  are 
more  strictly  defined.  Inflammatory  and  infective  disorders  are  widely 
distributed  and  more  virulent  in  action,  and  the  affections  dependent 
on  an  endogenous  failure  of  nutrition,  or  abiotrophy,  show  themselves 
most  frequently  in  early  life.  Disease  is  less  influenced  by  the  prolon- 
gation of  injurious  habits  of  life  and  the  degenerative  affections  due  to 
age,  changes  in  the  organs  or  environment.  Pathologicalprocesses  occur 
in  their  simplest  forms,  and  are  less  complicated. 

The  child  is  the  father  of  the  man,  but  is  by  no  means  a  miniature 
adult.  Although  there  are  comparatively  few  special  diseases  in  children, 
the  manifestations  of  disease  in  them,  and  to  a  greater  extent  in  infants, 
differ  much  from  what  is  seen  in  adults.  Diagnosis  is  not  necessarily  more 
difficult,  and  in  one  way  is  easier,  for  examination  can  be,  and  has  to  be, 
conducted  more  thoroughly.  There  is,  consequently,  less  likelihood  of 
overlooking  important  facts.  An  adult  is  apt  to  direct  attention  to  one 
particular  symptom  or  organ,  so  the  remainder  may  escape  examination. 
The  interpretation  of  nervous  symptoms  in  particular  is  difficult.  Always 
there  is  a  liability  to  misinterpret  facts  from  lack  of  acquaintance  with  the 
peculiarities  of  illness  in  early  life. 

A  thorough  knowledge  of  disease  at  this  period  implies  a  wider 
appreciation  of  the  problems  of  life  and  pathology  than  is  necessary  for 
those  whose  work  is  mainly  among  adults.  In  the  one  case  we  have  to 
deal  with  life  in  the  making,  in  the  other  with  the  finished  product,  by  no 
means  a  perfect  work  of  art.  Most  affections  of  later  life  are  seen  at  some 
time  or  other  in  children  and,  in  addition,  a  certain  number  incompatible 
with  prolongation  of  life. 

It  is  essential  that  a  special  knowledge  of  diseases  in  early  life  should  be 
accompanied  by  a  sound  practical  acquaintance  with  those  of  later  life, 
for  the  child  grows  into  the  adult,  and  the  life  of  the  adult  constantly 
depends  on  the  proper  management  of  the  child  in  its  earliest. years.  - 

B 


2  Chapter  I. 

Definitions. — The  period  of  infancy  terminates  at  the  completion 
of  the  first  dentition,  roughly  about  the  middle  of  the  third  year  of  life. 
This  can  be  subdivided  into  three  different  stages.  During  the  first  week 
the  child  may  be  spoken  of  as  the  "  Newborn."  Strictly  speaking,  a  new- 
born child  enters  the  world  at  the  end  of  the  fortieth  week  of  pregnancy. 
Born  before  that  date  it  is  spoken  of  as  premature,  and  according  to  the 
degree  of  prematurity  it  requires  special  treatment.  It  passes  from  an 
equable  temperature  and  a  watery  bed  into  a  world  where  the  temperature 
is  variable  and  exposure  to  injury  constantly  liable  to  occur.  The  change 
is  enormous.  During  the  first  fortnight  the  newborn  may  suffer  from 
effects  of  the  confinement,  and  these  effects  may  be  prolonged  or  even 
permanent.  Thus,  it  may  be  born  asphyxiated,  due  to  strangulation  by 
the  cord  ;  or  the  lungs  may  be  unexpanded  (atelectasis)  ;  or  it  may  have 
a  cephal-hamiatonia  or  tumour  of  the  sterno-mastoid ;  or  it  may  exhibit 
one  or  other  of  the  birth  palsies ;  or  suffer  with  ophthalmia  or  from  septic 
infection.  During  this  period  the  alimentation  of  the  child  undergoes  an 
abrupt  change.  From  dependence  for  food  on  the  maternal  blood  supply, 
it  suddenly  is  compelled  to  live  upon  a  different  kind  of  food  introduced  into 
an  untrained  stomach.  Bad  feeding,  especially  the  giving  of  artificial 
foods  during  the  first  few  days  of  life,  may  upset  digestion  and  assimilation 
to  such  an  extent  as  to  prove  fatal. 

Up  to  the  end  of  the  ninth  month  the  child  may  be  spoken  of  as  the 
"  Suckling  "  or  the  "  Baby  "  ;  the  term  "  Infant  "  being  reserved  for  the 
subsequent  period  up  to  the  end  of  the  middle  of  the  third  year.  Some 
writers  use  the  term  premiere  enfance  to  mean  the  period  before  the 
eruption  of  the  milk  teeth  begins,  and  others  use  it  to  denote  the  whole 
of  the  first  year.  During  this  period  life  is  mainly  vegetative,  and  the 
reflex  functions  predominate.  This  is  especially  so  during  the  first  few 
months.  Growth  is  very  rapid,  and  great  strain  is  thrown  on  digestion 
and  metabolism.  The  result  is  that  many  of  the  affections  of  the  first 
year  are  due  to  dietetic  errors,  which  lead  to  disorders  of  digestion, 
marasmus,  scurvy,  and  rickets. 

It  is  during  later  infancy,  after  the  suckling  period,  that  the  effect  of 
bad  feeding  on  the  osseous  and  muscular  systems  is  most  marked;  the 
deformities  due  to  rickets  developing  when  the  child  begins  to  crawl,  stand, 
.and  walk. 

The  name  "  Childhood,"  or  seconde  enfance,  is  sometimes  used  for 
the  period  extending  from  the  commencement  of  the  first  to  that  of  the 
second  dentition.  It  is  preferable  to  use  the  term  "  Early  Childhood  " 
to  cover  the  period  from  the  end  of  the  first  to  the  commencement  of  the 
second  dentition.  During  this  stage  growth  is  very  active,  and  the 
dependence  on  digestion  and  assimilation  very  great. 

"  Late  Childhood,"  or  Youth,  extends  from  the  onset  of  the  second 
dentition  up  to  puberty.    During  this  period  there  are  comparatively  few 


Introductory.  3 

affections    peculiar   to    children,    beyond    those    dependent   upon    undue 
strain  on  the  nervous  system  by  education. 

"  Adolescence  "  commences  with  puberty,  at  about  twelve  to  fourteen 
years  of  age,  and  ends  about  the  eighteenth  year. 

The  Examination  of  Children. — It  is  of  little  value  spending  much  time 
on  the  details  of  the  mode  of  examination  of  the  very  young.  There  are 
many  methods  equally  satisfactory  in  the  hands  of  those  who  adopt 
them.  Examination  must  be  much  less  prolonged  than  in  adults,  and 
great  reliance  has  to  be  placed  on  objective  signs.  An  important  point  to 
remember  is  that  a  child  is  a  young  animal,  nervous,  on  the  watch,  and  very 
easily  startled  or  frightened.  Anyone  who,  unaided,  has  succeeded  in  hal- 
tering a  foal  for  the  first  time,  will  understand  how  to  undertake  the 
examination  of  a  child.  The  chief  difficulties  arise  from  the  liability  to 
fright,  crying,  and  struggling,  and  from  the  inability  to  describe  and 
localize  pain  and  other  symptoms.  Counterbalancing  advantages  are  the 
ease  with  which  the  child  can  be  stripped  and  completely  overhauled, 
the  ease  with  which  it  can  be  moved  about  during  examination,  and  the 
absence  of  prevarication. 

A  child  is  distrustful  of  strangers,  still  more  so  if  the  doctor  has  been 
held  up  as  a  bogey,  instead  of  the  child's  best  friend,  or  if  a  previous  visit 
to  a  dentist  has  caused  the  infliction  of  pain.  Never  look  a  baby  in  the 
eyes,  although  inspection  is  of  chief  importance.  Children,  even  babies, 
like  animals,  intensely  dislike  being  stared  at.  On  entering  the  sick  room, 
or  if  the  child  is  brought  into  the  consulting  room,  it  is  rarely  advisable 
to  try  at  once  to  make  friends.  First  talk  to  the  mother  or  nurse  and 
learn  the  history  of  the  present  and  previous  illnesses,  the  number  of 
children,  and  where  the  patient  comes  in  the  family ;  the  number  and 
health  of  those  living ;  the  causes  of  death  of  any  which  are  dead  ;  the 
mother's  health  during  pregnancy ;  the  nature  of  the  confinement,  and 
of  any  difficulties  or  abnormalities  at  birth  ;  the  number  of  miscarriages, 
and  the  mode  of  feeding.  Inquire  as  to  a  history  of  asphyxia  or  fits  at 
birth,  the  weight,  the  rate  of  growth,  the  date  of  teething,  sitting  up, 
walking,  talking,  etc.  In  the  history  of  past  ailments,  inquire  more 
particularly  as  to  snuffles,  rashes,  bronchitis,  vomiting  and  diarrhoea, 
infectious  disease,  and  ear  and  throat  troubles.  It  is  much  better  to 
make  such  inquiries  before  investigating  the  particular  illness,  or  the 
parent  may  assume  that  you  are  trying  to  ascribe  its  causation  to  something 
in  the  family  or  past  history.  Ready  as  a  parent  may  be  to  transmit  disease 
to  the  child,  there  is  a  natural  objection  to  taking  the  blame  thereof,  and 
it  may  be  both  inadvisable  and  unnecessarily  unkind  even  to  suggest  its 
possibility.  Heredity  is,  however,  an  important  factor  in  so  many  diseases 
that  the  family  history  should  not  be  neglected.  The  terms  used  must  be 
analysed,  for  such  expressions  as  decline,  consumption  of  the  lungs  or 
bowels,  nervous  disease,  etc.,  have  varied  meanings. 


4  Chapter  I. 

It  is  equally  important  to  pay  serious  attention  to  the  history  of  the 
illness  given  by  the  mother  or  attendant,  noting  especially  what  has  led 
to  medical  advice  being  sought,  even  though  it  involves  delay,  repetition, 
and  garrulity.  The  baby  cannot  talk,  a  child  may  be  able  to,  but  is  quite 
incompetent  to  describe  symptoms  or  to  locate  pain  with  trustworthy 
accuracy.  An  observant  mother  or  nurse  can  give  valuable  information, 
which  must  be  carefully  weighed,  for  stress  is  constantly  laid  on  the  trivial 
features  to  the  neglect  of  the  serious  points  in  the  case.  Much  importance 
should  be  attached  to  her  opinion  of  the  progress  of  the  illness.  Ascertain 
the  date  of  onset,  or  when  the  child  last  seemed  quite  well,  and  the  state  of 
appetite,  digestion,  sleep,  irritability,  languor,  and  debility.  Personally 
examine  urine  and  faoces,  and  do  not  trust  even  a  trained  nurse's  descrip- 
tion. The  diseases  of  infancy  are  comparable  to  those  of  animals,  for  in 
each  case  we  are  dependent  on  the  observation  of  onlookers,  and  on  physical 
examination,  and  are  neither  assisted  nor  deceived  by  subjective  symptoms. 
The  character  of  the  cry  may  indicate  discomfort,  pain,  hunger,  indigestion, 
weakness,  temper,  or  i  fc  may  be  due  to  mere  habit. 

It  is  of  great  assistance  if  the  child  is  stripped  and  wrapped  in  a 
blanket,  or  is  in  bed  before  the  doctor  enters  the  room,  for  the  removal 
of  the  clothes  at  an  unusual  time  and  in  the  presence  of  a  stranger  often 
leads  to  distress  and  temper  in  even  good  children.  No  examination  is 
complete  without  stripping.  If  the  child  is  not  too  ill,  examine  it  on  the 
nurse's  knee  rather  than  in  bed,  for  the  child  feels  safer  in  a  sitting  posture. 
While  in  the  room  and  obtaining  the  history  the  doctor  should  not  sit 
close  to  and  stare  at  the  child,  but  by  occasional  glances  can  acquire  some 
idea  of  its  expression  and  general  appearance,  and  can  say  a  few  words 
to  it  or  indulge  in  trivial  play.  With  gentleness  and  tact  it  is  almost  always 
possible  to  obtain  the  confidence  of  any  child,  provided  all  movements  are 
unhurried,  patience  is  unlimited,  and  the  cerebral  state  is  normal. 

Note  the  size  and  shape  of  the  head,  the  degree  of  interest  in  surround- 
ings and  toys,  and  the  facial  expression  when  not  masked  by  emotion.  It 
indicates  how  the  child  is  feeling  and  is  expressive,  for  the  furrows  of  age 
are  absent.  The  facies  of  disease  is  only  learnt  by  observation  and  much 
practice.  Facial  diagnosis  is  of  assistance,  but  must  not  alone  be  relied 
upon.  To  the  expert  the  location  of  the  disease  in  the  cranial  cavity, 
respiratory  organs,  heart  or  abdomen  is  often  clearly  written  on  the  face. 
Thus  the  head  may  be  retracted  in  simple  meningitis,  the  expression  dull 
and  vacant  in  tuberculous  meningitis,  the  face  drawn  and  lined  in  abdominal 
disease,  the  mouth  open  in  the  presence  of  adenoids,  and  so  on.  The 
appearance  of  impending  death  is  indicated  by  the  Facies  Hippocratica, 
and  that  of  acute  diarrhoea  or  acute  nephritis  is  also  characteristic.  On 
simple  observation  one  may  note  the  flushed  face  and  bright  eyes  of  fever  ; 
hurried  respiration,  dusky  complexion  and  blue  lips  of  pulmonary  and 
some  cardiac  affections  ;    or  that  the  hand  is  frequently  raised  to  the  head 


Introductory.  5 

or  ear,  because  of  headache  or  earache.  Simple  inspection  affords  infor- 
mation as  to  the  mental  condition  of  the  child,  cretinism,  infantile  myxce- 
dema,  idiocy,  mongolism,  or  congenital  syphilis.  Note  the  presence  of 
squint,  the  state  of  the  pupils  and  eyes,  the  response  to  light,  and  mucus 
on  the  cornea  ;   nasal  discharge  ;  state  of  the  tongue  and  mouth. 

Normal  peculiarities  of  configuration  must  not  be  mistaken  for  signs 
of  disease.  Up  to  the  age  of  three  years  the  head  is  relatively  large.  For 
many  years  the  abdomen  is  prominent  and  the  chest  is  round,  not  acquiring 
the  oval  shape  for  some  time.  Malformations  of  the  chest,  a  bulging 
precordium,  and  venous  dilatation  may  be  obvious  on  inspection. 

If  the  child  is  asleep,  note  its  posture,  facial  expression,  character 
of  the  sleep,  and  count  the  pulse  and  respirations.  The  pulse  is  often 
irregular  during  sleep.  While  awake  it  is  of  comparatively  little  value  as  a 
sign  of  disease,  unless  it  is  abnormally  infrequent,  and  intermittent  or 
irregular.  Blood  pressure  is  low.  Breathing  is  often  strange  to  the 
inexpert.  A  child  may  hold  its  breath  for  an  extraordinary  long  time,  or 
there  may  be  inversion  of  the  respiratory  rhythm.  The  rate  of  breathing 
may  be  counted  if  the  child  is  not  excited,  and  is  often  very  rapid  in  fever. 
Retraction  of  the  epigastrium  and  lower  ribs  indicates  respiratory 
obstruction.  Puerile  breathing  may  be  mistaken  for  bronchial  breathing, 
unless  the  two  sides  are  compared,  and  bronchial  breathing  is  normally 
heard  in  certain  situations.  It  is  quite  a  common  mistake  to  diagnose 
bronchial  breathing  on  one  side,  when  the  condition  is  really  one  of 
exaggerated  puerile  breathing,  with  enfeebled  breath  sounds  on  the 
opposite  side.  Rales  are  liable  to  be  mistaken  for  friction,  and  abnormal 
sounds  are  readily  transmitted  to  the  opposite  side. 

Percussion  must  be  light  for  heavy  percussion  hurts  the  child  and 
affords  inaccurate  information,  because  of  the  conductivity  of  the  chest. 
Percuss  in  the  same  phase  of  respiration  or  one  side  may  sound  less  resonant 
than  the  other.  Dulness  over  the  manubrium  may  indicate  a  large  thymus 
or  glands.  The  yielding  chest  wall  readily  permits  the  production  of 
crack-pot  sound  when  the  glottis  is  closed,  but  it  must  not  be  mistaken  for 
that  due  to  a  cavity  in  the  lung.  Collapse  of  the  lung  gives  rise  to  dulness. 
It  is  easily  produced  by  obstruction  from  secretions,  and  may  equally 
easily  disappear.    It  is  constantly  mistaken  for  pneumonic  consolidation. 

During  the  general  examination  of  the  body  it  is  important  to  note 
the  state  of  nutrition,  of  flabbiness,  undue  fatness,  anaemia,  and  the  presence 
of  rickets  or  rashes.  Palpation  should  be  conducted  with  a  warm  hand. 
It  is  well  borne  by  babies  for  they  are  accustomed  to  being  handled. 
Begin  with  the  head  and  note  the  state  of  the  fontanelles,  sutures,  bossing, 
and  craniotabes.  Examine  the  neck  for  enlarged  glands.  Note  whether 
the  skin  is  unduly  hot,  dry,  moist,  or  has  lost  elasticity.  Examine  the  chest 
for  beading  of  the  ribs,  and  take  special  care  to  locate  the  apex  of  the 
heart,  the  presence  of  any  abnormal  pulsation  to  the  right  of  the  sternum 


6  Chapter  I. 

or  in  the  epigastrium,  and  note  the  force  of  the  cardiac  impulse  and  the 
presence  of  thrills.  Note  whether  there  is  any  respiratory  fremitus.  Some- 
times coarse  friction  can  be  felt.  Gentle  percussion  may  be  then  tried,  but 
should  be  postponed  until  after  auscultation  if  the  child  is  inclined  to  cry. 
Be  sure  that  the  child  is  sitting  straight,  and  that  the  sound  is  not  deadened 
by  any  support. 

For  auscultation  use  a  binaural  stethoscope  with  a  short  vulcanite 
reversible  chest  piece  of  different  sizes  at  either  end.  A  soft  rubber  cover 
on  the  mouthpiece  is  useful  to  secure  proper  approximation  to  the  chest 
wall  in  thin  or  wasted  infants.  A  wooden  stethoscope  is  often  preferable, 
but  it  must  be  carefully  held  in  the  hand  so  that  there  is  little  pressure  on 
the  chest  wall.  If  a  metal  stethoscope  is  used  the  end  must  be  warm. 
Direct  auscultation  of  the  back  is  often  less  alarming  and  more  satisfactory. 
Occasionally  it  is  useful  for  the  front  of  the  chest.  The  best  position  for 
the  examination  of  the  front  of  the  chest  is  while  the  child  is  sitting  up  or  on 
the  back.  For  examining  the  back  it  should  sit  up  or  rest  with  the  face  over 
the  nurse's  shoulder.  A  child  is  rarely  frightened  of  the  stethoscope  if 
allowed  to  play  with  it  first,  if  the  chest  piece  is  warm,  and  if  no  undue 
pressure  is  exerted.  It  is  generally  best  to  listen  to  the  back  first  for 
evidence  of  fluid  and  crepitations.  In  delicate  and  wasted  infants,  and  in 
collapse,  it  is  sometimes  necessary  to  make  the  child  cry  in  order  to  get 
it  to  breathe  sufficiently  deeply.  Without  such  a  precaution  patches  of 
collapse  and  consolidation,  and  intrapulmonary  crepitations  may  be 
missed.  Listen  to  the  heart  sounds  and  remember  that  up  to  the  fourth 
year  the  pulmonary  second  sound  is  normally  accentuated. 

While  examining  the  chest  in  a  sitting  posture  the  temperature  can 
be  taken  in  the  groin.  Palpate  the  abdomen  in  a  sitting  posture,  and  at 
first  while  covered  up,  and  examine  for  enlargement  of  the  liver  or  spleen, 
normal  kidneys,  and  abnormal  glands.  The  softness  and  smallness  of 
the  body  lends  itself  to  full  examination  by  this  method.  Note  specially 
the  condition  of  the  navel,  and  the  presence  of  an  adherent  prepuce  or 
undescended  testes.  Examine  the  limbs  and  note  whether  they  are  moved 
normally,  are  paralysed,  or  tender.  Test  the  reflexes.  Finally,  look  at  the 
lips,  tongue,  teeth,  gums,  palate,  and  throat.  To  make  an  unwilling  child 
open  the  mouth,  hold  the  nostrils  closed  and  press  the  upper  lip  over  the 
front  teeth,  or  the  cheek  between  the  gums,  or  introduce  the  handle  of 
a  teaspoon  to  the  back  of  the  throat  until  it  retches. 

Special  Features  of  Disease  in  Children. — The  nervous  system  is  abnor- 
mally irritable  and  susceptible  to  irritation,  reflex  and  direct.  General 
convulsions  and  local  spasms,  e.g.,  laryngospasm  and  carpo-pedal  con- 
tractions, depend  upon  this.  Convulsions  are  often  said  to  take  the  place 
of  the  rigors  which  occur  in  adults  at  the  onset  of  many  diseases.  Occasion- 
ally this  is  so,  but  more  commonly  acute  diseases  are  ushered  in  by  vomiting. 
Croupous  pneumonia  may  be  mistaken  for  meningitis  when  the  nervous 


Introductory.  7 

phenomena  markedly  predominate  and  the  signs  of  consolidation  are 
delayed.  Functional  nervous  derangement  is  common  and  especially 
apt  to  occur  in  toxaemic  cases,  with  severe  and  even  fatal  symptoms,  though 
nothing  abnormal  is  found  post  mortem. 

The  temperature  rises  easily,  and  perhaps  to  a  height  which  may  be 
alarming.  It  should  be  taken  in  the  groin  or  rectum,  and  normally  ranges 
from  98-99-5°  F.  in  babies.  The  younger  the  child  the  more  unstable 
is  the  temperature  for  the  heat-regulating  centre  is  incompletely  developed 
or  imperfectly  controlled.  A  rise  of  temperature  is  not  as  proportionately 
serious  as  in  the  adult,  nor  a  reliable  measure  of  the  severity  of  the  exciting 
cause.  More  importance  must  be  attached  to  the  general  symptoms. 
It  may  even  be  due  to  hot  bottles,  or  too  many  blankets,  and  insufficient 
ventilation.  The  pulse  and  respiration  rates  are  disproportionately 
accelerated  by  any  pyrexia. 

A  remarkable  absence  of  pain  or  complaint  of  pain  is  often  noticeable 
in  acute  tonsillar  affections  and  diphtheria.  The  generalisation  of  disease 
is  another  characteristic.  A  local  tuberculosis  is  a  most  uncommon  cause 
of  death.  Miliary  tuberculosis  is  frequent  in  infancy,  and  comparatively 
rare  in  adults.  Affections  of  the  mucous  membranes  are  widely  distributed, 
for  instance,  enteritis  associated  with  broncho-pneumonia. 

Some  diseases  are  almost  peculiar  to  children.  Many  of  these  are 
incompatible  with  life,  such  as  severe  forms  of  congenital  heart  disease 
and  amaurotic  family  idiocy.  Others  rarely  occur  except  in  children, 
viz.,  rickets,  broncho-pneumonia,  infantile  paralysis,  chorea,  and,  less 
notably,  specific  fevers.  Some  affections,  e.g.,  achondroplasia  and  mon- 
golism are  present  at  birth  and  persist  in  adults.  Many  diseases  are 
common  to  both  children  and  adults,  but  are  usually  regarded  and  described 
from  their  course  in  adults,  e.g.,  acute  rheumatism  and  typhoid  fever. 
Congenital  cardiac  bruits  are  common,  but  endocarditis  is  rare  before  the 
age  of  two  years.  Hoemic  murmurs  may  be  present  in  earliest  infancy. 
The  alimentary  and  respiratory  systems  and  the  brain  are  most  liable 
to  disease. 

From  another  point  of  view,  that  of  therapeutics,  the  child  is  a  more 
satisfactory  subject  than  the  adult.  It  has  great  reparative  powers. 
It  is  growing,  going  up,  not  down  the  hill  of  life.  Its  tissues  are  likely  to  be 
healthier,  and  to  respond  better  to  treatment.  A  child  does  not  overwork, 
has  few  mental  worries,  no  responsibilities,  and  can  be  efficiently  guarded, 
nursed,  and  controlled.  Even  in  the  matter  of  transference  from  place  to 
place,  the  advantage  is  on  the  child's  side,  for  it  can  be  easily  wrapped  up, 
carried  about,  protected  from  cold  and  draughts,  and  not  subjected  to 
anxiety  or  fatigue. 

Growth  and  Development.— Excluding  ante-natal  conditions,  and 
those  arising  from  the  act  of  birth,  the  health  and  development  of  the 
child  depend  upon  its  environment.     Under  this  are  included  those  factors 


8  Chapter  I. 

which  directly  or  indirectly  influence  and  modify  physical,  mental,  and 
moral  growth.  These  factors  are  hygienic,  i.e.,  all  that  pertains  to  air, 
exercise,  washing,  clothing,  dwellings,  and  drainage ;  dietetic  ;  and 
educational,  including  amusements.  It  is  by  these  means  that  the  physician 
mainly  influences  the  child  during  health  and  disease.  Their  relative 
importance  varies  at  different  periods  of  childhood. 

Certain  anatomical  peculiarities  depend  on  the  necessities  of  birth, 
the  passage  through  a  narrow  canal,  or  on  physiological  causes.  The 
cord  soon  shrivels  after  being  tied  ;  and  the  umbilical  vein  is  represented 
by  a  thin,  flat,  yellow  band  with  the  two  dark  tortuous  umbilical  arteries 
winding  round  it.  Around  the  base  is  a  reddened  areola,  where  separation 
shortly  takes  place.  At  birth  the  liver  is  large,  extending  from  one-half 
to  one  inch  below  the  costal  margin,  and  high  up  in  the  chest.  The  bladder 
is  usually  distended  with  urine,  and  presents  a  dull  area  above  the  pubes. 

The  head  measures  13-14  inches  in  circumference,  round  the  forehead 
and  occipital  prominence.  At  3  months  it  measures  15  inches,  and  it 
increases  by  1  inch  in  circumference  in  each  successive  3  months  up  to 
18  inches  at  1  year  of  age.  At  5  years  it  measures  20  inches.  The  anterior 
fontanelle  is  on  a  level  with  the  surrounding  bones,  or  a  little  depressed  at 
first.  It  is  diamond-shaped,  and  varies  in  size,  being  about  h  in.  wide 
and  |  in.  long.  The  posterior  fontanelle  is  small,  triangular,  and  at 
birth  overlapped  by  the  bones.  In  rare  instances  the  fontanelles  and  sutures 
are  ossified  at  birth,  and  interfere  with  labour. 

The  face  is  remarkably  small  in  comparison  with  the  cranium.  The 
nose,  like  that  of  a  monkey,  has  no  bridge  to  it.  The  naso-pharynx  and 
posterior  nares  are  small,  so  that  slight  causes  may  produce  dangerous 
obstruction.  The  Eustachian  tube  runs  nearly  horizontally.  The  external 
auditory  meatus  is  placed  more  anteriorly  than  in  the  adult.  The  jaws 
are  small  and  rudimentary.  The  gums  are  composed  of  fibrous  tissue, 
covered  by  mucous  membrane,  and  do  not  meet. 

The  head  and  face  may  be  extraordinarily  misshapen  from  pressure 
at  birth.  The  cranium  may  be  elongated,  flattened,  and  bulge  unequally, 
but  the  normal  shape  is  gradually  acquired  as  the  brain  and  skull  grow. 
Deformity  is  rarely  permanent,  though  a  certain  degree  of  asymmetry  is 
constant. 

At  birth  the  child  is  covered  with  a  secretion  of  sebaceous  matter, 
called  the  vernix  caseosa.  This  may  even  be  absent  or  vary  in  amount,  up 
to  a  covering  so  thick  and  impenetrable  as  to  prove  fatal.  It  is  washed  off 
gently  in  the  first  bath,  leaving  the  skin  of  a  healthy  brick-red  colour. 
The  head  looks  unduly  large,  may  be  bald  or  covered  with  fair  hair,  and 
occasionally  dark  hair,  an  inch  or  two  in  length.  The  eyes  are  dull,  half 
open  and  expressionless.  The  abdomen  is  prominent  on  account  of  the 
large  size  of  the  liver.  The  limbs  are  smooth  and  rounded,  the  arms  being 
better  developed  and  more  muscular  than  the  legs.     The  grasp  of  the 


Introductory.  9 

hands  is  strong,  and  the  child  can  usually  support  its  weight  by  its  grasp 
on  the  two  fingers. 

Certain  milestones  on  the  road  of  growth  and  development  should  be 
noted  as  indications  of  normal  childhood.  The  fontanelle  is  closed  at 
18-24  months  of  age,  often  earlier.  Early  closure  may  occur  as  a  sign  of 
microcephaly.  Delay  may  indicate  rickets,  hydrocephalus,  or  cleido- 
cranial dysostosis.    The  order  of  eruption  of  the  teeth  will  be  discussed  later. 

Sucking  is  an  instinctive  reflex,  and  so  is  the  grasp  of  the  hands  in 
the  newborn.  Lack  of  this  instinctive  grasp  indicates  mental  or  physical 
defect.  The  earliest  muscular  movements  are  spontaneous  or  reflex,  aimless 
movements  of  the  eyes,  head,  face,  neck,  and  limbs.  As  a  rough  guide 
it  may  be  stated  that  the  child  can  hold  its  head  up  at  3-4  months,  and 
makes  efforts  to  grasp  at  objects  in  an  inco-ordinate  manner.  It  can  sit 
up  at  6-9  months,  crawl  and  stand  at  9-12  months,  walk  at  12-18 
months,  and  talk  at  18-24  months  of  age.  Children  vary  much  in  the 
mode  of  acquirement  of  these  various  functions.  The  majority  crawl 
on  hands  and  knees  or  feet  before  learning  to  walk.  A  few  never  crawl, 
but  propel  themselves  rapidly  about  the  floor  on  the  buttocks.  At  first 
the  child  raises  itself  by  grasping  some  object  with  the  hands,  and  is  able 
to  stand  with  the  aid  of  the  hands  and  arms.  In  the  next  stage  it  is  able 
to  stand  unassisted.  Then  for  a  month  to  6  weeks  it  stumbles  about  with 
an  uncertain,  ataxic  gait,  using  all  available  support.  In  the  next  stage, 
lasting  2  or  3  weeks,  it  tries  to  walk  without  supports,  sways  the  trunk 
from  side  to  side  and  waves  its  arms  wildly  about  in  order  to  maintain  its 
balance,  just  like  a  person  learning  to  skate.  Painful  falls  at  this  period 
may  frighten  the  child  and  delay  its  progress. 

All  these  functions  vary  much  in  their  time  of  development,  partly 
according  to  family  peculiarities,  partly  in  accordance  with  the  weight  of 
the  child  and  the  mental  activity.  Premature  and  marasmic  infants  are 
backward.  Marked  delay  often  leads  to  medical  advice  being  sought.  In 
some  cases  the  power  has  not  been  acquired,  in  others  it  has  been  lost 
although  once  developed.  It  is  chiefly  for  delay  in  learning  to  walk,  or 
because  the  child  has  "  gone  off  its  legs,"  that  the  physician  is  called  in. 
Hypertonicity  of  the  muscles  is  common  in  the  very  young,  and  may 
suggest  spastic  diplegia.    It  disappears. 

Inability  to  support  the  head  at  a  proper  age  is  very  suggestive  of 
mental  defect  or  cretinism.  Hypotonia  occurs  in  imbeciles,  especially 
mongols,  and  also  in  rickets.  A  child  unable  to  walk  at  18  months  is 
generally  rachitic,  paralysed,  or  idiotic. 

Fat,  heavy  children  should  never  be  encouraged  to  stand  or  walk. 
It  is  even  advisable  that  they  should  be  discouraged,  especially  if  there  is 
the  least  indication  of  rickets.  If  not,  bending  of  the  bones  is  apt  to  ensue. 
A  child  who  has  not  learnt  to  walk,  should  be  examined  for  affections  of 
supporting  structures  and  the  neuro-muscular  system.     The  defect  may 


10  Chapter  I. 

be  due  to  the  loss  of  muscular  tone  and  lax  ligaments  of  rickets  ;  congenital 
dislocation  of  the  hips  ;  myatonia  congenita,  a  condition  of  idiopathic 
muscular  flaccidity  in  which  the  knee  jerks  are  present ;  cerebral  or  spinal 
paralysis,  mental  defects,  spina  bifida,  poliomyelitis,  post-pertussal 
hsematomyelia  or  cretinism. 

The  child  that  has  "  gone  off  its  legs  "  must  be  examined  for  evidence 
of  infantile  paralysis,  scurvy,  hip  disease,  rheumatism,  epiphysitis  or 
osteomyelitis.  Often  the  loss  of  function  is  due  to  malnutrition  or  weakness, 
the  result  of  acute  illness,  the  art  having  been  forgotten.  Sometimes  the 
loss  of  function  is  associated  with  an  apparent  paralysis  due  to  pain. 
The  epiphysitis  of  congenital  syphilis  occurs  so  early  in  life,  usually  a 
few  weeks  after  birth  and  rarely  after  six  months,  that  it  does  not  affect 
these  functions  to  a  very  conspicuous  extent,  but  the  immobility  of  the 
limb  is  found  if  looked  for. 

The  circumference  of  the  thorax  is  about  equal  to  that  of  the  head  in 
the  second  year  of  life,  and  should  exceed  it  in  the  third  year.  Lack  of 
development  of  the  chest  may  mean  lung  mischief. 

Weight.— Increase  in  weight  is  a  good  indication  of  satisfactory 
progress.  A  baby  should  be  weighed  daily  during  the  first  month,  and 
once  or  twice  a  week  in  the  succeeding  9  months.  The  same  scales  should 
be  used  on  each  occasion,  such  as  those  made  by  Messrs.  Avery,  or  an 
elongated  basket  tray  supported  on  a  recording  dial  and  weighing  up  to 
281bs.  by  ounces.  The  absence  of  gain  in  weight  or  an  actual  loss  in  weight 
may  indicate  defects  in  the  food  supply,  some  disturbing  factor,  such 
as  teething,  rapid  growth,  or  the  onset  of  some  morbid  process.  The  most 
common  causes  during  infancy  are  dietetic  defects,  insufficient  clothing,, 
cold  weather,  teething,  dyspepsia,  and  diarrhoea.  Increase  in  weight 
should  be  accompanied  by  progressive  increase  in  height.  Apart  from 
this  it  may  be  due  to  the  mere  deposition  of  fat,  as  in  a  rickety  infant 
fed  on  condensed  milk.  Occasionally  it  is  due  to  dropsical  effusions  or 
simple  oedema.  A  temporary  gain  in  weight  may  occur  in  hospital  patients 
although  suffering  from  serious  disease,  because  of  the  better  quality  of  the 
food,  regular  feeding,  warmth  and  nursing.  The  weekly  weighing  should 
take  place  on  a  fixed  day,  such  as  Sunday,  and  at  the  same  hour  of  the  day. 
The  weight  may  be  as  much  as  5-7  oz.  less  in  the  morning  than  in  the 
evening  in  an  infant  of  4-6  months  of  age,  because  more  food  is  taken 
during  the  day  time.  The  child  should  be  washed,  wrapped  in  a  warm 
flannel  and  then  weighed,  the  weight  of  the  flannel  being  subtracted 
subsequently.  Suitable  charts  for  recording  the  weight  on  can  be  obtained 
from  Messrs.  J.  &  A.  Churchill. 

The  weight  of  a  child  at  birth  varies  considerably,  3,000  grammes 
or  6£  lbs.  may  be  taken  as  a  fair  average,  but  it  is  often  exceeded,  and 
anything  from  6-9  lbs.  may  be  regarded  as  normal.  Boys  are  generally 
heavier  than  girls,  and  firstborns  smaller  than  other  children.    The  largest 


Introductory.  1 1 

babies  are  generally  those  of  women  from  25-30  years  of  age.  Giant 
fcetuses  have  been  reported  weighing  from  14  up  to  24£  lbs.  They  are 
born  dead.  The  size  of  the  normal  baby  depends  chiefly  on  the  physical 
health  and  build  of  the  mother  ;  her  food  supply,  amount  of  rest,  and 
freedom  from  worry  during  pregnancy  ;  and  the  period  of  gestation.  A 
limited  diet  at  this  period  diminishes  the  size  of  the  child,  lessens  its  vitality, 
and  makes  labour  more  easy. 

During  the  first  3  days  of  life  weight  is  lost  on  account  of  the  passage 
of  urine  and  meconium,  evaporation  of  water  from  the  skin  and  lungs,  and 
lack  of  food.  The  greatest  loss  takes  place  in  the  first  24  hours.  The 
heavier  the  babe,  the  greater  is  the  loss.  Boys  lose  less  than  girls.  The 
child  of  a  primipara  is  more  likely  to  lose  a  greater  percentage  of  its  original 
weight,  and  recover  it  less  quickly  than  the  child  of  a  multipara,  because 
the  milk  supply  is  not  so  quickly  established.  The  drying  up  and  separation 
of  the  cord  accounts  for  a  loss  of  about  f-1  oz.  The  total  loss  varies 
from  5-10  per  cent,  of  the  original  weight,  from  3-12  oz.,  generally 
averaging  7-8  oz.,  and  it  is  often  not  regained  until  the  end  of  the  second 
week.  The  initial  loss  can  be  prevented  by  utilising  a  wet  nurse  or  artificial 
feeding,  but  there  is  no  special  advantage  in  such  measures  unless  the 
infant  is  premature  and  weak. 

Subsequently  weight  may  be  regained  with  remarkable  regularity  or 
by  fits  and  starts.  Periods  of  retardation  are  followed  by  periods  of 
acceleration  in  both  breast-fed  and  artificially  fed  babies.  Speaking  generally, 
the  initial  weight  is  doubled  in  5  months,  and  trebled  in  12-15  months; 
such  results  are  often  exceeded.  The  following  table  in  a  simple  form 
fairly  well  represents  the  rate  of  gain  : — 


Birth 

..       7  lbs 

5  months 

. .     14  lbs 

15  months 

..     21  lbs 

6  years 

. .     42  lbs 

14  years 

. .     84  lbs 

All  such  figures  and  measurements  are  merely  averages,  sufficiently  near 
to  afford  evidence  as  to  whether  the  child  is  developing  at  a  more  or  less 
normal  rate.  The  rate  of  gain  is  more  or  less  proportionate  to  the  initial 
weight  of  the  infant.  Some  abnormally  small  infants  gain  weight  much 
more  rapidly  than  those  who  are  very  much  larger  at  birth.  During  the 
first  3  months  of  life  the  child  gains  5-7  oz.  per  week  ;  during  the  second 
3  months,  4-6  oz.  ;  and  during  the  third  3  months,  3-5  oz.  Sunlight 
is  beneficial  to  increase  of  growth,  and  fresh  air  is  of  importance.  The 
maximum  gain  takes  place  between  July  and  October. 

Growth  in  Length. — The  length  of  the  newborn  child  varies  according  to 
its  weight,  degree  of  development,  and  the  duration  of  gestation.  The 
measurement  in  inches  is   equivalent   to  the    lunar    month    of   gestation 


12  Chapter  I. 

multiplied  by  two.  This  gives  an  average  of  20  inches  at  term  for  a  male 
infant,  the  female  being  about  J  in.  less.  Subsequent  rate  of  growth  is 
about  |  in.  per  month  during  the  first  year.  The  length  is  doubled  in  five 
years.  Growth  takes  place  most  rapidly  during  the  early  months  of  the  year, 
from  March  up  till  the  end  of  June,  and  is  less  rapid  in  the  winter  months. 
The  yearly  increase  is  from  2-3  inches  for  many  years.  A  period  of  rapid 
growth  in  height  is  often  preceded  by  considerable  increase  in  weight,  and 
accompanied  by  retardation  of  gain  in  weight  or  even  actual  loss.  The 
two  processes  rarely  take  place  at  the  same  time,  the  body  appearing  to 
store  up  material  preparatory  to  increase  in  height.  Series  of  figures 
representing  the  weight  and  height  of  children  of  different  ages  are  of 
very  little  value.  Individual  differences  depend  upon  racial  and  family 
tendencies.  The  size  of  the  child  must  be  considered  in  relation  to  that 
of  the  parents,  and  other  children  in  the  family,  and  more  importance 
attached  to  the  relative  progress  from  month  to  month,  and  year  to  year, 
rather  than  to  the  actual  measurements  in  comparison  with  other  children. 
As  soon  as  the  period  of  infancy  is  passed,  the  rate  of  growth  may  be  so 
great  that  a  child  appears  to  be  rapidly  wasting.  Occasionally  delay  in 
growth  in  height  may  be  the  only  indication  of  thyroid  deficiency. 


Chapter  II. 

HEREDITARY    AND    ANTE-NATAL    CONDITIONS. 

Heredity — Pre-conceptional  Factors — Intra-uterine  or  Congenital  Factors 
— Mental  Impressions —  Direct  Transmission  of  Disease — Immunity — 
Treatment. 

The  child  is  the  product  of  inheritance  modified  by  environment, 
a  house  composed  of  many  bricks,  a  mosaic  of  many  ancestors.  Like  tends 
to  beget  like,  an  idea  expressed  in  the  biblical  sayings  that  "  you  cannot 
grow  grapes  from  thorns,  nor  figs  from  thistles,"  and  "the  sins  of  the 
fathers  are  visited  on  the  children  even  unto  the  third  and  fourth  genera- 
tions." The  first  quotation  indicates  true  heredity,  and  the  other  contains 
the  idea  of  the  transmission  of  acquired  characters.  It  is  evident  that  the 
scientific  study  and  care  of  children  includes  a  knowledge  of  the  factors 
which  are  liable  to  affect  them  before  birth,  and  even  before  conception. 
Healthy  infants  imply  healthy  parents,  and  healthy  conditions  during 
intra-uterine  life.  The  socialistic  statement  that  all  men  are  equal  implies 
a  profound  ignorance  of  heredity,  as  well  as  of  physiology  and  pathology. 
Yet  there  is  an  hereditary  tendency  to  health  and  to  a  normal  average. 
Sex,  family,  and  racial  peculiarities  arise  through  a  process  of  selection,  a 
survival  of  the  fittest,  or  an  inheritance  of  adaptations  and  mutations. 
A  racial  tendency  to  particular  diseases  is  sometimes  characteristic,  e.g., 
amaurotic  family  idiocy  among  the  Jews. 

In  the  consideration  of  abnormal  heredity  we  have  to  bear  in  mind  the 
occurrence  of  variations,  fluctuating  in  degree  and  kind,  and  not  breeding 
true  ;  mutations  of  any  size  and  degree,  which  are  transmitted  ;  and  the 
possibility  of  the  transmission  of  acquired  characters.  Many  of  the  lesions 
transmitted  are  omissions  in  evolution,  flaws  in  development,  and  not 
acquired  defects. 

We  must,  therefore,  investigate  the  pre-conceptional  factors,  i.e., 
heredity  ;  the  intra-uterine  or  congenital  factors,  and  their  modification 
by  the  state  of  health  and  environment  of  the  mother  during  pregnancy  ; ; 
the  natal  factors,  strictly  speaking,  those  which  affect  the  child  during  birth 
and  described  subsequently.  After  birth  the  child  is  exposed  to  all  those' 
factors  in  the  etiology  of  development  and  disease. which  are  summed  up 
under  the  name  of  environment.     It  passes  from  an  existence  in  the  dark, 


14  Chapter  II. 

almost  entirely  protected  from  violence,  surrounded  by  a  fluid  medium 
of  constant  high  temperature,  into  surroundings  of  a  totally  different 
character.  It  acquires  a  separate  existence,  and  becomes  an  individual 
with  multiple  possibilities  for  good  and  evil. 

Its  previous  existence  may  be  divided  into  three  stages  : — 

(1)  The  germinal  stage,  including  : — 

(a)  The  germ  cells,  the  ovum  and  spermatozoon,  liable  to  damage 
by  constitutional  disease  at  the  time  of  or  before  conception  ; 

(6)  The  pre-embryonic  period,  before  the  differentiation  of  the 
impregnated  ovum  has  begun,  during  which  it  is  liable  to  be 
damaged  by  morbid  agents  in  the  maternal  blood. 

(2)  The  embryonic  stage  of   5-7   weeks   during   which   the   different 

organs  are  formed    and  may  be    affected,  via   the    placental 
attachment,  after  the  third  week  of  intra-uterine  life. 

(3)  The  foetal  stage,  that  of  growth,  lasting    32-34  weeks,  but  not 

abruptly  separated  from  the  embryonic  stage. 

The  inheritance  of  disease,  etc.,  should  be  clearly  distinguished  from 
transmission.  Heredity  affects  the  germinal  period.  Malformations  and 
monstrosities  occur  in  the  embryonic  stage,  but  the  liability  to  them  may 
depend  on  hereditary  defects  in  the  germ  plasm.  Later,  the  child  is  liable 
to  the  same  diseases  as  after  birth.  Many  peculiarities  are  acquired,  arise 
de  novo,  are  due  to  extraneous  agencies.  For  instance,  deformities  may  be 
caused  by  amniotic  bands. 

Various  theories  of  heredity  have  been  advanced.  Lamarck,  in  1809, 
held  that  species  are  not  fixed,  but  are  evolved  from  earlier  and  generally 
less  organised  forms,  and  he  ascribed  the  transformation  to  the  effect 
of  use  or  disuse.  According  to  Darwin,  1850,  organisms  vary,  and  no  two 
are  alike.  They  tend  to  increase  to  the  utmost  limits  of  subsistence,  and 
in  the  struggle  for  existence  only  the  fittest  survive,  a  process  of  "  Natural 
Selection."  In  1868  he  advanced  the  theory  of  "  Pangenesis,"  according 
to  which  every  cell  of  the  body  throws  off  gemmules,  which  accumulate  in 
the  reproductive  organs  and  grow  into  similar  cells.  Neumann,  in  1884, 
put  forward  the  theory  of  "  Cellular  Continuity."  The  germ  cells  are 
separated  early  from  the  general  body  cells,  remain  unchanged,  and  are 
transmitted  directly  from  parent  to  offspring.  Weismann,  in  1885,  argued 
that  heredity  is  due  to  "  Continuity  of  the  Germ  Plasm."  He  assumed 
that  the  reproductive  cell  consists  of  two  parts  ;  one,  somatic,  from  which 
the  body  cells  are  formed ;  the  other,  reproductive,  remaining  inactive 
and  giving  rise  to  the  next  generation.  Thus  a  father  and  son  are  relatively 
brothers.  He  maintained  that  acquired  characters  are  not  transmissible. 
Hereditable  modifications  may  be  somatogenic  or  germinal  in  origin,  due 
to  a  potentiality  for  variation  dependent  on  environment.  The  germ 
plasm  is  situated  in  the  chromosomes  of  the  nucleus,  and  the  number 
of  the  chromosomes  varies  in  different  animals,  but  is  constant  in  the  same 


Hereditary    and   Ante- Natal  Conditions.  15 

species.  The  number  in  an  ovum  or  sperm  cell  is  half  that  of  a  body  cell, 
and  union  is  necessary  to  raise  the  number  to  that  of  a  body  cell.  He 
regarded  the  chromosomes  as  made  up  of  an  immense  number  of  small 
parts  or  "  determinants,"  and  the  characters  of  the  offspring  as  dependent 
on  the  relative  combinations  and  arrangements  of  these  male  and  female 
determinants.     Hence  arise  variations. 

The  most  interesting  theory  of  heredity  is  that  advocated  by  Mendel, 
and  it  has  the  great  advantage  of  being  supported  by  many  experimental 
data.  His  conclusions  are  based  on  the  results  of  experiments  on  the 
edible  pea,  in  order  to  discover  the  law  of  inheritance  in  hybrid  varieties. 
Of  two  contrasting  characters,  e.g.,  size,  colour,  shape  of  seed,  there  is 
always  one  in  each  cross  which  appears  exclusively  in  the  offspring,  and 
this  he  called  the  "  dominant,"  and  one  which  does  not  appear,  named 
by  him  the  "  recessive."  A  dominant  parent  only  produces  dominant 
"  gametes,"  and  a  recessive  produces  recessives.  Therefore,  the  offspring 
are  dominants. 

Thus. — DxR  =  D  (R),  the  recessive  being  latent. 

On  allowing  the  hybrids  to  become  self-fertilised  the  characters  of 
both  parents  appear  in  the  offspring  in  the  form  of  one  pure  dominant,  one 
pure  recessive,  and  two  impure  dominants  ;  that  is,  apparently  dominants 
but  containing  a  latent  and  unrecognisable  recessive  factor.  This  proves 
that  the  recessive  character  is  present,  though  latent,  in  the  hybrid  pro- 
duced by  the  union  of  a  dominant  and  a  recessive.  From  this  it  follows 
that  two  kinds  of  germ  cells  are  produced  by  the  hybrids,  the  parental 
characters  being  segregated  into  dominant  and  recessive  "  gametes " 
in  equal  numbers.  The  union  of  a  dominant  sperm  cell  (male  gamete) 
with  a  dominant  ovule  (female  gamete)  produces  a  pure  dominant.  A 
pure  recessive  is  due  to  the  union  of  a  recessive  with  a  recessive.  The 
impure  dominants  are  formed  by  the  union  of  a  dominant  male  or  female 
gamete  with  a  recessive  female  or  male  gamete.  The  pure  dominants  and 
recessives  are  called  "  homozygotes,"  and  the  impure  dominants  "  heterozy- 
gotes."  The  dominant  factor  is  present  in  three  out  of  four  zygotes. 
The  descent  may  be  tabulated  thus  : — 
D(R). 

MALE.    GAMETES.    FEMALE. 

D  unites  with  D  to  form  DD  Homozygote. 

D         „         ,,  R  ,,  DR  Heterozygote. 

R        .,         .,  D  .,  DR  Heterozygote. 

R         .,         ,,  R  ,,  RR  Homozygote. 

Each  gamete  contains  only  the  unsplittable  inherited  factor,  and 
only  one  of  a  contrasting  pair,  that  is,  is  pure  for  that  factor.  The  zygotes 
contain  two,  being  formed  by  the  union  of  two  gametes,  and  these  two 
characters  are  splittable,  that  is,  are  segregate  from  each  other  in  the  zygote. 
If  similar  gametes  unite  into  a  zygote,  segregation  is  into  like  gametes. 


16  Chapter  II. 

But  a  mixed  zygote,  a  heterozygote  or  hybrid,  contains  both  factors, 
and  segregates  or  splits  into  gametes  of  each  kind.  Hence,  it  is  obvious 
that  the  mating  of  hybrids  will  produce  a  certain  number  of  pure  offspring, 
which  will  subsequently  breed  true. 

The  blue  Andalusian  fowl  affords  an  excellent  illustration  of  this 
principle  for  it  is  a  hybrid,  an  impure  dominant,  and  will  not  breed  true. 

Blue  x  Blue  =1  Black,  2  Blue,  1  White. 
Blue  x  Black  =2  Black,  2  Blue- 
Blue  x  White  =2  White,  2  Blue. 
Black  x  Black  =  Black  only. 
White  x  White-  White  only. 
Black  x  White  =  Blue  only. 

Here  black  is  dominant  and  white  recessive.  This  applies  to  these 
colours  in  the  edible  pea,  and  in  this  plant  the  quality  of  tallness  is  dominant 
to  dwarfness.  The  descent  of  the  Andalusian  fowl  supports  the  statements 
that  pure  dominants  and  recessives  breed  true  ;  that  impure  dominants 
always  produce  the  same  kind  of  offspring  as  their  parents,  viz.,  one 
dominant,  one  recessive,  two  impure  dominants  ;  that  an  impure  dominant 
united  with  a  dominant  produces  an  equal  number  of  pure  and  impure 
dominants  ;  that  an  impure  dominant  united  with  a  recessive  produces  an 
equal  number  of  pure  recessives  and  impure  dominants. 

These  observations  have  been  confirmed  in  the  case  of  various  species 
of  plants,  snails,  moths,  mice,  rats,  rabbits,  and  poultry.  Immunity  and 
susceptibility  to  rust  in  wheat  also  obey  the  Mendelian  law.  The  application 
to  the  inheritance  of  the  varied  characters  of  man,  disease,  and  deformity, 
is  more  difficult,  but  claims  have  been  made  for  the  accuracy  of  the  theory 
in  the  transmission  of  the  colour  of  the  eyes,  tufts  of  white  hair,  greyness 
and  premature  baldness,  keratosis  or  tylosis  palmaris  et  palmaris,  epider- 
molysis bullosa,  brachydactyly,  the  short  tail  of  Manx  cats,  the  aborted 
coccyx  of  rumpless  fowls,  split  hand  and  foot,  abortion  of  the  fingers, 
ptosis,  coloboma,  cataract,  ectopia  lentis,  night  blindness,  retinitis  pigmen- 
tosa, diabetes  insipidus,  and  hereditary  chorea.  The  transmission  is 
generally  through  an  affected  parent  in  whom  the  peculiarity  is  a  special 
or  dominant  factor.  Many  of  the  abiotrophies  are  transmitted,  affections 
which  depend  on  early  degeneration  before  development  is  completed, 
such  as  grey  hair  and  baldness,  Friedreich's  disease,  hereditary  optic  atrophy, 
and  various  myopathies  ;  notably  pseudohypertrophic  palsy,  which  is 
transmitted  by  females  only,  and  the  facial  type  of  Landouzy-Dejerine, 
which  may  be  transmitted  by  males.  Possibly  in  the  case  of  pseudo- 
hypertrophic palsy  the  males  do  not  transmit,  because  they  do  not  reach 
procreative  age.  The  female  transmits  it  to  her  sons,  but  not  to  all  sons. 
She  must,  therefore,  possess  a  defect  in  that  part  of  the  ovum  which  becomes 
the  germ  plasm.  Similarly,  in  haemophilia,  the  ova  of  the  mother  are 
affected  though  the  bodv  cells  are  normal.  .   .. 


Hereditary    and   Ante- Natal  Conditions.  17 

Possibly  other  affections  will  be  found  to  conform  to  this  law,  when  they 
have  been  traced  through  a  sufficient  number  of  generations.  Among  these 
may  be  mentioned  asthma  and  hay  fever,  exostoses,  accessory  auricles  and 
helical  fistula?.  The  law  may  be  disguised  or  interfered  with  by  the  sex 
factor,  as  in  pseudohypertrophy  and  haemophilia  ;  and  by  the  transmitter! 
character  being  a  recessive,  perhaps  attracting  no  attention. 

Malformations  in  the  embryo  chick  have  been  produced  by  shaking 
the  egg,  warming  one  side,  varnishing  the  shell,  and  the  injection  of  toxins. 
So,  too,  interference  with  the  mammalian  embryo  in  the  very  early  stage 
may  cause  abnormality,  which  must  be  distinguished  from  an  inherited 
peculiarity.  Dimpling  may  arise  from  inflammatory  adhesions  between 
the  amnion  and  the  integuments.  Distortions  and  amputations  may 
possibly  be  due  to  a  like  cause  or  to  constriction  by  the  umbilical  cord. 

Reference  may  be  made  to  some  of  the  affections  above  mentioned. 
Slight  or  gross  peculiarities  of  structure  are  often  transmitted  through  several 
generations.  A  family  likeness  is  constantly  seen,  especially  if  there  is  a 
characteristic  feature,  such  as  the  nose  or  chin.  Sometimes  the  resemblance 
is  to  a  more  distant  ancestor  than  the  parent.  This  is  spoken  of  as  Reversion. 
Atavism  is  the  appearance  of  a  character  indicative  of  the  evolutionary 
ancestry  of  the  species.  Atavistic  tendencies  are  present  in  all  infants. 
The  newly  born  babe,  even  though  premature,  is  strikingly  strong  in  the 
hands  and  arms,  and  in  many  cases  can  support  its  own  weight  for  as 
long  as  two  minutes.  Its  upper  limbs  are  relatively  more  developed  than 
the  lower  ones.  This  has  been  assigned  as  evidence  of  descent  from  a  tree- 
climbing  ancestor,  since  it  would  be  essential  for  the  infant  to  be  able  to 
cling  firmly  to  its  mother  when  climbing  or  escaping  from  her  foes.  It  is 
not  due  to  the  peculiarities  of  the  foetal  circulation,  for  this  is  the  same 
in  mammals  in  whom  the  hind  limbs  predominate  in  growth.  Possibly, 
congenital  hyperplasia  of  the  pylorus,  and  rumination  or  merycism,  are 
evidence  of  a  still  more  remote  descent  from  a  vegetarian  ancestor. 
Polymastia  and  polythelia  are  probably  atavistic. 

The  transmission  of  characteristic  habits,  attitudes,  and  gaits,  may  be 
the  result  of  conscious  or  unconscious  imitation.  Often  this  explanation 
can  be  excluded  by  the  death  or  disappearance  of  the  parent ;  or  the 
peculiarity  may  have  been  transmitted  from  a  remote  ancestor.  Moral 
and  psychical  characters  follow  the  same  law.  It  is  a  happy  explanation 
when  a  parent  can  satisfy  himself  that  unpleasant  deviations  from  the 
normal  in  the  temper,  intellect,  or  morals  of  the  child,  are  the  result  of  a 
reversion  to  a  more  distant  ancestor.  Generally  it  is  the  parent  from  whom 
the  peculiarity  is  inherited.  Often  it  is  due  to  unsuitable  methods  of 
education,  bad  example,  and  unsatisfactory  environment. 

A  trivial  peculiarity  may  be  transmitted  in  a  most  persistent  manner. 
A  tuft  of  white  hair  has  been  handed  on,  always  in  the  same  shape,  to  the 
first  and  last  children  of  the  family  for  seven  generations.     In  another 

c 


18  Chapter  II. 

instance  it  was  transmitted  by  unaffected  daughters  to  their  sons.  In 
a  third  family  it  was  only  present  in  alternate  children.  In  a  family  of 
piebalds,  studied  for  six  generations,  24  out  of  138  individuals  exhibited 
a  partial  albinism,  a  white  forelock  and  an  underlying  white  patch  of 
skin  down  the  centre  of  the  forehead.  Transmission  was  by  direct  descent; 
in  one  case  to  all  the  children  (N.  Bishop  Harman).  In  albinism  there 
is  a  lack  of  pigment  forming  power.  The  descent  of  this  is  peculiar.  Thus, 
two  apparently  normal  parents  had  seven  albino  children  out  of  eight. 
In  a  negro  family  (Farabee)  the  union  of  a  normal  and  an  albino  negro 
produced  three  normal  sons  of  whom  two  bred  true.  The  third  married 
twice,  and  had  one  albino  child  out  of  six  by  the  first  wife,  and  three  out  of 
nine  by  the  second  wife.  Both  these  wives  must  have  carried  albinism 
as  a  recessive  and,  indeed,  the  peculiarity  was  by  no  means  uncommon 
in  the  locality.  Another  difficulty  in  the  study  of  albinism  is  the  tendency 
to  regard  those  in  whom  pigment  is  deficient  as  partial  albinos.  Darwin 
noted  a  curious  fact  that  albino  cats  with  blue  eyes  are  born  deaf.  Albinism 
may  be  associated  with  various  diseases.  It  is  most  likely  to  appear  in 
the  children  of  first  cousins,  who  are  heterozygous  and  contain  the 
recessive  factor. 

Colour-Blindness  also  illustrates  sex  limited  descent.  Females  must 
be  pure  in  colour-blindness  in  order  to  exhibit  the  defect.  Males  exhibit 
it,  if  they  receive  one  dose,  and  alone  are  affected,  unless  an  affected  male 
marries  a  female  who  carries  the  colour-blind  factor,  pure  or  impure. 
The  affected  and  the  sisters  of  the  affected  transmit  it  to  their  sons.  The 
female  may  be  a  pure  colour-blind  or  an  impure  colour-blind,  that  is,  not 
colour-blind  but  containing  the  factor  as  a  recessive.  The  male  may  be 
colour-blind  though  only  having  one  dose  of  the  factor  which  is  dominant 
for  sex.  So,  too,  the  colour-blind  female  must  have  a  colour-blind  father, 
and  will  have  colour-blind  sons.  The  colour-blind  male  will  have  sons, 
half  of  whom  are  colour-blind,  and  daughters,  half  of  whom  can  transmit 
the  peculiarity. 

Mendel's  work  strongly  supports  Weismann's  views  on  the  transmission 
of  characters  by  the  germ  cells  (germinal  or  blastogenic),  and  not  by 
modification  of  the  body  cells  (somatogenic).  Acquired  characters  are  not 
transmitted,  and  changes  in  type  can  only  arise  by  modification  of  the 
germ  cell.  Superficial  and  slight  mutilations  are  unlikely  to  be  transmitted, 
for  they  do  not  affect  the  composition  of  the  blood,  and,  therefore,  cannot 
affect  the  germ  cells.  Centuries  of  circumcision  have  left  the  foreskin 
of  Hebrew  children  unaltered.  Serious  damage  to  nerve  tissues  and  viscera 
is  said  to  cause  the  transmission  of  abnormality  in  such  organs.  Massin 
states  that  severe  damage  to  the  liver  of  rabbits,  bitches,  and  guinea  pigs 
may  result  in  affections  of  the  liver  in  the  offspring.  A  form  of  epilepsy, 
due  to  severe  injury  to  the  sciatic  nerves  in  guinea  pigs,  can  be  transmitted 
to  the  offspring,  and,  according  to  Brown-Sequard,  a  similar  form  of  spinal 


Hereditary    and   Ante- Natal  Conditions.  19 

epilepsy  can  be  produced  by  hemisection  of  the  dorsal  cord  in  these  animals, 
and  is  transmissible.  There  are  many  instances  of  new  types  arising, 
appearing  quite  suddenly  as  "  Sports,"  and  breeding  true  to  their  particular 
type.  The  white  sweet  pea  developed  suddenly  as  a  sport  or  mutation 
from  a  purple  parent,  long  before  any  of  the  intermediate  grades  in  colour. 
Other  similar  instances  are  the  Ancon  race  of  sheep,  now  extinct,  the 
Merino  sheep,  the  blotched  tabby  cat,  and  the  dwarf  bean.  In  the  realm 
of  medicine  we  can  quote  deformities,  such  as  webbed  fingers,  Polydactyly, 
brachydactyly,  split  foot,  cleft  palate,  microcephaly,  Mongolian  idiocy, 
congenital  hernia,  and  diseases,  such  as  alkaptonuria,  haemophilia,  and  so 
on.  Brachydactyly  has  been  traced  through  seven  generations  of  174 
individuals  (Drinkwater).  Half  the  children  of  abnormal  parents  were 
affected,  but  the  unaffected  did  not  transmit  the  disease. 

From  the  above  considerations  we  may  state  that  congenital  abnor- 
malities, consistent  with  life  and  the  propagation  of  the  species,  may  be 
transmitted  and  become  permanent  in  the  family,  provided  that  they 
arise  as  mutations  or  sports,  due  to  some  germinal  factor.  Mutilations 
are  not  reproduced.  Variations  in  the  offspring  are  due  to  the  inter- 
mixture of  dissimilar  germ  plasma,  the  spermatozoon  and  the  ovum. 
They  depend  greatly  on  selective  breeding,  for  instance,  in  pigeons,  horses, 
dogs,  cats,  sheep,  cattle,  etc.  Pigeons  revert  to  the  common  rock  pigeon 
type  if  allowed  to  breed  indiscriminately.  Hereditable  diseases  and 
malformations  can  only  be  prevented  by  not  allowing  those  affected,  or 
possessing  the  hereditable  factor  as  a  recessive,  to  have  offspring. 

Preconceptional  conditions  affecting  the  Germ  Plasm,  Male  or  Female. 

— It  is  almost  certain  that  the  constitutional  state  of  the  parents,  before 
or  at  the  time  of  conception,  may  affect  the  germ  plasm.  Any  change  in  the 
blood  or  tissues  of  either  parent,  whether  by  toxins,  ferments,  poisons,  or 
general  privation,  may  affect  the  nutrition  of  the  germ  cells,  and  thus  exert 
an  influence  on  the  offspring.  Similar  influences  may  affect  the  fertilised 
ovum,  via  the  maternal  tissues,  in  all  stages  of  its  existence.  Such  nutritive 
vacillations  are  likely  to  cause  variations  and  mutations  in  the  offspring. 

Consanguineous  marriages  are  not  to  be  countenanced  as  a  general 
rule,  for  consanguinity  emphasises  heredity.  Yet  the  marriages  of  first 
cousins  should  not  be  prohibited,  if  the  family  is  certainly  sound.  There 
is  nothing  in  such  marriages  which  necessarily  tends  towards  deterioration 
in  the  progeny,  for  sound  health  is  transmitted  equally  well  as  ill  health. 
When  ill  results  arise  they  are  due  to  the  effect  of  a  hereditable  defect 
which  is  naturally  present  in  both  parents.  Insanity  in  the  parent,  if 
breaking  out  in  the  mother  during  pregnancy,  causes  an  unduly  high 
mortality  in  the  offspring.  Apart  from  this,  it  has  no  effect  on  the  mental 
or  physical  state  of  the  child  per  se,  but  if  the  insanity  is  dependent  on  a 
morbid  heredity,  this  influence  may  be  transmitted  to  the  child,  and  cause 
insanity  or  allied  affections  in  later  life.    If  only  one  parent  is  insane,  and 


20  Chapter  II. 

there  is  no  family  history,  that  is,  if  the  insanity  is  due  to  an  accidental 
factor  and  is  an  acquired  disease,  the  child  is  likely  to  be  unaffected. 

Even  if  one  or  both  parents  are  insane,  and  the  family  tendency  is 
pronounced,  it  is  rare  for  all  the  children  to  be  affected.  On  the  other 
hand  mental  deficiency  in  the  offspring  may  depend  on  disease  in  the 
mother,  such  as  cretinism,  on  alcoholism  in  one  or  both  parents,  or  on  injury 
or  disease  at  and  after  birth.    Often  no  explanation  can  be  found. 

In  estimating  the  effect  of  poisons  such  as  alcohol,  lead,  opium,  and 
the  toxins  of  disease,  we  have  to  remember  that  the  poison  may  affect  the 
sperm  cell  or  ovum  before  or  at  the  time  of  impregnation,  and  the  impreg- 
nated ovum  during  its  nine  months  existence  in  the  maternal  womb.  Hence 
the  continued  action  of  the  poison  on  the  mother  is  more  likely  to  damage 
the  offspring,  through  the  medium  of  the  blood  supply,  than  paternal 
poisoning.  Alcohol  has  acquired  a  very  bad  reputation  in  this  respect. 
Many  sources  of  error  arise  in  judging  its  effect.  It  is  even  asserted  that 
there  is  no  evidence  that  parental  drinking  is  a  cause  of  inherited  weakness, 
and  there  is  no  inherent  reason  why  germ  cells  should  be  affected  by 
alcohol  to  such  an  extent  as  to  be  incapable  of  recovery.  Many  secondary 
causes  come  into  play  after  the  birth  of  a  child  of  alcoholic  parentage. 
A  drinking  parent  is  liable  to  neglect  the  child.  Food,  clothing,  warmth, 
and  general  hygiene  are  likely  to  be  bad  or  insufficient,  and  the  child 
suffers  from  these  secondary  factors  rather  than  from  a  direct  inherited 
debility.  Again,  the  association  of  alcoholism  and  mental  instability  does 
not  prove  that  the  mental  state  is  the  result  of  alcohol.  It  is  quite  probable 
that  there  is  a  primary  mental  defect,  and  that  this  is  exaggerated  second- 
arily by  alcohol  and  imitation.  On  the  other  hand,  Robinovitch,  of  Paris, 
in  1900,  ascribed  criminality  and  immorality  to  alcoholism  in  the  parents  ; 
over  90  per  cent,  in  the  father  only.  Of  127  children,  40  died  in  infancy  or 
prematurely,  and  only  27  were  in  good  condition.  Wigglesworth  found 
parental  intemperance  in  one-sixth  of  his  insane  patients.  It  is  probably 
as  frequently  an  antecedent  of  sanity.  Crothers,  in  1902,  stated  that 
parental  intemperance  gives  rise  to  "  a  drink  craving,  a  neurosis  or  a  mental 
defect,"  and  obtained  a  direct  alcoholic  heredity  in  1080  out  of  1744  in- 
ebriates. On  the  whole  we  may  conclude  that  parental  intemperance  is 
often  due  to  a  neurotic  or  insane  heredity,  and  that  the  combination  of 
these  two  factors,  or  of  alcoholism  with  tuberculosis  or  syphilis,  exerts 
great  influence  on  the  vitality,  the  mental  and  the  physical  degeneration 
of  the  offspring,  and  is  a  cause  of  idiocy,  mental  and  moral  imbecility, 
feeble-mindedness,  and  a  neurotic  temperament. 

Lead  and  copper  may  be  conveyed  to  the  foetus.  Arsenic  passes  the 
placenta  with  greater  difficulty,  and  mercury  not  at  all,  though  it  accumu- 
lates therein  (Porak,  1894).  Oliver  fed  pregnant  animals  on  white  lead, 
causing  death  of  the  young  in  utero,  and  found  lead  in  the  foetal  liver. 
Legrand  and  Winter,  in  1889,  reported  a  remarkable  case  in  which  both 


Hereditary    and    Ante- Natal  Conditions.  21 

parents  suffered  from  plumbism.  Five  children  were  stillborn.  The  sixth 
lived  15  days,  had  small  sclerotic  kidneys,  and  general  circumlobular 
cirrhosis  of  the  liver,  and  much  lead  in  this  organ.  Plumbism  is  a  common 
cause  of  abortion  or  feeble  infants.  The  results  are  the  same,  but  less 
severe,  when  the  father  is  affected  than  if  the  mother  suffers.  The  poison, 
therefore,  affects  both  germ  cells  and  foetus.  Diachylon  is  frequently 
taken  to  produce  abortion,  often  with  fatal  results. 

The  uric  acid  diathesis,  lithsemia,  gravel,  renal  calculus,  and  gout 
are  prevalent  in  many  members  of  a  family.  Before  accepting  this  as  a 
proof  of  inheritance,  the  fact  that  there  is  a  regional  distribution  for 
calculus  must  be  considered,  and  that  the  same  conditions  of  life  and 
environment  may  have  been  co-existent.  Gout  appears  more  liable  to 
affect  the  younger  than  the  elder  children  of  a  family,  and  at  an  earlier  age 
period.  If  this  be  true,  it  might  be  urged  as  an  argument  in  favour  of  the 
transmission  of  acquired  characters. 

Chlorosis  affects  many  girls  in  the  same  family  at  about  the  same  age. 
Perhaps  there  is  a  congenital  imperfect  development  of  the  uterus  or 
ovaries.  Virchow  has  ascribed  it  to  hypoplasia,  an  unduly  small  heart 
and  narrow  blood  vessels  ;  the  symptoms  not  arising  until  an  extra  tax 
falls  on  these  structures  at  puberty.  Bunge  holds  that  the  anaemia  is  due 
to  the  body  storing  up  iron  in  the  liver  and  tissues  as  a  supply  for  the 
f  oetus,  if  impregnation  takes  place. 

In  these  affections  there  is  no  true  inheritance  of  disease,  but  rather 
the  inheritance  of  a  predisposition  dependent  on  the  inherent  qualities  of 
the  protoplasm  of  the  germ  cells.  The  future  may  perchance  reveal  to  us 
that  there  is  a  true  heredity,  a  transmission  of  ferments  or  lack  of  ferments 
which  set  up  or  prevent  these  affections. 

Intra-Uterine  or  Congenital  Factors. — Some  of  the  features  of  this 
period  overlap  those  of  the  preconceptional  stage.  Thus,  tuberculosis, 
syphilis,  rheumatism,  and  other  infective  disorders  may  affect  the  nutri- 
tion of  the  germ  cell  before  conception,  the  impregnated  ovum,  and  the 
foetus  in  its  intra-uterine  life.  The  better  the  general  environment  of  the 
mother,  the  better  is  it  for  the  child  in  utero,  though  healthy  babies  have 
been,  and  will  continue  to  be  born  under  the  most  deleterious  conditions 
affecting  the  mother  during  pregnancy.  A  liberal  diet  is  important,  for  the 
nutrition  of  the  child  depends  on  the  blood  and  lymph  conveying  nutriment 
to  the  ovum  and  foetus.  In  tadpoles  an  alteration  in  the  diet  may  determine 
the  sex.  The  effect  of  alcohol  has  been  discussed  above.  Exercise  is  good 
in  moderation,  for  it  maintains  the  general  health  and  helps  to  prevent 
constipation.  Hard  work  should  not  be  continued  up  to  the  end  of 
pregnancy.  With  moderate  rest  in  the  later  stages,  the  duration  of 
pregnancy  is  more  likely  to  be  continued  up  to  or  beyond  full-time,  and  tho 
infant  heavier  and  better  nourished. 

All  strong  emotions  and  mental  excitement  should  be  guarded  against. 


22  Chapter  II. 

It  is  a  popular  belief  that  mental  impressions  may  be  the  cause  of  defor- 
mities, although  there  are  no  nerve  fibres  in  the  umbilical  cord  to  carry 
the  nerve  impulses.  The  idea  dates  back  to  the  time  of  Jacob  and  the 
flocks  of  Laban  (Genesis,  Chap.  xxx).  Maternal  impressions  are  common, 
but  deformities  are  rare.  In  many  cases  there  is  no  history  of  such  an 
impression.  In  others  the  mother  is  anxious  to  find  some  excuse  for 
bearing  an  imperfect  child.  It  is  difficult  to  admit  the  possibility  of  the 
impression  affecting  the  foetus  in  the  earliest  stages  of  its  existence,  before 
the  umbilical  cord  is  formed,  and  yet  the  different  structures  are  differen- 
tiated very  early.    The  cases  must  be  regarded  as  mere  coincidences. 

Accidents,  injury  to  the  mother,  and  intra-uterine  disease  are  likely 
to  affect  the  fcetus  at  all  stages  of  its  career,  and  may  cause  imperfect 
development,  malformations,  intra-uterine  death,  and  miscarriage. 

It  is  still  more  difficult  to  believe  in  Telegony,  in  spite  of  the  evidence 
in  its  favour.  According  to  this  theory  a  female  who  has  been  once 
impregnated  by  the  male  may  subsequently  bear  young  by  another  sire, 
which  resemble  the  sire  of  the  first-born.  Such  resemblance  is  more 
probably  due  to  reversion  to  a  more  remote  ancestor. 

The  actual  transmission  of  infective  diseases  is  almost,  if  not  quite, 
impossible,  provided  that  the  placenta  is  healthy.  There  is  not  always 
evidence  of  disease  in  this  organ,  yet  it  may  be  sufficiently  affected  to 
render  it  imperfect  as  a  filter.  White  infarction  of  the  placenta  has  been 
ascribed  to  rheumatism  and  to  salicylates,  and  is  a  cause  of  abortion. 
In  the  case  of  infective  organisms,  they  must  either  reach  the  foetus  via  the 
umbilical  vein,  or  be  swallowed  with  liquor  amnii.  Infection  via  the  vein 
causes  a  general  blood  infection,  so  the  disease  in  the  foetus  will  have  a 
different  distribution  to  that  in  the  parent.  For  instance,  erysipelas 
may  give  rise  to  endocarditis  in  the  child.  Hence,  placental  infection  may 
mean  the  transmission  of  organisms,  or  of  toxins  in  both  directions.  The 
placenta  has  undoubtedly  a  selective  action,  transmitting  some  poisons 
more  readily  than  others,  and  forms  a  generally  efficient  barrier. 

Ante-natal  tuberculosis  is  illustrative  of  many  points  in  the  action  of 
parental  disease  on  the  offspring.  Its  toxic  effects  on  the  germinal  plasm 
may  prove  a  cause  of  neuroses.  The  children  of  tuberculosis  parents  are 
often  precocious,  and  abnormally  excitable.  Morselli,  in  1904,  ascribed 
to  parental  tuberculosis,  idiocy  or  imbecility  dependent  on  cerebral  arrest 
of  development,  and  many  other  mental  defects.  Tubercle  bacilli  some- 
times exist  in  the  semen,  but  it  is  incredible  that  a  sperm  cell  could  convey 
the  organism  and  infect  the  ovum.  Much  more  probably  it  would  impair 
its  nutrition,  and  render  it  useless  for  impregnation.  The  same  argument 
holds  good  for  the  ovum.  Possibly  teratological  results  arise  from  toxic 
action  during  the  embryonic  stage.  Many  instances  of  foetal  infection  are 
now  on  record,  but  congenital  tuberculosis  must  be  regarded  as  distinctly 
rare.    Newborn  calves  rarely  react  to  tuberculin,  and  the  non-reacting  calves 


Hereditary    and   Ante-  Natal  Conditions.  23 

of  tuberculous  dams  do  not  become  tuberculous  if  they  are  segregated 
and  properly  fed.  Schmorl  found  tuberculous  nodules  in  the  placenta  in 
9  out  of  20  tuberculous  women,  some  in  the  stage  of  incipient  phthisis. 
This  observation  suggests  that  the  liability  to  infection  is  greater  than 
generally  supposed.  Sitzenfrey  (1909)  found  tuberculous  changes  in  the 
vessels  of  the  cord.  It  must,  therefore,  be  accepted  that  any  tuberculous 
mother  is  liable  to  disease  or  malnutrition  of  the  placenta,  which  may  then 
permit  the  transmission  of  the  bacillus  and  general  blood  infection  of  the 
foetus.  The  extent  of  the  disease  in  the  child  is  proportionate  to  its  inten- 
sity in  the  placenta.  It  may  be  limited  to  a  local  tumour.  The  possibility 
of  infection  by  swallowing  liquor  amnii  must  be  included.  The  lungs  may 
escape  infection,  because  they  are  unexpanded,  and  have  a  small  blood 
supply.  In  late  infections,  ending  in  early  death  of  the  child,  inoculation 
experiments  may  be  necessary  to  demonstrate  tubercle  bacilli  in  the  blood 
and  tissues. 

Similar  objections  to  the  transmission  of  syphilis  by  an  ovum  or  sperm 
cell,  infected  by  the  Treponema  pallidum,  hold  good  as  in  the  case  of 
tuberculosis.  The  sperm  cell  is  devitalised  by  the  disease ;  perhaps 
sufficiently  to  destroy  its  fertilising  power,  perhaps  enough  to  render  the 
development  of  the  impregnated  ovum  unsatisfactory,  leading  to  congenital 
defects  of  structure,  function,  and  vitality.  The  mode  of  transmission  to  the 
offspring  is  discussed  in  the  chapter  on  syphilis.  It  is  analogous  to  that  of 
tuberculosis,  almost  certainly  so  since  Schaudinn's  discovery  of  the 
treponema. 

With  the  exception  of  diphtheria  pregnant  women  are  less  sus- 
ceptible to  specific  fevers.  The  transmission  of  these  fevers,  and  of  other 
diseases  due  to  ascertained  organisms,  depends  on  the  duration  and  severity 
of  the  disease,  and  the  effect  on  the  placenta.  A  general  blood  infection  is 
produced.  In  variola  and  measles  the  foetus  may  die  before  the  rash 
appears,  may  be  born  with  a  rash,  may  develop  a  rash  after  birth  though 
infected  in  utero,  or  may  be  infected  at  birth.  Mauriceau,  the  French 
obstetrician,  was  born  with  the  marks  of  small -pox.  Typhoid  fever  causes 
abortion  in  two-thirds  of  the  cases.  The  foetus  may  die  from  acute  blood 
poisoning,  and  the  placenta  appear  healthy,  though  containing  typhoid 
bacilli.  Ulceration  of  the  agminated  glands  is  exceptional.  Measles  is 
likely  to  cause  abortion  in  over  half  the  cases.  The  fifth  month  is  the  most 
dangerous  time  in  all  fevers.  It  has  even  been  recorded  that  the  mother 
has  transmitted  measles  and  small-pox,  without  being  herself  infected. 
Such  cases  are  open  to  suspicion  of  erroneous  diagnosis.  The  streptococcus 
pyogenes  and  the  bacillus  of  symptomatic  carbuncle  have  been  shown 
experimentally  to  pass  to  the  foetus.  Hydrophobia  may  be  transmitted, 
even  to  only  one  of  a  litter  of  pups  (Peroncita  and  Carita).  Erysipelas, 
glanders,  anthrax,  cerebro-spinal  meningitis,  relapsing  fever,  rheumatic 
fever,  yellow  fever,  and  malaria  have  all  been  handed  on  to  the  foetus. 


24  Chapter  II. 

A  woman  had  malaria  in  early  pregnancy,  and  gave  birth  to  a  child  4  months 
after  coming  to  England.  At  the  age  of  7  weeks  the  child  was  intensely 
anaemic,  and  had  numerous  malarial  parasites  in  the  blood  (Moffat). 

The  parasites  have  been  found  in  the  blood  of  newborn  infants  of 
women  with  malaria.  Some  develop  the  fever  directly  after  birth,  others 
later.  Some  exhibit  no  symptoms  and  grow  normally.  The  spleen  may  be 
enlarged  at  birth.  The  later  the  mother  is  infected  the  more  likely  is  the 
infant  to  suffer.  Paroxysms  of  shaking  during  intra-uterine  life  have  been 
reported  by  Felkin  in  two  cases,  the  children  being  born  with  enlarged 
spleens,  and  having  attacks  of  fever. 

Immunity. — This  is  a  property  due  to  the  formation  of  antibodies 
(antitoxin)  in  the  blood  and  lymph.  It  is  an  increased  cellular  resistance 
acquired  by  the  leucocytes,  not  by  the  germ  cells.  The  antitoxin  combines 
with  the  specific  toxin  and  arrests  its  action.  The  two  bodies  are  not 
physiological  antagonists,  though  they  directly  affect  and  combine  with 
each  other  ;  as  a  rule,  but  not  invariably,  in  proportionate  amounts.  The 
degree  of  neutralisation  may  vary  in  accordance  with  the  degree  of  con- 
centration or  with  the  duration  of  contact. 

The  duration  of  immunity  varies  in  different  diseases  and  in  different 
individuals.  It  is  often  very  short  in  influenza,  and  may  last  a  lifetime  in 
variola.  Two-thirds  of  the  infants  of  women  vaccinated  during  pregnancy 
take  just  as  well  as  usual,  and  the  rest  will  take  in  six  months. 

Congenital  immunity  is  probably  always  transmitted  by  the  mother, 
via  the  placenta.  It  is  improbable  that  an  immune  male  can  transmit 
immunity  to  his  offspring  by  a  normal  female.  Experiments  have  shown 
that  immunity  to  diphtheria  toxins  can  be  transmitted  to  young  guinea 
pigs  from  the  mother.  Ehrlich  rendered  young  mice  immune  to  tetanus, 
through  the  mother's  milk,  by  inoculating  the  mother  with  serum  from  an 
immune  horse.  Thus,  there  is  a  conveyance  of  antibodies  from  the  maternal 
blood  to  the  child,  a  transmission  and  not  an  inheritance,  not  a  cellular 
immunity. 

The  blood  of  the  child  of  a  woman  with  typhoid  fever  may  give  Widal's 
reaction,  either  because  the  foetus  produces  its  own  agglutins  or  they  are 
transmitted.  Possibly  the  children  of  tuberculous  parentage  inherit  a 
slight  immunity.  The  liability  to  infection  is  great,  but  the  incidence 
is  very  little  larger  in  these  children.  Limit  the  chance  of  infection,  and 
the  disease  is  limited.  The  age  of  onset  is  earlier,  unless  contact  can  be 
excluded.  If  it  is,  the  liability  is  no  greater  than  in  those  of  non-tuberculous 
parents.  The  acquisition  of  partial  immunity  as  the  result  of  infected  glands, 
and  the  survival  of  the  fittest  complicate  the  study  of  this  question.  Measles 
and  syphilis  become  milder  in  type  in  the  course  of  years,  and  are  extremely 
virulent  when  introduced  among  a  new  people.  Negroes  and  Mongols  are 
relatively  immune  to  yellow  fever.  The  English  are  more  susceptible  than 
the  Boers  to  typhoid  fever.    Thus,  it  is  probably  mainly  due  to  the  survival 


Hereditary  and   Ante- Natal  Conditions.  25 

of  the  insusceptible.  Nevertheless,  it  is  certain  that  antibodies  are  trans- 
mitted from  the  mother  to  the  offspring  by  the  maternal  blood  and  by 
the  milk.  The  liability  to  infections  is  much  greater  in  the  infants  who 
are  not  breast-fed,  especially  during  the  first  few  days  of  life.  Immunity 
from  infections  in  the  first  weeks  of  life  is  probably  due  to  transferred 
immunity  from  the  mother  against  the  infections  she  has  suffered. 

Treatment. — Ante-natal  treatment  is  often  ignored.  The  mother  must 
be  put  under  the  best  available  conditions  of  environment,  diet,  hygiene, 
and  freedom  from  mental  disturbance.  Local  and  general  health  must  be 
attended  to.  Tuberculosis  may  improve  during  pregnancy,  remain  fairly 
stationary,  or  progress  rapidly  and  end  fatally  before  confinement.  The 
treatment  of  syphilis  in  either  parent  is  essential,  and  produces  excellent 
results  on  the  offspring.  Drugs  and  other  means  for  procuring  abortion 
must  be  avoided.  They  generally  fail,  produce  serious  or  fatal  illness  in 
the  mother,  or  result  in  the  birth  of  a  defective  or  malformed  infant. 


CHAPTER    III. 

DIET    AND    NUTRITION. 

The  Mother  or  Wet  Nurse — Physiology  and  Chemistry — Breast  Feeding — 
Human  Milk — Cow's  Milk — Bacteriology — The  Effect  of  Heat  and 
Attenuants — Subsidiary  Methods  of  Feeding — Proprietary  Foods — 
Diet  after  Weaning  ;   in  Early  Childhood ;   in  School  Life  ;   in  Illness. 

The  Mother  of  the  Child,  or  Wet  Nurse.— Every  child  should  be  brought 
up  on  human  milk,  preferably  by  the  mother,  and  especially  during  the 
first  three  months  of  life.  For  a  few  days  after  birth  the  milk,  known 
as  the  Colostrum,  appears  to  contain  antigens,  substances  which  produce 
antibodies  in  the  blood  of  the  child,  rendering  it  much  less  liable  to  infection. 
Maternal  nursing  is  particularly  important  during  this  period,  for  these 
antigens  disappear  almost  entirely  in  the  course  of  a  week  or  two.  The 
mortality  of  infants  depends  mainly  on  digestive  disturbances,  which 
result  from  an  unsuitable  diet,  and  are  much  less  apt  to  occur  in  the  breast- 
fed. Maternal  nursing  conduces  to  the  complete  involution  of  the  uterus, 
and  sometimes  lessens  the  chance  of  impregnation  at  too  short  intervals. 
It  is  also  beneficial  to  the  mother  through  the  mode  of  life  and  regular 
diet  necessary,  and  gives  her  a  much  greater  sense  of  responsibility  in  the 
management  of  the  child.  Even  if  the  mother  cannot  suckle  the  child 
entirely,  or  for  a  prolonged  period,  it  is  almost  invariably  advantageous 
that  she  should  do  so  to  the  best  of  her  ability,  and  should  not  neglect  this 
important  duty  for  what  are  often  trivial  or  inexcusable  causes.  Economic 
conditions  may  prevent  the  mother  nursing,  because  she  is  compelled  to  go 
out  to  work. 

A  wet  nurse  is  often  the  only  means  of  saving  the  child's  life,  but  is 
by  no  means  always  reliable  or  available.  Such  a  nurse  is  an  expensive 
luxury,  and  may  have  to  be  obtained  from  Paris.  Her  milk  will  not 
necessarily  suit  the  baby  for  whom  it  is  required.  There  is  no  fear  that 
immoral  or  inborn  propensities  can  be  transmitted  by  the  milk  to  the  child. 

Seeing  that  the  care  of  the  child  begins  before  birth,  and  even  before 
conception,  the  mode  of  life  of  the  expectant  mother  must  be  supervised. 
The  more  healthy  the  mother,  the  sounder  and  more  healthy  will  be  the 
offspring.  The  diet  should  be  rather  more  generous  than  at  other  times, 
and  contain  a  liberal  supply  of  lime  salts,  protein,  and  foods  suitable  to 
maintain  regular  action  of  the  bowels.    A  little  more  milk,  meat,  and  bread 


Diet    and   Nutrition.  27 

will  supply  all  the  nutriment  necessary  for  the  growing  foetus.  Alcohol  is 
unnecessary,  and,  taken  in  excess,  may  be  injurious.  Occasionally,  mild 
purgatives,  such  as  cascara,  aloes,  liquorice  powder,  or  Apenta  water,  are 
required.  Violent  exercise,  lifting  heavy  weights,  any  mode  of  progression 
causing  much  jolting,  and  sea-sickness  must  be  avoided.  Regular  walking 
exercise  at  a  moderate  pace  should  be  taken  morning  and  afternoon,  and 
continued  up  to  the  end  of  pregnancy,  unless  rendered  impossible  by 
swelling  of  the  legs  or  pain.  Swimming  is  permissible.  The  relief  from 
household  worries  and  troubles,  and  the  advantages  derived  from  rest  and 
good  food  by  women  admitted  to  Lying-in  Hospitals  for  at  least  10  days 
before  confinement,  are  shown  in  the  increased  average  weight  of  their 
children. 

Mental  excitement  and  emotion,  if  excessive,  are  deleterious,  but  most 
ordinary  amusements  and  entertainments  are  valuable  in  preventing  the 
mother  thinking  too  much  about  her  condition.  All  the  usual  hygienic 
factors  of  ordinary  life  are  more  necessary  for  the  expectant  mother. 
She  should  rest  for  at  least  an  hour  in  the  middle  of  the  day  during  the  later 
months  of  pregnancy,  and  have  a  good  long  rest  at  night.  Her  clothing 
must  not  interfere  with  the  respiratory  movements  or  exert  pressure  or 
friction  on  the  breasts  and  nipples.  A  broad  strong  jean  or  flannel  bandage 
may  be  worn  to  support  the  lower  part  of  the  abdomen. 

The  breasts  and  nipples  must  be  kept  clean,  and,  if  pendulous,  the  folds 
below  the  breasts  must  be  freely  dusted  night  and  morning  with  Emol 
Keleet,  zinc  oxide  and  starch,  or  other  drying  powder.  For  three  months 
before  confinement  the  nipples  should  be  washed  daily  in  warm  water,  and 
massaged  with  pure  vaseline,  lanoline,  or  cacao-butter.  No  astringent  or 
spirituous  lotion  should  be  used,  for  it  hardens  the  skin,  and  makes  it  much 
more  liable  to  crack.  Small  and  retracted  nipples  can  be  increased  in 
size  and  drawn  out  by  careful  manipulation,  and  rendered  more  prominent 
by  the  gentle  use  of  Bier's  suction  cups.  During  the  later  months  swollen 
prominent  nipples  must  be  protected  by  absorbent  salicylic  wool,  frequently 
changed  if  there  is  much  overflow  of  milk. 

Most  drugs  can  be  taken  in  moderation  with  impunity,  but  strong 
purgatives,  large  doses  of  quinine,  ergot  of  rye,  and  similar  drugs,  must  be 
avoided.  Salicylates  are  harmless,  although  they  have  been  supposed  to 
give  rise  to  the  "  white  infarction  "  of  the  placenta,  which  is  liable  to 
occur  in  rheumatic  women,  causing  intra-uterine  death  of  the  child. 

The  perfect  mother  or  wet  nurse  is  25  to  35  years  of  age,  truthful, 
placid,  and  equable  in  temper,  cheerful,  good-natured,  affectionate,  un- 
emotional or  well  controlled,  and  active.  She  should  already  have  had  one 
healthy  child,  and  experience  in  the  mode  of  management.  Many  previous 
pregnancies,  in  rapid  succession,  impair  the  general  health  and  quality  of  the 
milk.  She  should  be  temperate  in  food  and  drink,  though  not  necessarily  a 
total  abstainer.     Above  all  she  must  have  plenty  of  patience,  and  realise 


28  Chapter  III. 

that  for  the  time  being  nursing  is  her  paramount  duty,  and  that  all  other 
duties  and  amusements  must  be  put  on  one  side  if  they  interfere  with  the 
proper  performance  of  her  functions  as  a  nurse.  She  should  present  on 
examination  the  appearances  of  perfect  health  ;  be  strong,  robust,  and 
well  nourished.  There  is  no  advantage  in  being  fat,  and,  indeed,  some 
thin  women  are  most  excellent  nurses.  The  teeth  should  be  good,  free 
from  caries,  appetite  and  digestion  excellent,  and  bowels  open  daily 
without  the  aid  of  medicine.  She  should  be  in  the  habit  of  taking  daily 
exercise  and  sleeping  well.  In  the  case  of  a  wet  nurse  more  particularly, 
there  should  be  no  evidence  of  past  or  present  constitutional  disease,  more 
especially  tuberculosis,  congenital  or  acquired  syphilis,  gonorrhoea,  and 
former  rickets.  The  mouth  and  throat  must  be  carefully  examined  ;  and 
the  hair  and  skin,  to  see  that  she  is  free  from  rashes  and  vermin.  The 
physical  examination  must  never  be  omitted,  but  it  is  an  absurd  refinement 
to  apply  the  tuberculin  test,  as  has  been  suggested.  The  nurse's  child,  if 
living,  should  be  examined  for  evidence  of  disease,  and  as  regards  its 
general  nutrition  and  cleanliness.  For  this  reason  it  should  be  at  least  a 
month  or  six  weeks  of  age.  The  child  should  be  under  six  months,  but  it  is 
not  necessary  that  it  should  be  of  the  same  age  as  the  infant  for  whom  the 
nurse  is  required.  Beware  of  a  substituted  child.  Chemical  and  micro- 
scopical examination  of  the  milk  are  unnecessary. 

The  breasts  of  a  primipara  are  generally  conical  or  pyriform  in  shape, 
not  necessarily  large,  firm  to  the  touch,  with  prominent  nipples.  In  a 
multipara,  and  sometimes  in  a  primipara,  they  are  pendulous.  The  actual 
size  of  the  breast  is  no  measure  of  its  functional  capacity,  for  the  glandular 
structure  may  be  relatively  small  in  proportion  to  the  amount  of  fat.  A 
large  breast  of  this  kind  diminishes  little  in  size  during  suckling,  whereas  a 
well-developed  gland  becomes  smaller  and  less  tense.  Even  this  is  not  an 
absolutely  reliable  indication  of  the  functional  value,  for  in  some  women 
the  secretion  of  milk  takes  place  rapidly  during  the  process  of  suckling,  and 
only  to  a  slight  extent  during  the  intervening  period.  By  weighing  the 
mother's  child  before  and  after  nursing,  on  several  occasions,  a  fair  estimate 
of  the  secretory  activity  of  the  breast  can  be  arrived  at.  The  nipples  should 
be  prominent  and  erectile.  Occasionally  they  are  too  large,  but  more 
commonly  they  are  too  small,  or  flat  and  retracted,  rendering  suckling  a 
mechanical  impossibility. 

While  nursing,  the  mode  of  life  should  be  regular  and  placid,  and 
include  personal  cleanliness  as  well  as  a  certain  amount  of  exercise  or 
physical  work  daily.  The  diet  should  be  generous,  nutritious,  and  easily 
assimilable,  but  excess  of  food,  especially  indigestible  food,  strongly 
aromatic  foods,  highly  seasoned  dishes,  and  strong  tea,  are  to  be  avoided. 
Wet  nurses  constantly  are  overfed.  Having  previously  been  in  reduced 
circumstances,  and  on  a  plain  and  insufficient  diet,  as  soon  as  they  get  the 


Diet    and  Nutrition.  29 

chance  they  drink  too  much  milk,  eat  an  excess  of  meat,  and  often  take  an 
undue  supply  of  stout  or  other  malt  liquor,  on  the  plea  that  it  is  essential 
in  order  to  provide  good  milk  for  the  baby.  The  usual  result  is  that  the 
quality  of  the  milk  becomes  such  that  it  upsets  the  digestion  of  the  child. 
As  a  general  principle  alcohol  is  unnecessary,  but  one  or  two  glasses  of 
burgundy  or  port,  or  |  to  1  pint  of  light  ale  or  stout,  may  be  taken  daily 
by  women  who  are  accustomed  to  it.  An  extra  pint  of  milk  in  the  course 
of  the  day,  and  the  ordinary  three  meals  are  quite  sufficient  under  most 
conditions.  Bread  and  milk,  gruel,  or  cocoa  may  be  taken  at  bed  time. 
Fruit  and  vegetables  may  be  given  freely  to  counteract  the  tendency  to 
constipation,  common  when  an  excess  of  milk  is  taken.  Sixty  grammes  of 
extra  protein  in  the  diet  will  supply  the  20  grammes  in  a  litre  of  human 
milk,  and  a  surplus  of  carbon  available  for  the  formation  of  fat.  During  the 
early  days  of  lactation,  while  the  mother  is  in  bed,  the  diet  should  be  light, 
easy  of  digestion,  and  not  too  nutritious.  Many  mothers  take  too  much 
milk  and  an  excess  of  food,  which,  combined  with  lack  of  exercise,  leads  to 
the  secretion  of  milk  rich  in  solids,  and  sets  up  indigestion  in  the  child. 

If  the  wet  nurse's  child  is  alive,  the  employer  should  see  that  it  is 
properly  cared  for,  and  the  nurse  consequently  free  from  anxiety.  A 
moral  obligation  lies  upon  the  employer  not  to  allow  the  child  to  suffer 
while  he  is  paying  the  mother  to  deny  it  its  natural  food  supply.  The 
mortality  among  these  children  is  enormous,  most  of  them  dying  under 
three  months  of  age.  For  this  reason  a  wet  nurse  should  be  preferred  whose 
child  has  reached  the  fourth  month  in  life.  If  the  supply  of  milk  is  over- 
abundant, it  must  be  drawn  off,  or  given  to  another  child,  otherwise  stasis 
and  loss  of  function  result.  This  is  especially  important  when  the  foster 
child  is  a  weak  or  newborn  baby,  for  it  is  not  at  all  likely  to  be  able  to  empty 
the  breasts.  Under  such  circumstances  it  is  advisable  to  allow  the  nurse  to 
suckle  her  own  child,  either  at  the  beginning  of  or  at  the  end  of  the  nursing 
period,  according  to  which  portion  of  the  milk  is  required  for  the  foster 
child.  The  nurse  must  not  be  allowed  to  go  home  for  this  purpose,  for  she 
might  convey  infectious  disease,  and  all  control  is  lost  over  her  diet  and 
habits  of  life.  She  must  be  watched  to  see  that  she  does  not  attempt  to 
supplement  any  deficiency  in  her  milk  supply  by  giving  cow's  milk  or  other 
food,  and  that  she  does  not  soothe  an  infant  irritable  from  indigestion  or 
insufficient  food  by  means  of  opiates.  The  child  must  be  watched  to  see 
that  it  is  not  overfed. 

It  is  a  pure  experiment  in  every  case  where  a  wet  nurse  is  tried  for  a 
delicate  infant.  If  the  child  is  extremely  weak  it  may  be  too  dangerous  to 
attempt  it,  and  safer  to  rely  upon  carefully  supervised  substitute  feeding. 

Physiology  and  Physiological  Chemistry. — Sometimes  a  few  drops  of 
milk  can  be  squeezed  out  of  the  gland  during  the  early  months  of  pregnancy. 
Usually  secretion  is  active  in  the  last  few  months,  and  on  pressure  milk 


30  Chapter  III. 

will  flow  out  in  jets  from  the  nipple.  That  secreted  during  the  first  three 
days  after  delivery  ( Colostrum)  is  scanty,  nutritive,  and  laxative.  Active 
secretion  generally  begins  on  the  third  or  fourth  day,  and  increases  with  the 
age  of  the  child.  It  is  most  active  while  the  child  is  suckling.  Females, 
human  and  animal,  occasionally  secrete  milk  without  having  been  pre- 
viously pregnant.    In  rare  instances  the  male  has  done  so. 

The  secretion  of  milk  is  not  a  process  of  filtration.  It  is  the  result  of  the 
metabolic  activity  of  the  secretory  cells  of  the  mammary  gland.  These 
cells  manufacture  the  milk  from  the  nutrient  materials  brought  to  them  by 
the  blood.  That  the  fat  of  milk  is  not  derived  from  the  fat  in  the  food  is 
evident  in  many  cases.  Cows  out  at  grass  yield  much  more  butter  fat  than 
can  be  accounted  for  by  the  fat  in  the  food,  and  carnivorous  animals  secrete 
a  milk  rich  in  fat.  Generally  speaking,  the  quantity  of  fat  in  milk  is  increased 
by  protein  and  diminished  by  fat  in  the  diet.  Protein  increases  metabolic 
activity,  whereas  fatty  food  diminishes  it.  Possibly,  some  of  the  fat  may  be 
taken  up  by  the  gland  cells  from  the  blood  directly. 

Caseinogen,  another  constituent  of  milk,  is  not  found  in  the  blood, 
and  must,  therefore,  be  formed  by  the  metabolism  of  the  cells.  The 
lact-albumin  is  closely  allied  to  the  serum-albumin  of  the  blood,  but  differs 
in  several  respects.  It  is  probably  formed  or  modified  by  the  cellular 
metabolism.  If  the  normal  activity  of  the  gland  is  disturbed,  the  per- 
centage of  albumin  is  increased  at  the  expense  of  the  caseinogen. 

The  lactose  or  milk  sugar  is  not  found  in  any  other  part  of  the  body, 
except  in  the  alimentary  canal  when  it  has  been  taken  as  food,  nor  has  it 
been  found  in  the  blood.  In  carnivora  it  is  present  in  abundance  in  the 
milk,  although  little  carbohydrate  food  is  taken.  In  these  animals,  it  is 
clear  that  the  lactose  is  little,  if  at  all,  dependent  upon  the  consumption 
of  carbohydrates. 

All  these  considerations  prove  that  milk  is  a  true  secretion  dependent 
upon  cell  activity,  that  the  metabolic  processes  in  the  cells  are  influenced 
by  the  nature  of  the  food,  and  that  an  increase  of  one  particular  food 
stuff  does  not  necessarily  produce  an  increase  of  the  same  constituent  in  the 
milk.  Like  other  secretions  it  is  controlled  and  modified  by  the  nervous 
system. 

Proportionately  to  its  weight  the  child  requires  more  food  than  the 
adult,  in  order  to  provide  for  growth  and  development  as  well  as  for  energy 
in  the  form  of  work  and  heat,  the  supply  of  secretions,  the  repair  of  waste, 
and  the  general  maintenance  of  nutrition.  More  heat-producing  food  is 
required  during  the  early  months  of  life  to  counterbalance  the  deficient 
heat-production  from  lack  of  muscular  energy,  and  the  great  loss  of  heat  by 
the  skin,  relatively  to  the  bulk  of  the  body.  The  loss  of  heat  by  the  skin 
varies  directly  as  the  superficial  area,  and  inversely  as  the  body  weight ; 
the  percentage  loss  is  consequently  greater  in  small  animals  than  in  larger 


Diet    and   Nutrition.  31 

ones.  In  proportion  to  weight  the  superficial  area  in  the  baby  is  quite  three 
times  greater  than  in  the  adult.  More  than  two-thirds  of  the  loss  of  heat 
is  due  to  conduction,  radiation  and  evaporation  from  the  surface. 

The  value  of  a  food  is  equal  to  the  sum  of  the  values  of  its  component 
parts,  or  proximate  principles,  namely,  water,  proteins,  carbohydrates,  fats, 
and  salts.  It  also  depends  on  the  nature  of  the  food,  assimilability,  mode  of 
preparation  and  administration,  the  composition  of  the  digestive  juices, 
the  condition  of  the  absorbing  surface,  and  the  age  and  idiosyncracy  of  the 
individual.  (. 

Water  is  lost  in  sweat,  the  expired  air,  and  the  excreta.  The  infant 
requires  a  liberal  supply  because  of  the  extent  of  the  body  surface.  When 
the  ordinary  processes,  by  which  water  is  eliminated,  are  increased,  more 
fluid  should  be  supplied,  e.g.,  the  sweating  of  rickets  and  febrile  conditions, 
in  respiratory  affections,  polyuria,  and  infantile  diarrhoea.  Infants  fre- 
quently suffer  from  thirst,  and  should  be  given  plain  boiled  water,  hot  or 
cold,  not  iced,  rather  than  milk  for  its  relief.  Water  assists  digestion, 
increases  the  various  secretions,  is  of  value  as  a  solvent  and  diluent  of 
food  substances,  and  assists  in  absorption  from  the  alimentary  canal.  It 
aids  in  elimination,  keeps  the  blood  in  a  fluid  condition  and  lessens  the 
liability  to  thrombosis,  and  promotes  activity  of  the  circulation  of  fluids 
and  of  cell  metabolism. 

Protein  food  is  the  source  of  nitrogen,  and  is  essential  to  the  structure 
of  protoplasm  and  every  body  cell.  A  growing  child  requires  a  free  supply, 
relatively  more  than  the  adult.  Development  of  young  animals  depend 
very  much  on  the  percentage  of  protein  in  the  milk.  An  infant  doubles  its 
weight  in  5  months  on  a  1-2  per  cent,  protein  diet,  a  calf  doubles  its 
weight  in  1  or  2  months  on  4  per  cent.  Possibly  the  albumin  is  merely 
nutritive,  and  the  casein  is  essential  for  growth.  An  adult  man  weighing 
67  kilogrammes  requires  about  100  grammes  of  protein  daily.  A  six  months 
old  baby,  one-tenth  of  the  weight,  takes  a  litre  of  milk  containing  20  grammes 
of  protein.  For  the  growing  animal  vegetable  proteins,  though  free  from 
crystalline  extractives,  are  not  as  valuable  nor  as  digestible  as  animal 
proteins. 

An  excess  of  protein  in  the  milk  is  liable  to  set  up  indigestion,  colic, 
and  constipation,  or  simply  loss  in  weight.  The  stools  are  green  or  yellow, 
and  contain  curds,  especially  if  the  caseinogen  is  in  excess.  Excess  of  urio 
acid  in  the  urine,  gravel,  and  renal  colic  may  occur.  Evil  results  are  un- 
common in  older  children  because  of  their  active  metabolism.  Headache, 
migraine,  and  renal  colic  may  be  due  to  this  cause. 

On  a  diet  defective  in  protein  the  child  becomes  anaemic,  languid,  weak, 
and  short  of  breath  on  exertion.  The  muscles  are  flabby  and  soft,  dentition 
is  delayed,  the  child  ceases  to  grow,  and  rickets  may  develop.  The  absence 
of  the  ordinary  gain  in  weight  and  height  is  a  fair  indication  that  the  diet 


32  Chapter  III. 

of  school  children  is  deficient  in  protein.  In  breast-fed  infants,  and  those  fed 
on  whey,  a  low  percentage  of  protein  may  lead  to  curds  in  the  stools, 
disappearing  when  more  protein  is  added.  This  has  been  ascribed  to  the 
formation  of  an  insoluble  curd  by  uncombined  acid,  or  to  the  abnormality 
in  the  relative  proportions  of  fat  and  protein.  Caseinogen  with  a  dilute  acid 
forms  a  loose  precipitate  completely  soluble  in  sodium  chloride  solution,  but 
with  an  excess  of  acid  an  insoluble  precipitate  is  formed.  With  a  low 
percentage  of  protein  in  the  food  there  is  liable  to  be  an  excess  of  free  acid. 

Fat  is  present  in  all  tissues,  especially  adipose  and  nervous  tissues 
and  bone  marrow.  Fat  in  the  food  is  chiefly  of  value  for  the  maintenance  of 
the  body  temperature.  There  is  no  proof  that  the  fat  in  the  tissues  is  stored 
up  from  the  fat  taken  as  food,  but  the  stored-up  fat  is  soon  drawn  upon  if 
the  diet  is  deficient  in  this  respect,  and  hence  the  tissues  may  suffer 
indirectly.  Fat  aids  in  the  absorption  of  inorganic  salts,  especially  earthy 
phosphates,  from  the  alimentary  canal,  more  of  these  salts  being  found  in  the 
faeces  if  the  fat  is  deficient  in  the  food.  It  delays  protein  digestion,  lessens 
gastric  peristalsis,  diminishes  the  secretion  of  gastric  juice,  and  is  partially 
split  up  by  gastric  juice  and  the  enzyme  lipase.  In  the  duodenum  it  is 
split  up  into  fatty  acids  and  glycerine.  As  a  rule  it  is  very  completely 
absorbed,  but  there  is  often  more  fat  in  human  milk  and  other  diets  than  is 
necessary,  from  4  to  5  per  cent,  escaping  digestion,  and  appearing  in  the 
stools  in  the  form  of  fatty  acids  chiefly,  neutral  fats  and  soaps. 

An  excess  of  fat  interferes  with  the  gastric  digestion  of  protein,  and 
may  lead  to  "  fat  dyspepsia  "  or  "  fat  diarrhoea."  The  dyspepsia  is  charac- 
terised by  constant  vomiting  of  curdled  milk  and  mucus,  with  the  odour  of 
rancid  cream,  due  to  butyric  acid.  Vomiting  occurs  from  half-an-hour  to  an 
hour  after  food,  and  the  fat  may  resemble  lumps  of  casein.  If  there  is 
diarrhoea,  the  stools  are  loose,  yellowish  green,  acid,  greasy,  and  contain 
much  mucus.  It  is  usually  associated  with  colic,  flatulence,  intestinal 
catarrh,  and  loss  of  weight.  Other  symptoms  ascribed  to  excess  of  fat  are 
refusal  of  food,  capricious  appetite,  constipation  with  pasty,  foul  stools, 
excess  of  ammonia  in  the  urine,  irritability,  and  convulsions.  These 
children  are  often  excessively  fat,  and  have  a  much  enlarged  liver. 

Deficiency  of  fat  impairs  digestion  and  nutrition,  causes  constipation, 
and  the  appearance  of  earthy  phosphates  in  the  stools.  It  is  generally 
regarded  as  the  cause  of  rickets,  possibly  by  interfering  with  the  absorption 
of  lime  salts  in  the  form  of  lime  soaps.  The  deficiency  in  fat  cannot  be 
replaced  by  additional  carbohydrates  with  success. 

Carbohydrates  are  of  use  for  the  production  of  heat  and  muscular 
energy.  Infants  practically  never  suffer  from  deficiency  of  this  food,  for 
the  percentage  in  milk  varies  within  comparatively  small  limits.  An  excess 
of  sugar  in  human  milk  rarely  produces  ill  effects,  though  the  infant  may 
become  very  fat.    Artificially  fed  babies,  especially  those  fed  on  condensed 


Diet    and   Nutrition.  33 

milk,  often  become  fat,  flabby,  unwieldy,  and  rachitic.  They  suffer  from 
intestinal  disturbances,  and  fermentation  of  the  food  in  the  alimentary 
tract,  with  the  production  of  flatulence  and  offensive  diarrhoea.  In  artificial 
feeding  either  milk  sugar  or  cane  sugar  is  added.  Commercial  milk 
sugar  is  often  impure,  and  liable  to  be  contaminated  during  prepara- 
tion. It  is  probably  not  identical  with  that  of  human  milk.  On  fermenta- 
tion it  is  converted  into  lactic  acid.  Perhaps  there  are  several  kinds 
of  lactic  acid,  just  as  there  are  many  varieties  of  bacilli  causing 
lactic  acid  fermentation.  Cane  sugar  is  cheaper,  more  handy,  and 
sweeter.  On  account  of  its  sweetness  it  cannot  be  given  in  such  large 
quantities  as  lactose.  In  the  small  intestine  it  is  converted  into  dextrose,, 
in  which  form  it  is  absorbed.  Possibly  lactose  can  be  absorbed  without 
such  conversion,  but  this  is  uncertain.  There  is  no  serious  objection, 
to  the  use  of  cane  sugar  in  preference  to  milk  sugar,  if  it  is  given  in 
proper  amount.  The  digestive  disturbances  induced  by  its  use  are  due  to 
excess  rather  than  to  its  chemical  composition.  The  starchy  foods  are 
referred  to  later. 

Salts. — Bunge  has  shown  that  the  percentages  of  the  salts  in  the  ash  of 
the  newly  born  animal  are,  with  certain  exceptions,  practically  the  same 
as  the  percentages  in  the  ash  of  the  mother's  milk.     Milk  contains  more 
potassium  and  less  sodium  salts,  for  as  the  animal  grows  there  is  a  relative 
increase  of  the  muscles  rich  in  potassium,  and  a  diminution  of  the  cartilages 
rich  in  sodium.    The  percentage  of  iron  is  very  much  less  in  the  milk  than  in 
the  newborn.    To  compensate  for  this,  a  young  animal  stores  up  iron  in  the 
liver  previous  to  its  birth,  this  iron  being  used  up  as  the  animal  grows. 
Animals  can  live  on  milk,  but  die  if  the  salts  are  extracted.     Even  if  the 
salts  after  extraction  are  again  added  to  the  mixture,  the  animal  cannot 
live  on  it,  for  it  is  unable  to  utilise  the  salts  except  in  organic  combination 
with  protein.    Hence,  some  of  the  defects  ascribed  to  deficiency  of  protein 
may  depend  on  the  deficiency  of  assimilable  salts.     When  cow's  milk  is- 
diluted  the  percentage  of  iron  is  reduced  below  that  present  in  human  milk 
and  may  lead  to  anaemia  and  debility.     To  counterbalance  this,  organic 
combinations  of  iron  may  be  given,  such  as  the  yolk  of  egg,  raw  meat  juice, 
and  various  proprietary  foods  made  from  blood.     The  iron  in  the  yolk 
of  egg  has  been  estimated  as  0-04  per  cent,  of  the  dried  solids,  and  as 
18-3  mg.  per  100  gms.  of  dried  substance.      The  iron  in  haemoglobin  is 
more   firmly  combined  than  that  in  the   nucleo-albuminous   compound 
present  in  yolk  of  egg.     Nevertheless,  meat  juice  and  the  red  gravy  from 
undercooked  meat  are  valuable  additions  to  the  diet  of  anaemic  babies.     After 
the  age  of  one  year  potatoes  and  small  quantities  of  green  vegetable  can 
be  added  to  the  diet.     Cabbage  and  spinach  contain  the  highest  per- 
centage of  iron,  and  this  may  partly  account  for  the  maxim  that  "  green, 
vegetables  are  excellent  for  the  blood." 

D 


34 


Chapter  III. 


IRON   IN    FOODS. 

Milligrammes  per  100  grammes  of  dried  Substances. 


White  Bread   . . 

.      1-4 

Potatoes 

.      6-2 

Apples,  Sweet . . 

.      1-7 

GreenPeas 

.      6-8 

Pears 

.      2-2 

French  Beans 

.      8-5 

Cow's  Milk       . . 

.      2-3 

Carrots 

.      8-9 

Goat's  Milk      .. 

.      2-5 

Lentils 

.      9-3 

Brown  Bread  . . 

.      2-5 

Asparagus 

.    10-5 

Bed  Currants 

.      3-6 

Yolk  of  Egg 

.    18-3 

Rice 

.      4-5 

Green  Chicory 

.    22-0 

Barley 

.      4-7 

Cabbage 

.    30-5 

Black  Grapes  . . 

.      5-8 

Spinach 

.    40-0 

-(The  Hospital,  May  18th,  1908). 


There  is  more  sodium  chloride  in  cow's  milk  than  in  human  milk, 
so  common  salt  need  not  be  added  to  milk  mixtures  in  artificial  feeding. 
It  has,  however,  some  advantages  for  it  delays  rennet  curdling  and  makes 
it  less  complete.  It  stimulates  the  appetite,  increases  the  secretion  of 
hydrochloric  acid,  and  thus  assists  digestion.  Later  od,  when  much 
vegetable  food  is  taken,  the  sodium  is  required  to  neutralise  the  potassium 
in  the  vegetables.  For  this  reason  it  is  advantageous  to  add  it  to  barley 
water.  There  is  one  cereal,  namely  rice,  which  contains  remarkably  little 
potassium. 

The  percentage  of  lime  in  human  milk  is  0-0243,  in  cow's  milk,  1-51,  and 
in  yolk  of  egg,  0-38.  Meats,  cereals,  and  leguminosse  contain  very  much  less. 
Phosphates  of  lime  and  magnesium  are  most  important  for  cell  growth  and 
bone  formation.  The  addition  of  lime  water  to  milk  exerts  some  influence 
by  virtue  of  its  alkalinity.  Lime  water  does  not  contain  as  much 
lime  as  cow's  milk,  and  probably  lime  cannot  be  absorbed  except  in  the 
form  of  organic  compounds.  Prolonged  heat  injures  milk  by  rendering  the 
lime  salts  insoluble. 

Phosphorus  is  of  importance  in  the  formation  of  bones,  and,  perhaps, 
in  the  prevention  of  rickets.  Cereals,  leguminosae,  and  potatoes  contain 
considerably  more  than  human  milk  ;  while  lean  beef,  yolk  of  egg,  and 
cow's  milk  contain  6  times  as  much.  Lecithin  and  nuclein  contain  phos- 
phorus, and  are  found  in  considerable  quantities  in  ova  and  nervous 
tissues.  It  is  uncertain  whether  they  are  digested  and  absorbed,  but  it 
is  harmless  to  give  calves'  brain  and  the  hard  roes  of  fishes  to  children. 
Nuclein  is  present  in  cow's  milk,  but  Koplik  states  that  it  is  not  assimilated 
by  the  infant.  If  more  phosphorus  is  required  in  the  diet  it  is  best  given 
in  the  form  of  the  yolk  of  egg.  Sulphur  is  found  in  cereals,  leguminosse, 
potatoes,  and  some  fruits,  such  as  cherries  and  peaches ;  lettuce  and  leeks 
contain  a  high  proportion.     Its  importance  is  not  thoroughly  understood. 


Diet   and  Nutrition.  35 

The  Chemical  Composition  of  an  Infant's  Diet. — A  baby,  six  months 
old,  taking  1,000  grammes  of  human  milk  daily,  ingests  protein  20  gms., 
fat  40  gms.,  carbohydrates  66  gms.  An  adult,  ten  times  as  heavy,  takes, 
on  an  average,  protein  100  gms.,  fat  100  gms.,  carbohydrates  250  gms. 
Thus,  weight  for  weight,  the  infant  requires  a  much  more  liberal  supply  of 
each  constituent  than  the  adidt  does.  Halliburton  estimates  the  needs  of  an 
infant  under  a  year  and  a  half  old  at  protein  20-36  gms.,  fat  30-45  gms., 
and  carbohydrates  60-90  gms.  The  requirements  of  the  individual  child 
are  very  variable.  In  regard  to  protein  Waller  has  pointed  out  that  in 
proportion  to  weight  the  infant  requires  more  than  the  adult,  but  in 
proportion  to  body  surface  the  amount  is  approximately  the  same.  Body 
surface  is,  therefore,  a  better  proportional  indicator  than  body  weight. 
Weight  is  a  better  indicator  than  age.  All  three  factors  should  be  taken 
into  consideration. 

Attempts  have  been  made  to  regulate  the  diet  according  to  the  calorie 
value.  A  calorie  is  the  amount  of  heat  needed  to  raise  1  kilo,  of  water 
1  degree  of  centigrade.  The  number  of  calories  required  per  kilo,  of  weight 
is  called  the  Energy-  Quotient.  Now  the  calorie  value  of  1  gramme  of 
protein  or  sugar  is  4-1,  and  of  fat  is  9-3.  The  calorie  value  of  1  oz.  of  human 
milk  is  about  19,  and  of  cow's  milk  about  20.  One  hundred  calories  per 
kilo,  is  equal  to  45  per  lb.  From  these  figures  the  necessary  calculations  can 
be  made.  An  adult  needs  from  30-35  calories  per  kilo,  per  day.  An  infant 
requires  during  the  first  3  months  of  life  100  calories,  during  the  second 
3  months  90-100,  and  from  6-12  months  80-90  per  kilo,  daily. 
Atrophic  and  premature  children  may  need  120  calories  or  more.  These 
calculations  are  interesting,  but  not  of  very  much  value  in  practice. 

Breast  Feeding. — The  child  should  be  put  to  the  breast  as  soon  as  the 
mother  has  recovered  somewhat  from  the  fatigue  of  labour,  say,  in  6-12 
hours.  The  excitation  of  the  nipple  reflexly  induces  uterine  contraction, 
and  lessens  the  risk  of  post-partum  haemorrhage.  The  child  has  an  oppor- 
tunity of  drawing  out  the  nipples  if  they  are  small  or  retracted,  before  the 
rapid  swelling  of  the  breast,  usually  occurring  on  the  third  day,  makes 
such  nipples  so  depressed  below  the  surface  that  it  is  difficult  or  impossible 
for  the  child  to  get  hold  of  them.  A  small  amount  of  colostrum  is  obtained, 
valuable  for  nutrition  and  its  laxative  action.  It  is  unnecessary,  and  often 
injurious,  to  give  castor  oil  or  other  purgatives,  or  the  concoction  of  butter 
and  brown  sugar  administered  for  this  purpose.  Such  treatment  may  start 
troublesome  gastric  and  enteric  disturbance,  which  may  end  fatally. 
Suckling  stimulates  the  secretion  of  milk.  The  amount  obtained  varies 
with  the  vigour  of  sucking,  and  the  state  of  the  breasts.  Exhausted  by  its 
entrance  into  the  world,  change  of  temperature  and  bathing,  the  newborn 
sleeps  most  of  the  first  24  hours.  Usually  from  one-third  to  two-thirds  of 
an  ounce  is  taken  in  two  meals  in  the  first  24  hours  ;  3  oz.  in  4-6  meals  on 
the  second  day  ;   and  then  7,  10,  12,  14,  and  16  oz.  on  successive  days. 


36  Chapter  III. 

Nothing,  not  even  milk  and  water  is  to  be  given.  From  the  fact  that 
lactation  is  not  established  until  the  third  day,  and  often  later,  it  is  evident 
that  no  food  other  than  the  colostrum  is  required  before  that  time.  Food 
given  diminishes  the  activity  of  suckling  and  the  consequent  stimulation  of 
milk  production.  Boiled,  cooled  water  may  be  given  during  the  first  three 
days,  sweetened  with  saccharin,  if  necessary  to  render  the  urine  less 
concentrated  and  irritating.  If  at  the  end  of  the  third  day  the  supply  of 
milk  is  insufficient,  it  may  be  supplemented  by  a  mixture  of  milk,  cream, 
water,  and  milk  sugar.  The  child  should  be  fed  every  2  hours,  on  the  breast 
and  the  milk  mixture  alternately,  or  put  to  the  breast  every  time  and 
allowed  to  take  some  of  the  mixture  afterwards  if  not  satisfied.  Weakly  and 
premature  infants  may  have  to  be  fed  during  the  first  three  days.  Begin 
with  a  teaspoonful  or  two  of  a  5  per  cent,  solution  of  milk  sugar,  and  add 
small  quantities  of  milk  and  cream  gradually,  if  the  child  has  to  be  brought 
up  artificially. 

During  suckling  the  child  should  be  held  partially  on  its  side  with  the 
head  and  back  supported  on  the  right  or  left  arm  of  the  mother,  according 
as  it  is  fed  from  the  right  or  left  breast,  and  the  mother  must  bend  her  body 
somewhat  forward  so  that  the  nipple  falls  easily  into  the  infant's  mouth. 
The  breast  must  be  steadied  by  the  index  and  middle  fingers  of  the  disen- 
gaged hand  placed  above  and  below  the  nipple. 

Pressure  with  these  fingers  will  enable  the  mother  to  prevent  the  child 
taking  the  milk  too  quickly,  or  to  assist  the  flow  by  gentle  pressure  on  the 
breast.  The  child  obtains  the  milk  by  compression  of  the  sinus  and  base  of 
the  nipple,  and  not  by  suction,  in  a  similar  manner  to  the  way  milk  is 
obtained  in  milking  cows.  During  the  first  week  the  child  should  be  put  to 
both  breasts  at  each-nursing,  and  after  that  to  alternate  breasts  every  other 
feed,  unless  it  is  weakly  and  the  milk  supply  scanty.  The  mother  should 
express  a  little  of  the  milk  first  to  get  rid  of  organisms  present  in  the  ducts. 
The  duration  of  each  nursing  is  from  10-20  minutes,  but  varies  with  the 
strength  of  the  child  and  its  requirements,  the  rapidity  of  suckling,  the 
frequency  of  feeding,  the  state  of  the  nipple,  and  the  quantity  and  quality 
of  the  milk.  A  healthy  child,  taking  milk  from  a  full  breast,  may  nurse 
until  satisfied.  It  should  not  be  allowed  to  go  to  sleep  with  the  nipple  in  its 
mouth.  After  nursing,  the  mouth,  especially  the  corners,  should  be  wiped, 
but  the  inside  must  be  left  alone  for  fear  of  injuring  the  delicate  mucous 
membrane.  During  the  first  few  days  the  infant  may  be  put  to  the  breast 
every  2  hours,  while  the  mother  is  awake,  or,  if  very  feeble,  every  1  \  hours. 
The  stomach  is  rarely  empty  in  less  than  2  hours.  It  is  sometimes  better 
that  the  breast  should  be  given  every  6  hours  on  the  first  day,  4  hourly  on 
the  second  day,  and  after  that  every  2  hours.  The  more  frequent  nursing 
during  the  first  two  days  is  advantageous  to  the  child,  and  stimulates  the 
secretion  of  milk.  "When  lactation  is  fully  established  the  child  should 
be  given  the  breast  every  2  hours  from  5  a.m.  to  11  p.m.  during  the  first 


Diet    and   Nutrition.  37 

month  ;  every  2-|  hours  from  5  a.m.  to  10.30  p.m.  during  the  second  month  ; 
and  after  that  every  3  hours  from  5  a.m.  to  11  p.m.  Some  babies  require 
feeding  less  frequently,  but  great  circumspection  must  be  employed  in 
lengthening  the  intervals,  and  even  more  in  shortening  them.  It  is  a  common 
custom  to  feed  the  child  whenever  it  cries,  on  the  supposition  that  the  cry 
indicates  hunger.  More  often  the  cry  is  due  to  indigestion,  and  the  indi- 
gestible character  of  the  milk  is  induced  by  too  frequent  nursing.  The  pain 
of  indigestion  can  be  relieved  by  any  warm  fluid,  such  as  hot  water,  but  the 
warm  milk  only  gives  relief  by  virtue  of  its  warmth  and  induces  fresh  colic 
in  a  short  time.  Very  feeble  infants,  and  occasionally  vigorous  ones  with 
active  digestive  organs,  require  an  extra  feed  during  the  six  hours  interval 
at  night.  During  the  later  months  of  nursing  the  5  a.m.  feed  may  be 
omitted,  if  the  child  sleeps  soundly  until  later.  Some  infants  do  better  on 
less  frequent  feeds  such  as  5  feeds  at  intervals  of  4  hours,  sleeping  soundly 
for  8  hours  at  night.  These  cases  are  exceptional,  and  show  the  necessity 
of  not  rigidly  adhering  to  a  hard-and-fast  rule,  although  it  applies  to  the 
majority  of  infants. 

Regularity  of  feeding  is  essential  to  success,  for  if  the  intervals  are 
irregular  in  duration,  the  quantity  and  quality  of  the  milk  vary  considerably. 
Both  the  babe  and  the  mammae  should  be  trained  to  exact  regularity. 
With  a  little  patience  the  babe  can  be  accustomed  to  waking  up  for  its 
meals  with  the  regularity  of  clockwork,  and  sleeping  6  hours  at  night. 
Too  frequent  nursing  increases  the  percentage  of  proteins  in  the  milk, 
renders  it  indigestible,  and  does  not  allow  the  child's  stomach  sufficient 
time  to  digest  its  contents  and  pass  them  on  into  the  duodenum.  Wake 
the  child  when  the  feed  is  due,  if  it  is  asleep.  If  it  is  difficult  to  keep  it 
awake,  shorten  the  duration  of  the  nursings,  so  that  in  future  it  will  wake 
up  hungry  at  the  proper  time.  If  the  interval  is  too  prolonged  the  child 
is  hungry,  sucks  greedily,  rapidly  fills  or  overfills  the  stomach,  and  then 
vomits  or  gets  an  attack  of  indigestion. 

At  night  the  child  should  sleep  in  a  cot  by  the  side  of  its  nurse,  and 
not  in  the  same  room  as  the  mother,  if  a  nurse  is  available.  If  the 
mother  is  disturbed  in  the  night  by  the  child's  cry,  the  temptation  to 
give  the  breast  is  almost  irresistible,  and  likely  to  be  encouraged  by  a  tired 
husband. 

Provided  the  mother  is  healthy  and  strong,  and  the  milk  supply 
satisfactory,  suckling  may  be  continued  for  9  months,  and  partial  suckling 
for  10-12  months.  Except  under  special  advice  it  should  never  be 
continued  after  12  months,  and  usually  it  is  advisable  to  discontinue  it  at 
the  end  of  10  months.  Few  mothers  are  unable  to  suckle  their  children 
during  the  important  first  three  months  of  life,  and,  if  possible,  artificial 
feeding  should  be  postponed  until  after  this  period.  By  the  fourth  or  fifth 
month  the  child's  stomach  is  more  fully  developed  as  a  receptacle  for  food. 
Its  digestive  powers  are  stronger,  and  there  is  less  liability  to  infections. 


38  Chapter  III. 

If  the  mother's  milk  becomes  unsuitable,  it  can  often  be  improved  by  altera- 
tion in  the  diet,  the  mode  of  life  or  the  frequency  of  nursing. 

Unduly  prolonged  suckling  is  injurious  to  the  mother,  and  may  give 
rise  to  headache,  ansemia,  debility,  muscular  pains,  and  increased  sus- 
ceptibility to  disease.  Amaurosis,  epilepsy,  and  insanity  are  rare  sequels. 
The  child  may  suffer  on  account  of  deterioration  in  the  quality  of  the  milk, 
a  reduction  in  protein  and  total  solids,  and  consequent  insufficiency  of  the 
diet. 

Among  the  lower  classes  a  child  is  often  nursed  for  2  or  even  3  years 
on  account  of  the  prevalent  idea  that  conception  does  not  occur  while  the 
mother  is  nursing.  Various  observations  show  that  impregnation  does  not 
take  place  quite  so  readily  during  lactation  as  at  other  times.  From  3-5-8 
per  cent,  of  suckling  women  conceive,  although  the  catamenia  have  not 
returned,  but  the  return  of  the  menses  is  the  best  indication  that  the 
mother  may  again  conceive.  Under  such  circumstances  the  continuation  of 
suckling  has  probably  little  or  no  effect  in  preventing  impregnation. 

Breast  feeding  may  be  injurious  to  either  the  child  or  the  mother. 
Gastric  disturbance  and  colic  in  the  infant  may  be  due  to  irregularity  in 
feeding,  milk  too  rich  in  protein,  or  other  changes  in  its  composition. 
Easily  digested  milk  is  not  always  sufficiently  nutritious,  by  reason  of  its 
small  percentage  of  solids.  Sometimes  there  are  defects  in  quantity  as  well 
as  in  quality. 

The  general  health  of  the  mother  may  be  unsatisfactory.  Tuberculous 
women  do  not  secrete  good  milk,  but  often  nurse  their  children  satisfactorily. 
Nursing  must  be  prohibited  if  there  is  active  lung  mischief.  In  the  presence 
of  latent  disease  suckling  must  not  be  long  continued.  It  is  possible  that 
the  tubercle  bacillus  may  reach  the  infant  through  the  milk  supply,  but  is 
still  more  likely  to  be  acquired  by  direct  infection,  if  there  is  actual  lung 
disease.  Past  tuberculous  disease  of  glands  or  bone  does  not  contra- 
indicate  nursing,  provided  the  child  is  weighed  every  week  and  the  general 
health  of  the  mother  is  maintained. 

Constitutional  syphilis  may  render  the  milk  supply  insufficiently 
nutritious,  but,  on  account  of  the  delicacy  of  the  baby,  the  mother  must 
nurse  her  child  and  supplement  the  diet  if  necessary.  A  neurotic  inherit- 
ance is  undesirable  in  that  the  insanity  of  lactation  may  develop,  or  that 
melancholia  may  follow  on  prolonged  lactation.  Epilepsy  is  not  necessarily 
a  bar  if  the  mother  is  under  observation,  but  she  might  injure  her  child  in 
a  fit,  or  her  milk  supply  may  be  affected.  The  emotional  temperament, 
associated  with  a  neurotic  heredity,  is  liable  to  cause  alterations  in  the 
milk  on  very  slight  provocation.  General  debility  from  any  cause  may 
render  it  necessary  to  stop  nursing.  Immediate  weaning  is  essential  in 
acute  diseases,  especially  those  of  the  infective  type.  The  rheumatic 
pains,  sometimes  called  the  "  rheumatism  of  lactation,"  mav  be  severe  and 


Diet    and  Nutrition.  39 

constant.  If  they  are  not  cured  by  a  nutritious  diet  and  tonics,  the  child 
must  be  wholly  or  partly  weaned.  Albuminuria  as  a  rule  does  not  interfere 
with  nursing.  Lactation  must  not  be  considered  a  serious  drain  on  the 
system,  if  the  food  supply  is  satisfactory  and  nutrition  well  maintained. 
It  is  important,  therefore,  never  to  recommend  weaning  except  after  most 
careful  consideration.  In  doubtful  cases  nursing  should  be  tried,  and  the 
effect  on  the  mother  and  child  carefully  noted. 

Local  affections  of  the  nipple  may  be  so  severe  as  to  render  suckling 
impossible.  Fissure  is  preceded  by  abrasion  or  excoriation  due  to  want  of 
cleanliness,  constant  moisture  from  galactorrhcea,  too  frequent  suckling,  or 
the  use  of  hardening  astringent  lotions.  Infection  of  the  raw  surface  and 
the  mechanical  effects  of  suckling  prevent  healing,  and  lead  to  adenitis. 
Preventive  treatment  consists  in  bathing  with  cold  water  before  and  after 
nursing,  rubbing  in  olive  oil  or  lanolin,  or  painting  with  raw  white  of  egg. 
Treat  excoriation  with  zinc  ointment ;  or  balsam  of  Peru,  one  drachm 
to  the  ounce  of  cold  cream  and  lanolin,  equal  parts  ;  or  tannic  acid, 
grs.  15,  balsam  of  Peru,  grs.  30,  vaseline,  1  oz.  For  the  treatment  of  fissure 
dry  the  nipple  carefully  and  paint  it  freely  with  boric  acid,  grs.  20,  to 
mucilage,  1  oz.  If  this  fails  to  cure,  touch  the  fissure  every  other  day  with 
a  finely  pointed  stick  of  nitrate  of  silver.  Or  wash  with  5  per  cent,  solution 
of  boric  acid,  anaesthetise  with  cocaine,  paint  on  10  per  cent,  solution  of 
nitrate  of  silver,  dry  with  absorbent  wool,  and  paint  on  egg  albumin.  For 
the  next  few  nursings  use  a  glass  nipple  shield.  Sometimes  it  is  necessary 
because  of  pain  or  bleeding  to  stop  nursing  entirely  for  the  time  being, 
maintaining  the  activity  of  the  gland  by  systematic  use  of  the  breast  pump. 
Pain  can  be  relieved  by  applying  a  5  per  cent,  solution  of  cocaine  half-an- 
hour  before  nursing,  but  the  nipple  must  be  washed  before  the  child  is  fed. 

Lymphangitis  of  the  breast,  abscess,  and  primary  tuberculosis  render 
nursing  impossible.  In  mastitis  even  the  use  of  the  breast  pump  must  be 
forbidden.  In  the  early  stages  of  congestion  of  the  breast  apply  hot  oil 
fomentations  and  massage  gently  from  the  periphery  towards  the  nipple. 
At  first  it  is  very  painful,  but  soon  milk  flows  freely,  and  the  child  can  be 
put  to  the  breast.  If  the  congestion  has  proceeded  further,  a  full  dose  of 
Epsom  salts  must  be  given  at  once,  and  two  grains  doses  of  quinine  3  or  4 
times  a  day.  Equal  parts  of  extract  of  belladonna  and  glycerine  are 
applied  locally.  Surgical  interference  is  necessary  if  there  is  evidence  of 
pus.  Tuberculosis  of  the  breast  may  take  the  form  of  irregular  disseminated 
nodules,  a  confluent  mass,  or  miliary  tubercles.  It  sometimes  leads  to 
abscess  and  sinus  formation.  The  axillary  glands  are  enlarged,  the  affected 
breast  smaller  than  normal,  and  the  nipple  often  retracted.  It  is  often 
painless.  Though  occasionally  seen  before  puberty  it  is  most  common  at 
20-35  years  of  age.  In  a  girl  of  17  years  there  was  no  other  evidence  of 
tubercle,  and  her  child  was  born  healthy  (E.  P.  Davis,  1897).     About  60 


40  Chapter  III. 

cases  are  on  record.  Old  mastitis  is  of  importance  as  an  indication  that 
the  breast  is  imperfect  and  incapable  of  full  physiological  activity. 

The  only  reliable  evidence  of  an  insufficient  milk  supply  is  a  lack  of  gain 
in  weight.  Few  women  anxious  to  suckle  their  infants  will  admit  their 
inability  to  do  so.  Occasionally  both  mother  and  nurse  are  deceived  on 
account  of  the  size  of  the  breasts,  and  the  duration  of  time  the  baby  suckles, 
although  it  is  wasting  rapidly.  Weighing  the  child  before  and  after  nursing 
will  give  the  weight  of  milk  obtained.  Chemical  and  microscopical  examina- 
tions afford  evidence  of  its  quality.  Observation  of  the  child  while  suckling 
may  show  where  the  fault  lies.  If  the  infant  sucks  vigorously  for  a  few 
minutes  and  then  drops  the  nipple  with  an  angry  cry  the  quality  is  probably 
good  but  the  quantity  deficient.  If  the  child  nurses  languidly  and  for  a 
long  time,  the  quality  is  probably  poor  but  the  quantity  abundant. 
Disturbed  sleep,  fretfulness  and  crying,  gastro-intestinal  disturbance,  and 
abnormal  stools  are  usually  due  to  milk  too  rich  in  protein.  This  is  not  an 
indication  for  weaning,  as  it  can  usually  be  reduced  by  regulation  of  the 
mother's  diet,  and  decreasing  the  frequency  of  nursing,  or  by  giving  the 
child  a  small  quantity  of  plain  boiled  water  or  lime  water  immediately  before 
it  is  fed. 

Human  Milk. — Human  milk  is  a  thin,  watery,  bluish-white,  sterile 
fluid,  with  a  peculiar  taste  and  odour.  It  is  generally  said  to  be  faintly 
alkaline,  but  according  to  Kerley,  Gieschen,  and  Myers  (1903),  it  is 
invariably  acid  if  tested  with  phenol-phthalein.  The  specific  gravity  ranges 
between  1030  and  1035  at  60°  F.  It  varies  a  little  with  the  temperature. 
With  a  low  percentage  of  fat  and  a  high  one  of  sugar  it  may  reach  1042. 
If  the  percentage  of  fat  is  high  it  may  fall  as  low  as  1024.  The  specific 
gravity  and  the  percentage  of  fat  afford  a  fair  estimate  of  the  quality. 
Milk  containing  3-5  per  cent,  of  fat  and  of  average  specific  gravity  may 
be  regarded  as  good  milk. 

The  fat  globules  vary  in  size  from  0-00015-0-005  mm.  in  diameter, 
and  their  number  is  in  direct  relation  to  their  size  ;  up  to  11  millions  per 
cm.,  averaging  5  millions.  The  best  milk  contains  a  medium  number  of  a 
medium  size,  and  the  worst  a  small  number  of  small  size.  It  is  impossible 
from  microscopical  examination  alone  to  say  that  the  milk  is  of  good  quality. 

Milk  varies  in  composition  in  different  women,  on  different  days,  at 
different  periods  of  the  day,  at  different  stages  of  each  nursing,  and  in  the 
two  glands.  It  is  modified  by  the  state  of  the  health,  diet,  exercise, 
menstruation,  prolonged  lactation,  and  other  causes.  It  contains  ferments, 
such  as  katalase  and  antibacterial  alexins.  In  general  composition  it 
resembles  the  mammary  secretion  of  other  animals.  It  does  not  curdle 
with  rennet,  unless  a  little  hydrochloric  acid  is  added,  and  then  only 
forms  a  fine  flocculent  coagulum. 

In  order  to  obtain  a  sample  for  analysis  a  breast  pump  must  be 


Diet    and   Nutrition.  41 

employed,  using  very  gentle  suction.  It  must  be  thoroughly  clean  and  both 
nipples  and  breasts  previously  washed.  The  sample  used  for  analysis  should 
be  taken  from  the  middle  of  the  nursing  ;  the  milk  first  poured  out  is 
watery,  and  poor  in  fat,  and  that  obtained  at  the  end  is  especially  rich  in  fat ; 
hence  the  conclusions  drawn  from  an  isolated  partial  sample  are  of  com- 
paratively little  value.  It  is  very  difficult  to  empty  the  breast  with  a 
breast  pump. 

Colostrum  differs  from  the  milk  secreted  when  lactation  is  fully 
established.  It  is  yellowish  in  colour,  more  alkaline  in  reaction,  of  a  higher 
specific  gravity,  and  contains  the  colostrum  corpuscles.  These  are  large 
nucleated  cells,  epithelial  in  character,  from  the  acini  of  the  glands, 
containing  granules  and  fat  globules,  but  not  yet  disintegrated.  Colostrum 
also  contains  mononuclear  and  polynuclear  leucocytes  and  lymphocytes. 
The  presence  of  colostrum  corpuscles  indicates  non-establishment  or 
disturbance  of  equilibrium  in  the  gland.  They  are  variable  in  number,  and 
may  be  absent  if  the  mother  is  feverish.  Usually  they  persist  for  7-10 
days.  They  disappear  more  slowly  from  the  milk  of  a  primipara  than  a 
multipara,  during  bad  health  and  in  puerperal  affections.  They  may 
reappear  during  ill -health  and  at  the  commencement  of  involution  of  the 
gland.  If  so,  the  milk  will  disagree  with  the  infant.  Colostrum  contains 
a  higher  percentage  of  protein  and  salts,  and  a  lower  percentage  of  sugar 
than  the  later  milk  secreted.  The  high  percentage  of  protein  is  due  to  the 
number  of  corpuscles.  The  amount  of  fat  is  variable,  and  the  fat  globules 
vary  in  size.  Colostrum  is  coagulable  by  heat,  and  may  coagulate  spon- 
taneously. Its  relative  composition  is  unimportant,  seeing  that  it  is  only 
secreted  for  a  few  days  and  may  vary  daily.  The  importance  of  the  anti- 
gens or  antibodies  which  it  contains  is  referred  to  above  (p.  25). 

An  approximate  clinical  examination  of  milk  can  be  made  by  Holt's 
method.  It  is  based  on  the  fact  that  the  percentages  of  salts  and  sugar  are 
nearly  constant,  that  the  percentages  of  fat  and  protein  vary,  and  that 
the  specific  gravity  averages  1031  at  70°  F.  An  increase  in  the  fat  lowers 
the  specific  gravity,  and  increase  in  the  protein  raises  it. 

The  apparatus  consists  of  a  small  hydrometer  graduated  from 
1010-1040,  a  pipette,  and  a  glass-stoppered  cylinder  graduated  in  100  parts 
and  holding  about  10  c.c.  Half  an  ounce  of  milk  is  required.  The  specific 
gravity  is  taken  by  the  hydrometer.  To  estimate  the  fat  the  glass  cylinder 
is  filled  by  means  of  the  pipette  to  the  upper  line  exactly.  The  cylinder  is 
then  stoppered  and  allowed  to  stand  for  24  hours  at  a  temperature 
66-72°  F.  Generally  the  lower  limit  of  the  cream  becomes  sharply  defined  in 
that  time,  but  an  additional  6  hours  may  be  allowed  if  necessary.  Chemical 
examination  shows  that  the  ratio  of  fat  to  cream  is  very  nearly  3  to  5,  and 
for  clinical  purposes  it  may  be  so  estimated.  The  amount  of  protein  can 
then  be  judged  from  the  following  table  : — 


42 


Chapter  III. 


Clinical  Examination  of  Milk  ( Holt). 


Specific  Gravity. 

Percentage  of  Cream. 

Protein  (Calculated). 

Average 

1031 

7 

1  "5  per  cent. 

Normal  variations 

1028-1029 
1032 

8-12 
5-6 

Rich  milk. 
Fair  milk. 

Abnormal  variations 

Below  1028 
Above  1032 

Above  10 
Below     5 
Above   10 
Below     5 

About  normal. 
Very  poor  milk. 
Very  rich  milk. 
About  normal. 

Holt  asserts  that  conclusions  drawn  from  this  mode  of  examination  are 
as  exact  as  those  obtained  by  the  ordinary  examinations  of  the  urine. 

Many  analyses  of  human  milk  have  been  recorded,  showing  marked 
discrepancies  in  the  percentages  of  protein  and  sugar,  though  comparatively 
little  in  the  total  of  these  two  bodies.  In  some  of  the  older  analyses  the  per- 
centage of  protein  is  too  high,  and  of  sugar  too  low.  The  next  table  shows 
the  results  obtained  in  recent  years  by  analysis  of  specimens  from  a  large 
number  of  women. 

Meigs'  results  are  included,  because  carefully  carried  out,  although  he 
probably  underestimated  the  percentage  of  protein,  and  overestimated  that 
of  sugar. 

The  Percentage   Composition  of   Human  Milk. 


Meigs. 

Sharpless 

and 
Darling. 

Adriance. 

Pfeiffer. 

Carter  and 

Droop, 
Richmond. 

Leeds. 

Average. 

Protein 

1-046 

1-34 

1-48 

1-944 

1-97 

1-995 

1-5-2-0 

Fat     .. 

4-283 

2-91 

3-83 

3-107 

3-07 

4-131 

3-0-4-0 

Sugar 

7-407 

7-01 

6-72 

6-303 

6-59 

6-936 

6-0-7-0 

Salts  .. 

0-101 

— 

0-17 

0-192 

0-26 

0-201 

0-2 

Estimations  of  the  relative  proportions  of  caseinogen  and  lact-albumin 
are  extremely  unequal,  although  in  the  majority  the  total  of  the  combined 
proteins  is  about  the  average,  e.g. : — 


Diet    and   Nutrition. 
The  Relative  Percentages  of  Caseinogen  and  Lad-  Albumin. 


43 


Observer. 

Caseinogen. 

Albumin. 

Total. 

Konig 

0-61 

1-27 

1-88 

Hirt    .. 

0*63 

1-50 

2-13 

Lehmann 

1-20 

0-50 

1-70 

Tolmatscheff 

1-28 

0-34 

1-62 

Wynter  Blyth 

2-40 

0-57 

2-97 

Although  milk  may  vary  considerably  in  its  composition  it  must  be 
regarded  as  normal  if  the  infant  takes  it  well,  digests  it  satisfactorily,  gains 
weight,  and  keeps  in  good  health.  Harrington  found,  in  the  milk  of  women 
whose  infants  were  doing  well,  that  the  protein  varied  from  1  -08-4-17, 
fat  2-02-5-16,  sugar  5-68-7-30,  salts  0-12-0-21.  More  importance  must 
be  attached  to  the  clinical  condition  of  the  child  than  to  the  chemical 
analysis  of  the  mother's  milk. 

Other  constituents  are  found  in  minute  quantities,  namely,  nuclein, 
lecithin,  cholesterin,  neurin,  and  a  yellow  lipochrome.  Various  enzymes 
are  present,  but  very  little  is  known  about  them.  There  are  no  microbes, 
except  such  as  have  got  into  the  ducts  of  the  nipple  from  outside,  and 
possibly  into  the  milk  in  certain  infective  disorders,  such  as  puerperal  sepsis. 
The  salts  are  present  in  the  proportions  suitable  to  the  needs  of  the  growing 
animal,  while  the  percentage  of  the  sugar  is  fairly  constant,  and  that  of 
protein  and  fat  more  variable.  The  two  latter  constituents  vary  under 
numerous  conditions,  and  are  generally  the  cause  of  intestinal  derangement 
or  lack  of  progress  in  the  child. 

Human  milk  may  vary  in  quantity  or  quality.  It  may  contain  an 
excess  of  water,  or  vary  in  the  relative  proportions  of  its  different  con- 
stituents ;  occasionally  it  contains  deleterious  substances.  The  fore  milk, 
that  first  secreted,  contains  more  water  and  much  less  fat  than  the 
strippings,  that  obtained  last  from  the  gland.  The  strippings  of  cows  is 
sometimes  so  rich  in  fat  that  it  is  sold  as  cream. 

The  quantity  secreted  daily  varies  with  the  age  and  needs  of  the 
child.  At  1-3  months  the  normal  average  amount  is  600-900  c.c,  roughly 
1-1£  pints,  but  this  amount  is  often  exceeded.  The  quantity  increases 
rapidly  up  to  the  end  of  the  second  month,  and  then  much  more  slowly. 
Babies  vary  in  size  and  appetite  and  mothers  in  milk  secreting  powers. 
During  the  first  2  or  3  months  large  babies  take  from  15-20  per  cent.,  and 
small  babies  10-15  per  cent,  of  their  weight  in  milk  ;  after  that  the 
proportions  are  smaller.  The  daily  quantity  has  been  calculated  from 
observations  by  Hsehner,  Laure,  and  Ahlfeld  as  : — 


44  Chapter  III. 

From  the  end  of  the  1st  to  4th  week  10  to  25  oz. 

During  the  2nd  month  . .  ..  20  to  30  oz. 

From  the  3rd  to  6th  month       . .  ..  25  to  35  oz. 

From  the  6th  to  9th  month       . .  . .  30  to  40  oz. 

The  quantity  can  be  increased  by  stimulation  of  the  breasts,  either  by 
use  of  the  breast  pump  or  the  suction  of  other  infants  ;  the  ingestion  of  an 
increased  amount  of  fluid,  preferably  nutritious  fluid  ;  the  moderate  use  of 
stimulants  ;  extra  food,  maltine  and  somatose  ;  drugs  such  as  iron,  arsenic, 
and  strychnia  ;  faridisation  of  the  breasts  ;  gentle  massage  of  the  breasts 
for  10  minutes  3  times  a  day,  and  massage  of  the  abdomen  in  an  upward 
direction.  Galactagogues  are  drugs  said  to  directly  influence  the  secretion 
of  milk.  Subcutaneous  injections  of  nitrate  of  pilocarpin,  gr.  i,  for  a  few 
successive  days  may  increase  diminished  secretion  or  restore  one  rapidly 
failing.  Drachm  doses  of  tincture  of  common  goat's  rue  (galega  officinalis) 
5  times  a  day,  and  tincture  of  the  stinging  nettle  in  doses  of  |-1  oz. 
have  been  recommended  by  Grinewitch.  Veterinary  surgeons  give  infusion 
of  aniseed  freely  internally,  and  apply  it  to  the  mammae  as  a  fomentation. 
Thyroid  extract  is  sometimes  used. 

The  quantity  may  be  diminished  by  reducing  the  amount  of  liquid 
in  the  diet  and  giving  saline  cathartics.  A  full  dose  will  sometimes  entirely 
stop  secretion  for  a  time.  It  is  rarely  necessary  to  diminish  the  quantity 
of  the  milk,  for  if  it  is  too  poor  in  quality  it  is  better  to  try  and  improve 
it  by  measures  which  increase  the  percentages  of  solids.  Preparations 
of  belladonna  or  atropine  taken  internally  or  applied  locally  lessen  the 
secretion.  Camphor,  grs.  3-5,  3  times  a  day  for  3  days,  may  completely 
arrest  the  flow,  and  sometimes  potassium  iodide  lessens  it.  Complete 
agalactia  may  result  from  fright  or  sudden  shock. 

Age  has  very  little  effect  on  the  quality.  Menstruation  may  cause  an 
alteration  of  such  a  nature  as  to  set  up  indigestion  or  diarrhoea  in  the 
child.  Usually  a  slight  disturbance  of  the  digestion  is  all  that  results,  but 
occasionally  the  infant  is  seriously  affected.  More  generally  the  milk  is 
unaltered  and  the  child  unaffected.  Dyspepsia,  colic,  and  enteric  catarrh 
are  more  often  coincident  than  due  to  this  cause,  and  should  be  treated 
in  the  usual  way,  and  not  by  weaning.  If  the  milk  markedly  disagrees  it 
will  probably  be  because  of  an  excess  of  protein,  and  all  that  is  necessary 
is  to  lengthen  the  interval  between  the  nursings,  give  a  little  water  to  the 
child  before  nursing,  or  temporarily  modify  the  diet  and  mode  of  life  of  the 
mother. 

Should  the  mother  become  pregnant  while  nursing  the  question  of 
weaning  depends  on  several  factors.  Supposing  the  child  is  gaining  weight, 
and  is  contented,  and  the  mother's  health  is  not  suffering,  suckling  may  be 
prolonged  to  the  fifth  or  even  the  sixth  month  of  pregnancy.  If  so,  the  child 
must  be  weaned  entirely  by  the  end  of  the  month,  and,  as  a  rule,  at  a  much 
earlier  date.    If  the  baby  is  delicate,  or  the  weather  hot,  suckling  should  be 


Diet    and   Nutrition.  45 

continued  as  long  as  possible.  If  the  mother  is  delicate  or  the  milk  supply 
insufficient,  partial  weaning  may  be  begun  at  the  end  of  the  fourth  month. 
The  slight  risk  of  reflex  miscarriage  being  set  up  by  suckling  is  so  small 
that  it  may  be  neglected,  except  in  women  who  are  very  prone  to  miscarry. 
Few  conceptions  take  place  before  the  sixth  month  of  lactation,  and  at 
that  age  a  baby  can  generally  be  weaned  with  little  risk,  if  it  is  thought 
advisable  for  the  sake  of  the  foetus,  or  on  account  of  the  health  of  the 
mother. 

The  percentage  of  fat  in  milk  can  be  increased  by  a  liberal  supply  of 
protein  food.  Malt  extracts  also  increase  the  amount  of  fat.  Vegetable 
diet  diminishes  both  the  amount  of  fat  and  protein  in  the  milk.  An  increase 
of  protein  in  the  diet  also  increases  the  amount  in  the  milk,  and  thus  makes 
it  more  indigestible.  To  counterbalance  this  the  increased  nitrogenous 
diet  must  be  supplemented  by  an  increase  in  the  amount  of  exercise  taken. 
To  convert  a  poor  milk  into  a  digestible  rich  one,  give  a  liberal  protein  diet 
and  walking  exercise  morning  and  afternoon,  or  even  order  a  moderate 
amount  of  riding,  cycling,  and  lawn  tennis.  A  nursing  mother  must  not 
fast.  Deficiency  of  food  is  bad  both  for  her  and  the  child ;  the  milk  is 
weaker  in  protein  and  fat,  and  the  mother  has  to  draw  on  her  reserve  stores 
of  nutriment  to  provide  even  this  imperfect  diet. 

Alcohol  is  said  to  increase  the  proportion  of  fat,  to  slightly  diminish 
the  amount  of  sugar,  and  to  have  no  constant  effect  on  protein.  A  moderate 
amount  can  be  taken  without  injury  and  without  any  alcohol  appearing  in  the 
milk.  It  should  not  be  prescribed  as  a  general  rule  for  fear  of  setting  up  the 
alcoholic  habit,  but  in  some  cases  it  will  help  the  mother  to  continue  nursing. 
Good  milk  depends  on  suitable  food,  not  upon  stimulants.  To  insist  on  the 
prolongation  of  nursing,  when  it  can  only  be  continued  by  means  of  a 
considerable  amount  of  stimulation,  is  bad  for  both  mother  and  child. 

Increasing  the  frequency  of  nursing  increases  the  percentage  of  solids, 
especially  protein,  in  the  milk  ;  resulting  in  colic  and  indigestion.  The  more 
frequent  the  feeding  the  more  indigestible  the  milk  becomes.  By  lengthening 
the  intervals  between  the  feeds,  the  milk  may  be  rendered  more  digestible. 

In  order  to  alter  the  composition  of  milk  we  can  adopt  the  following 
simple  methods.  The  percentage  of  protein  is  increased  by  increased 
frequency  of  nursing,  increased  protein  food,  and  insufficient  exercise  ; 
and  is  decreased  by  the  opposite  conditions.  The  percentage  of  fat  is  in- 
creased by  increased  protein  food,  malt  extracts,  and  possibly  alcohol  ; 
and  is  diminished  by  excess  of  fatty  foods,  deficiency  of  protein  and  fasting. 
The  percentage  of  water  is  increased  by  an  increased  fluid  diet,  and 
diminished  by  a  lessened  ingestion  of  fluid  and  the  use  of  saline  cathartics. 

Certain  drugs  given  by  the  mouth  to  the  mother  are  partly  excreted 
in  the  milk  and  may  affect  the  child,  but  the  amount  of  excretion  is 
unreliable  and  uncertain.  Citric  acid  and  hydrochloric  acid  produce  no 
change  in  the  milk.    Sodium  salicylate,  potassium  iodide,  iodoform  applied 


46  Chapter  III. 

externally,  iodine  injected  intramuscularly,  and  colchicum  may  all  pass 
into  the  milk.  Mercury  is  transmitted  only  feebly  and  irregularly.  Lead, 
arsenic,  and  antimony  have  been  excreted.  Rhubarb,  senna,  and  saline 
cathartics  may  pass  into  the  milk  and  purge  the  child.  Opium  and  morphia 
taken  by  the  mother  have  sometimes  produced  deep  sleep  in  the  infant  ; 
so,  too,  chloral  hydrate.  The  effect  of  bromides  is  variable.  Phenazone, 
phenacetin,  and  urotropin  may  appear  in  the  milk,  and,  possibly,  atropine 
and  belladonna.  Attempts  to  treat  the  child  through  the  medium  of  the 
milk  supply,  by  giving  drugs  to  the  mother,  are  foolish,  and  uncertain 
in  their  results. 

Cow's  Milk. — The  general  composition  of  cow's  milk  is  like  that  of 
human  milk.  The  percentage  composition  differs.  In  addition  it  is  crowded 
with  micro-organisms,  and  is  a  very  suitable  medium  for  their  growth. 
Its  specific  gravity  ranges  between  1028  and  1035.  When  secreted  it  has 
an  amphoteric  reaction,  turning  litmus  blue  and  turmeric  brown.  With 
phenolphthalein  it  is  acid.  With  litmus  the  reaction  may  be  amphoteric, 
due  to  the  salts,  acid  and  alkaline  sodium  phosphate.  Citrates  are  more 
abundant  in  cow's  milk  than  in  human  milk,  the  amount  being  equivalent 
to  1-2-2  gms.  per  litre  (Obermeyer).  On  boiling,  the  soluble  bicitrate  of 
calcium  is  converted  into  a  less  soluble  tricitrate.  Many  ferments  are 
present  and  are  readily  destroyed  by  heat.  Microscopical  examination 
reveals  extraneous  substances,  such  as  epithelial  cells,  particles  of  manure 
hairs,  etc. 

The  total  solids  vary  within  considerable  limits  dependent  upon  the 
breed  of  the  cow,  the  period  of  lactation,  and  the  nature  of  the  food.  The 
total  solids,  less  fat,  vary  within  comparatively  small  limits  from  8-5-11 
per  cent.  Each  cubic  millimetre  contains  in  suspension  from  2-3  million 
fat  globules.  The  fat  is  poorer  in  olein  than  is  the  fat  of  human  milk, 
but  amounts  to  over  40  per  cent.  It  is  a  mixture  of  neutral  olein,  palmitin, 
and  stearin,  and  glycerides  of  the  fatty  acids,  palmitic,  stearic,  and  oleic. 
Glycerides  of  certain  volatile  fatty  acids,  chiefly  butyric,  caproic,  and 
caprylic,  are  present  in  small  quantities.  Purin  bodies,  lecithin,  choles- 
terin,  and  mineral  salts  are  also  present.    The  sugar  is  in  the  form  of  lactose. 

The  proteins  are  caseinogen  and  albumin.  The  terminology  of  proteins 
varies  with  different  writers.  The  caseinogen  of  Halliburton  is  the  same 
as  the  casein  of  German  writers,  and  the  free  casein  of  Van  Slyke  and  Hart, 
i.e.,  it  is  equivalent  to  calcium  casein  or  bicaseinate  of  calcium,  for  it  is 
always  combined  with  calcium.  The  casein  of  Halliburton  is  the  same 
as  the  paracasein  of  the  Germans.  Caseinogenate  of  calcium  or  basic  cal- 
cium casein  is  formed  by  adding  lime  water  to  milk  ;  caseinogenate  of  K. 
or  Na.  by  adding  alkalies  of  K.  or  Na.  ;  basic  calcium  casein,  plus  antacid, 
by  adding  bicarbonate  of  soda  ;  sodium  casein  by  adding  citrate  of  soda  ; 
and  calcium  lactate  in  buttermilk.  None  of  these  compounds  is  coagulable 
by  rennet.      Calcium  casein  forms  with  rennet  in  a  faintly  acid  medium 


Diet    and  Nutrition.  47 

calcium  paracasein  or  curd.  If  the  milk  is  rendered  alkaline  it  will  not 
curdle,  but  the  addition  of  a  small  amount  of  alkali  only  delays  clotting 
until  it  is  neutralised.  Further  observations  are  required  on  the  necessity 
for  and  justification  of  this  nomenclature. 

The  average  composition  of  cow's  milk,  obtained  by  different  analysts, 
does  not  show  nearly  the  same  discrepancies  as  in  the  case  of  human  milk. 
Protein  is  estimated  by  Kjeldahl's  process,  fat  by  Babcock's  apparatus  or 
Gerber's  acido-butyrometer,  and  sugar  by  Fehling's  process.  Provided  the 
milk  has  not  been  tampered  with,  its  specific  gravity  depends  chiefly  on  the 
percentage  of  fat.  This  varies  considerably  in  different  cows,  in  the  same 
cow  at  different  times,  and  during  the  same  milking  according  as  the  fore 
milk,  middle  milk,  or  strippings  is  taken  for  analysis. 

The  chief  fraud  in  milk  dealing  consists  in  the  removal  of  cream. 
To  detect  such  a  fraud  place  100  c.c.  in  a  graduated  vessel,  or  fill  any  glass 
cylinder  graduated  in  100  parts,  take  the  specific  gravity,  and  after  allowing 
the  milk  to  stand  for  24  hours,  read  off  the  proportion  of  cream  which  rises 
to  the  surface.  If  the  specific  gravity  is  within  the  limits  of  1028  to  1035, 
and  the  percentage  of  cream  on  standing  not  less  than  9,  it  may  be  con- 
sidered good  average  milk.  The  higher  the  percentage  of  cream,  and  the 
lower  the  specific  gravity,  the  less  likely  is  the  milk  to  have  been  tampered 
with. 

The  difference  between  milk  and  cream  is  essentially  one  of  fat 
percentage.  There  are  two  kinds  of  cream  :  (1)  Gravity  Cream,  obtained  by 
skimming  the  milk  after  it  has  stood  for  24  hours;  and  (2)  Centrifugal 
Cream,  obtained  by  the  use  of  a  separator.  The  latter  is  fresher  if  it  is 
made  from  fresh  milk.  Possibly,  to  a  slight  extent  the  emulsion  is  broken 
up  by  the  centrifugal  force.  The  richest  centrifugal  cream  contains  40-50 
per  cent,  of  fat.  Much  of  it  contains  20  per  cent.  only.  Gravity  cream 
is  very  variable,  and  usually  contains  about  16  per  cent,  fat ;  sometimes  it 
is  merely  rich  milk.  It  does  not  keep  well,  and  is  often  preserved  by  means 
of  ice  or  the  addition  of  preservatives.  If  the  cream  is  obtained  by  skimming, 
it  should  be  taken  from  the  mixed  milk  of  a  herd  and  not  from  a  fancy 
cow.  The  milk  should  be  allowed  to  stand  at  the  same  temperature,  for 
the  same  length  of  time,  and  skimmed  by  the  same  person.  Centrifugal 
cream  is  separated  from  the  mixed  milk  of  many  animals.  The  milk  is 
filtered,  cooled  to  40°  F.,  pasteurised,  centrifugalised  and  again  cooled 
to  40°  F.  The  fat  globules  may  become  coherent  and  indigestible,  giving 
rise  to  vomiting  of  water,  fat,  and  curd  in  succession.  This  is  most  liable 
to  occur  if  the  bottles  have  not  been  kept  cool,  or  have  been  much  shaken 
in  transportation. 

The  gravity  process  can  be  used  for  obtaining  cream  of  various  per- 
centages of  fat.  According  to  Townsend  the  top  quarter  of  milk,  which  has 
stood  for  6-8  hours,  contains  10  per  cent,  of  fat.  The  upper  half  will  contain 
7-8  per  cent.    Chapin  uses  the  top  12  oz.  of  a  quart  of  milk,  and  says  it 


48  Chapter  III. 

contains  12  per  cent,  of  fat.  Holt  states  that  the  upper  half  contains  7  per 
cent.  ;  the  upper  third,  10  per  cent.  ;  the  upper  fourth,  13  per  cent.  ;  and 
the  upper  fifth,  15  per  cent,  of  fat,  if  the  milk  is  allowed  to  stand  4-5  hours. 
All  cream  should  be  sold  according  to  the  percentage  of  fat  it  contains.  It 
should  be  pasteurised  at  the  dairy,  cooled  down,  and  kept  in  ice. 

Only  the  milk  from  healthy  cows,  subjected  to  the  tuberculin  test, 
should  be  used.  It  is  preferable  to  use  mixed  milk  from  a  large  number  of 
cows,  as  by  this  means  a  more  uniform  standard  quality  is  obtained.  Milk 
from  one  cow  only  is  liable  to  great  variation  according  to  the  period 
of  lactation,  the  nature  of  the  food,  and  the  condition  of  its  health.  The 
best  cows  are  Shorthorns,  Ayrshires,  Kerrys,  Devons,  and  Red  Polled. 
Jersey,  Alderney,  and  Guernsey  cows  yield  a  milk  containing  a  higher 
percentage  of  fat,  but  they  are  more  liable  to  disease.  The  milk  of  new 
calved  cows  must  not  be  used  because  the  colostrum  corpuscles  are  liable 
to  disagree.  The  milk  of  old  cows,  or  of  those  which  are  calved  for  a  long 
time,  will  be  thin,  watery,  and  deficient  in  fat.  Cows  should  have  a  liberal 
supply  of  clean  water,  plenty  of  food,  a  ration  of  nitrogenous  food,  and 
comparatively  little  exercise.  They  must  not  be  fed  on  fermented  food, 
such  as  the  refuse  of  breweries,  nor  allowed  to  drink  stagnant  water,  and 
the  pastures  should  be  free  from  noxious  weeds.  Frequently  the  milk  of 
cows  fed  on  turnips  and  linseed  or  cotton  cake  disagrees  with  infants.  A 
diet  of  hay  and  oats  or  of  grass  is  the  best.  Cow  houses  should  be  built  on 
the  most  approved  principles,  well  drained,  kept  scrupulously  clean  and 
lime-washed,  and  the  stalls  roomy.  No  deposit  of  manure  should  be 
allowed  near  the  sheds.  The  bedding  must  consist  of  clean  straw,  peat- 
moss, sand  or  sawdust,  fresh  twice  a  day.  The  floor  ought  to  be  swept  an 
hour  before  milking.  Plenty  of  light  and  ventilation  are  essential,  but  the 
shed  should  not  be  draughty  ;  a  temperature  of  about  50°  F.  is  the  most 
suitable.  On  no  account  should  the  cows  be  hurried  or  frightened  before 
being  milked. 

The  cow  must  be  kept  clean,  and  before  milking  the  udder  and  teats 
should  be  gently  washed  with  warm  water  and  dried  with  a  soft  towel,  and 
the  hands  of  the  milker  also  washed.  The  milker  must  wear  a  clean  overall, 
and  the  pail  be  thoroughly  scalded  out  with  boiling  water.  The  milk 
should  be  aerated  by  pumping  in  pure  air  by  means  of  a  suitable  machine 
or  by  pouring  it  in  a  thin  stream  from  can  to  can  in  the  open  air.  It  must 
then  be  cooled  to  60°  F.,  or  under  ideal  conditions  down  to  40°  F.  When 
sent  by  rail,  it  should  be  placed  in  milk  cans  fitted  with  lids  to  exclude  dust, 
and  put  in  vans  built  on  the  principle  of  the  refrigerator.  It  would  be  still 
better  if  the  milk  were  cooled,  bottled,  and  sealed  at  the  dairy  in  the 
country,  and  delivered  direct  from  the  station  to  the  consumer.  The 
shorter  the  distance  the  milk  has  to  travel,  and  the  fresher  it  is,  the  better 
for  the  infant.  Even  in  towns  it  ought  never  to  be  more  than  12  hours  old, 
and  no  chemicals  should  be  added  as  preservatives.     Borax,  boric  acid, 


Diet    and   Nutrition.  49 

salicylic  acid,  and  formalin  are  the  ones  chiefly  used.  Hydrogen  peroxide 
is  probably  harmless,  though  it  may  enable  milk  to  be  used  which  is  not 
properly  fresh.  To  test  for  boric  acid  in  milk  put  20  c.c.  in  a  beaker,  add  a 
drop  or  two  of  phenolphthalein  solution,  and  then  drop  in  a  solution  of 
caustic  soda  of  about  normal  strength  until  a  faint  pink  colour  appears. 
Pour  the  mixture  into  two  test  tubes,  and  to  one  part  add  an  equal  bulk 
of  distilled  water,  to  the  other  an  equal  bulk  of  a  neutral  50  per  cent, 
solution  of  glycerol  in  water.  If  boric  acid  is  present,  the  mixture  in  the 
first  tube  will  become  more  pink,  while  that  in  the  second  will  turn  pale  or 
white. 

Formalin  (40  per  cent,  formaldehyde)  is  added  as  a  preservative  in  the 
proportion  of  one  drop  to  each  ounce.  It  delays  the  action  of  rennet, 
gastric  digestion,  and  the  pancreatic  digestion  of  fibrin  and  starch. 
Schiff's  re-agent  (fuchsine  decolourised  with  sulphurous  acid),  impregnated 
with  sulphurous  acid  gas,  is  used  as  a  test.  Precipitate  casein  and  fat, 
and  add  the  filtrate  to  the  re-agent ;  it  turns  pink  if  formalin  is  present. 
Another  test  is  that  devised  by  Manget  and  Marion.  If  a  few  crystals  of 
amidol  are  sprinkled  on  slightly  diluted  normal  milk  it  becomes  pink  or 
salmon  colour,  and  canary  yellow  if  formaldehyde  is  present.  Whey  con- 
taining formaldehyde  turns  yellow  on  adding  amidophenol. 

To  test  for  salicylic  acid  make  an  ether  solution,  evaporate  it,  dissolve 
the  residue  in  alcohol,  and  add  ferric  chloride  ;  a  violet  colour  is  produced. 

Cow's  Milk  compared  with  Human  Milk. — It  is  impossible  to  prepare 
from  cow's  milk  a  fluid  identical  with  human  milk,  even  though  the  chemical 
composition  of  the  two  fluids  appears  the  same.  The  proteins  in  different 
milks  are  not  homologous,  and  their  digestibility  depends  partly  on  their 
special  bio-chemical  characters.  Part  of  the  indigestibility  of  cow's  mdk  is 
due  to  the  fat,  the  globules  being  from  10-15  times  larger  than  in  human 
milk.  There  is  evidence,  too,  that  the  sugar  is  not  chemically,  physically,, 
and  physiologically  the  same  in  the  two  fluids.  All  observers  are  agreed 
that  the  proportion  of  protein  coagulable  by  acid  (caseinogen)  is  much 
greater  in  cow's  milk  than  in  human  milk.  In  some  respects  it  differs  in 
the  two  fluids,  for  it  is  precipitated  with  greater  difficulty  by  acetic  acid, 
and  more  readily  by  magnesium  sulphate  from  human  milk  than  from 
cow's  milk.  The  curd  formed  by  the  addition  of  acid  or  rennet  ferment 
to  human  milk  is  finer  and  more  flocculent,  and  more  readily  digestible. 
According  to  Biedert,  cow's  milk  coagulates  in  the  stomach  like  human 
milk,  if  the  ratio  of  fat  to  protein  is  the  same.  Schlossmann  states  that  the 
coagulum  is  the  same,  if  albumin  is  added.  It  is  largely  a  question  of 
dilution  for,  if  from  4-5  times  its  bulk  of  water  is  added  to  cow's  milk, 
the  curd  obtained  on  adding  dilute  acetic  acid  closely  resembles  that 
of  human  milk.  This  implies  that  there  is  4-5  times  as  much  caseinogen 
in  cow's  milk  as  in  human  milk.  If  it  is  sufficiently  diluted  and  agitated,  the 
curd  with  rennet  is  similar  to  that  of  human  milk.     The  following  table 


50 


Chapter  III. 


shows  the  relative  proportions  of  the  two  proteins,  and  the  average 
differences  between  cow's  milk  and  human  milk.  In  human  milk  the 
caseinogen  bears  to  the  albumin  a  proportion  of  about  2  to  3  ;  in  cow's 
milk,  about  4  to  1.  My  own  analyses  gave  the  high  proportion  of  albumin 
1-4,  caseinogen  2-6  in  cow's  milk. 


Human  Milk. 

Cow's  Milk. 

Protein 

1-2 

3-5-4-0 

Caseinogen 

0-6-1-3 

2-5-3-7 

Albumin 

0-5-1-2 

0-5-1-0 

Fat              

3-4 

3-5-4-0 

Sugar 

6-7 

4-4 

In  order  to  prepare  from  cow's  milk  a  mixture  as  nearly  as  possible 
identical  in  composition  with  average  human  milk,  we  must  start  with  an 
average  standard  for  each.  For  practical  purposes  the  following  is  a  useful 
and  simple  standard  table  : — 


Cow's  Milk. 

Protein 

.       4-0 

Fat     . . 

.       4-0 

Sugar.. 

.       4-4 

Salts  .. 

.       0-6 

Water 

.     87-0 

Human  Milk. 

2-0 
4-0 
6-6 
02 

87-2 


The  effects  of  diluting  milk  with  water  can  be  easily  calculated  from 
this  table.  Sometimes  it  is  essential  to  dilute  it  with  4  or  5  times  its  bulk 
of  water,  or  even  more,  in  order  to  enable  the  baby  to  digest  it.  This 
is  due  to  relative  excess  of  caseinogen  in  cow's  milk  compared  with  that 
present  in  human  milk,  and  is  further  proof  that  there  is  from  4-5  times  the 
amount  in  cow's  milk. 

Of  the  numerous  methods  of  devising  a  milk  mixture  for  an  infant 
the  following  is  by  far  the  simplest.  Once  the  initial  difficulty  of  obtaining 
a  superfatted  milk  of  definite  fat  percentage  is  overcome,  it  is  easy  to  devise 
a  suitable  weak  mixture  and  gradually  to  increase  its  strength.  The  top 
half  of  a  good  mixed  milk  which  has  stood  from  4  to  6  hours  will  contain 
about  the  following  percentages  :  protein  4,  fat  8,  sugar  4.  A  mixture  of 
10  drachms  of  milk  sugar,  lime  water  1  oz.,  and  water  up  to  20  oz.,  will 
contain  6-25  per  cent,  of  sugar.  If  there  be  taken  of  the  top  milk  amounts 
increased  gradually  from  5  oz.  to  10  oz.,  and  of  the  sugar  solution  sufficient 
to  raise  the  total  amount  to  20  oz.,  the  percentage  composition  of  the  first 
mixture  will  be,  roughly,  protein  1*0,  fat  2-0,  sugar  6-0,  and  of  the  last, 
protein  2-0,  fat  4-0,  sugar  5-5.     If  a  higher  proportion  of  fat  is  desirable, 


Diet    and   Nutrition.  51 

the  milk  must  be  allowed  to  stand  a  similar  time,  and  only  the  top  third  used. 
The  apparatus  required  consists  of  an  ice  box,  2  syphons,  pasteuriser,  ther- 
mometer, feeding  bottles,  bottle  brushes,  absorbent  and  non-absorbent 
wool,  straining  muslin,  mixing  pitcher,  8  oz.  and  20  oz.  graduated  measures, 
bottle  warmer,  rubber  nipples,  bicarbonate  of  soda  and  boric  acid. 

The  home  modification  of  milk  carried  out  in  this  manner  makes  it 
unnecessary  to  know  the  exact  percentages  of  fat  and  protein  in  the  milk 
used,  provided  always  that  the  same  amount  of  top  milk  is  taken  after  the 
same  period  of  standing.  From  the  effect  on  the  child,  as  judged  by  the 
digestion,  character  of  the  stools,  and  gain  in  weight,  it  is  easy  to  decide 
whether  the  food  should  be  made  richer  in  protein  or  fat,  or  both. 

Laboratory  methods. — To  secure  accuracy  of  composition,  and  to 
minimise  the  chances  of  food  contamination,  milk  mixtures  are  made  up  in 
milk  laboratories  by  various  companies,  in  much  the  same  way  as  medical 
prescriptions  are  made  up  by  chemists.  A  prescription  is  sent  stating  the 
percentages  of  proteins  (caseinogen  and  albumin),  fat,  and  sugar  required, 
the  degree  of  alkalinity,  the  number  of  feeds  and  the  quantity  in  each, 
and  the  temperature  to  which  it  is  to  be  heated,  e.g.,  pasteurised  at  158°  F. 
or  167°  F.  The  component  parts  of  the  food  are  derived  from  the  milk  of 
cows,  sometimes  tested  with  tuberculin  to  ensure  freedom  from  tuber- 
culosis, and  properly  cooled  down.  The  cows  are  kept  under  the  best 
conditions  of  diet  and  hygiene,  and  special  precautions  are  adopted  during 
milking  for  the  sake  of  cleanliness,  and  in  keeping  the  milk  at  a  low  tempera- 
ture subsequently  and  free  from  contamination.  Cream  of  known  per- 
centage of  fat,  fat-free  milk,  whey,  20  per  cent,  milk  sugar  solution,  lime 
water,  and  distilled  water  are  the  materials  used.  This  method  saves  both 
doctor  and  nurse  the  trouble  of  writing  down  accurate  directions  and 
carrying  them  out.  It  is  merely  necessary  to  start  with  a  weak  mixture  and 
gradually  increase  its  strength  according  to  the  results.  This  system  of 
feeding  has  had  a  very  thorough  trial,  and  has  not  proved  satisfactory, 
except  for  temporary  purposes.  Some  babies  do  badly  on  it,  possibly 
because  of  too  low  a  percentage  of  protein,  too  high  a  percentage  of  fat, 
or  the  continued  use  of  cooked  food.  Pasteurisation  is  strongly  condemned 
by  many  physicians.  Occasionally  injurious  organisms  get  into  the  mixtures 
in  spite  of  the  care  taken.  The  child's  stomach  is  net  a  test  tube,  nor  is 
feeding  merely  a  chemical  experiment.  The  strongest  argument  against 
percentage  feeding  lies  in  the  fact  that  nature  does  not  provide  milk  of 
unvarying  chemical  composition.  It  has  been  shown  that  milk  varies 
at  different  times  of  the  day,  in  either  breast,  and  at  different  stages  of 
each  nursing.  Consequently,  it  is  scientifically  unsound  to  keep  rigidly  to 
definite  percentages  of  the  various  constituents,  and  still  more  so  to  provide 
the  same  percentages  in  each  feed.  The  constant  repetition  of  meals 
identical  in  flavour,  quality,  and  quantity  is  entirely  opposed  to  nature's 
method  of  feeding. 


52  Chapter  III. 

Artificial  Feeding. — Artificial  feeding  may  be  necessary  from  birth 
or  not  until  the  commencement  of  weaning,  which  should  normally  take 
place  in  the  tenth  month  of  life,  partial  suckling  being  continued  for  4  or  5 
weeks  longer.  Weaning  may  be  delayed  if  the  child  is  debilitated,  and 
during  or  after  acute  illness.  It  is  better  to  wean  during  cold  weather  than 
when  it  is  hot,  and  not  to  begin  when  a  child  is  actually  teething.  In  sudden 
weaning  the  child  is  taken  entirely  from  the  breast  and  put  on  a  milk 
mixture  suitable  for  its  age.  It  may  refuse  the  food  for  some  hours,  or  even 
a  whole  day,  but  will  give  in  to  the  cravings  of  hunger,  if  the  mother 
perseveres.  Gradual  weaning  is  a  better  method,  as  by  this  means  the 
child's  stomach  and  digestion  become  accustomed  to  the  artificial  food, 
and  it  is  easier  to  find  out  the  particular  mixture  which  is  suitable.  During 
the  first  week  one  such  feed  is  given  at  8  a.m.  ;  in  the  second  week  a  second 
bottle  is  given  at  8  p.m.  ;  in  the  third  week  a  third  bottle  is  given  at  2  p.m., 
or  4  bottles  are  allowed  daily  ;  and  in  the  next  week  or  two  the  remaining 
breast  feeds  are  also  replaced  by  the  bottle  feeds.  The  composition  of  the 
food  and  the  amount  for  each  feed  depends  on  the  age  of  the  child. 

In  artificial  feeding  we  have  to  take  into  consideration  (1)  The  size 
of  the  child's  stomach.  The  age  and  weight  of  the  child.  (2)  The  quantity 
of  food  for  each  feed.  (3)  The  number  of  feeds  to  be  given  in  24  hours. 
(4)  The  composition  of  the  substitute  food.  (5)  The  mode  of  preparation 
of  each  feed.  (6)  The  kind  of  bottle  to  be  employed.  (7)  The  temperature 
of  the  food  and  the  mode  of  administration.  (8)  The  preservation  of  the 
food.     (9)  The  cleanliness  of  all  the  apparatus. 

The  size  of  the  child's  stomach  varies  at  different  ages,  in  different 
children  of  the  same  age,  and  is  more  or  less  proportionate  to  the  size  of 
the  child.  The  difference  in  weight  before  and  after  nursing  represents 
the  weight  of  food  taken,  but  is  not  an  accurate  measure  of  the  capacity 
of  the  stomach,  for  some  of  the  food  passes  into  the  intestine  during  feeding. 
Estimations  of  gastric  capacity  must  be  based  on  the  results  of  several 
such  weighings  and  not  on  one  alone,  because  of  the  variation  in  the  child's 
appetite  "and  the  amount  of  milk  obtainable.  The  gastric  capacity  varies 
in  different  infants  of  the  same  size,  and  only  a  rough  average  can  be 
ascertained.  Post  mortem  measurements  are  unreliable,  for  the  stomach 
is  likely  to  be  over-distended.  The  stomach  is  very  small  at  birth,  and 
increases  rapidly  during  the  first  two  months  of  life,  and  only  slowly 
afterwards. 

The  stomach  capacity  may  be  estimated  as  equivalent  to  1  per  cent, 
of  the  original  weight  of  the  child  at  birth,  and  an  increase  of  1  gm. 
allowed  daily  up  to  the  end  of  the  first  month.  Thus  a  child,  weighing 
6J  lbs.  (3,000  gms),  would  require  for  each  feed  during  the  first  week 
1  oz.  ;  the  second  week  1|-  oz.  ;  the  third  week  1^  oz.  ;  and  in  the  fourth 
week  If  oz.  A  larger  child  might  have  an  extra  drachm  or  two  in  each 
feed.     In  the  second  month  the  gastric  capacity  amounts  to  2|  oz.  ;  for 


Diet    and   Nutrition.  53 

the  next  four  months  to  3-4  or  5  oz. ;  and  from  six  to  nine  months  to  5-6  oz., 
and  occasionally  more. 

The  quantity  of  food  is  based  upon  the  gastric  capacity.  A  bulky 
food  is  not  necessarily  a  nutritious  one,  and  too  rich  food  may  give  rise 
to  digestive  disturbance.  A  child  lives  and  grows  by  the  aid  of  the  food 
it  digests  and  assimilates.  Hand-fed  infants  are  often  overfed  as  to 
quantity  or  quality  of  food  ;  or  both  may  be  in  excess.  In  healthy  infants 
the  weight  of  the  child  is  a  better  indication  of  its  needs  than  is  its  age, 
but  neither  age  nor  weight  alone  is  sufficient  guide.  A  wasted  infant  may 
require  a  much  larger  quantity  of  food  than  its  weight  indicates.  On 
the  other  hand  fat,  rachitic  infants  are  unduly  heavy,  but  do  not  require 
more  food  in  consequence.  The  best  indication  that  the  food  is  satisfactory 
in  quantity  and  quality  is  a  regular  weekly  gain  in  weight,  combined 
with  contentment,  satisfactory  stools  and  the  usual  indications  of  health. 
Overfeeding  is  indicated  by  irritability,  constant  crying,  indigestion, 
vomiting,  colic,  and  unsatisfactory  stools. 

The  artificially-fed  child  requires  the  same  number  of  feeds  and  at 
the  same  intervals  as  the  breast-fed.  It  certainly  should  not  be  fed  more 
frequently.  The  breast-fed  child  empties  its  stomach  in  1^-2  hours, 
while  a  bottle-fed  one  generally  requires  ^  hour  longer,  according  to 
the  size  and  the  quality  of  its  meal.  The  child  should  have  10  feeds  at 
intervals  of  2  hours  during  the  first  month  ;  8.  feeds  at  intervals  of  2 \  hours 
during  the  second  month  ;  and  7  feeds  at  intervals  of  3  hours  subsequently. 
Often  after  the  age  of  6  months,  and  occasionally  before,  the  number 
of  feeds  can  be  reduced  to  6  and  sometimes  to  5  per  diem.  Prolonged 
intervals  between  meals  should  not  be  encouraged,  because  the  consequent 
hunger  leads  to  the  food  being  taken  too  rapidly,  and  may  result  in 
vomiting  or  gastro-enteric  disturbance. 

Cow's  milk  is  the  usual  food  used  as  a  substitute  for  breast-milk. 
It  should  be  obtained  fresh  twice  a  day.  In  exceptional  cases  it  may 
have  to  be  diluted  with  7  or  8  times  its  bulk  of  water,  in  order  to  gradually 
accustom  the  child  to  digest  it.  It  is  rare  for  any  child,  unless  extremely 
marasmic  or  suffering  from  gastric  disturbance,  to  be  unable  to  digest 
cow's  milk  properly  diluted  and  given  in  suitable  quantities  at  the  usual 
intervals.  It  is  a  common  practice  to  increase  the  strength  of  the  food 
with  the  increasing  age  of  the  child.  This  is  theoretically  unsound,  for 
the  maternal  milk  supply  increases  in  quantity,  and  not  in  quality,  as  her 
infant  gets  older.  At  the  age  of  2  months  it  is  generally  possible  to  train 
a  child's  stomach  to  digest  equal  parts  of  cow's  milk  and  water — that  is, 
a  mixture  containing  about  2  per  cent,  of  protein.  In  strong,  healthy 
children,  who  have  reached  the  age  of  6  months  and  are  taking  6  oz.  feeds, 
and  appear  to  require  a  richer  food  or  more  in  quantity,  it  is  better  to 
increase  the  strength  of  the  food  rather  than  the  bulk.  The  advantages 
of  undiluted  milk  were  urged  by  Parrot  in  1887,  and  supported  by  Budin 


51 


Chapter  III. 


and  Chavane,  who  obtained  very  satisfactory  results  by  feeding  infants 
on  sterilised,  undiluted  cow's  milk.  Prolonged  heat  makes  milk  less 
coagulable  by  rennet,  and  thus  counteracts  the  effect  of  excessive  protein 
in  the  stomach  ;  but  there  is  no  reason  to  suppose  this  excess  of  protein 
is  advantageous  to  the  infant.  Certainly  such  a  diet  sometimes  sets  up 
troublesome  digestive  disturbance.  Satisfactory  mixtures  for  artificial 
feeding  can  be  prepared  according  to  the  simple  method  above  described 
(p.  50),  or  as  is  shown  in  the  following  tables,  which  have  been  found 
suitable  for  the  average  child,  though  necessarily  requiring  modification 
for  special  cases.  Gravity  cream,  16  per  cent,  fat,  should  be  used  in 
preparing  these  mixtures.  If  the  rich  centrifugal  cream  containing  40-50 
per  cent,  of  fat  is  used  only  one-third  the  quantity  must  be  added. 

Diet  during  the  First  Month. 


Week  of  Life. 

One. 

Two. 

Three. 

Four. 

Milk 

2 

3 

4 

5 

Cream 

1 

1 

1 

1 

Water 

5 

6 

7 

8 

Lime  Water 

1 

1 

1 

1 

Milk  Sugar 

* 

i 

2 

i 

i 

The  quantities  are  given,  in  drachms. 


Diet  after  the  First  Month. 


Month  of  Life. 

Two. 

Three  to  Six. 

Six  to  Nine. 

Milk 

1  oz. 

1^-2  oz. 

2£-3  oz. 

Water 

1     „ 

H-2    „ 

2£-3   „ 

Cream 

1  dr. 

2-4  drs. 

2-4  drs. 

Lime  Water 

3     „ 

4      „ 

4     „ 

Sugar 

1     „ 

1 

1-2      „ 

1 

2     „ 

After  the  second  month  thin  barley  water  can  be  used  instead  of 
water,  and  the  lime  water  omitted.  If  cream  is  omitted  the  top  half  of 
milk  after  standing  should  be  used. 

In  preparing  each  feed  the  quantities  of  cream,  milk,  and  water 
required  for  12  hours  must  be  measured  out  in  a  graduated  measure  glass. 
Ordinary  spoons  are  unreliable  for  they  differ  considerably  in  size.      The 


Diet    and   Nutrition,.  55 

necessary  milk  sugar  or  cane  sugar  is  dissolved  in  the  water,  and  the  whole 
thoroughly  mixed.  The  mixture  must  be  kept  in  a  clean  jug  or  tightly 
sealed  glass  jar  in  a  cool  place,  surrounded  by  ice  water,  or  in  a  refrigerator. 
The  amount  for  each  feed  is  taken  out,  after  thoroughly  stirring  with  a 
clean  glass  rod.  It  is  poured  into  a  milk  saucepan  and  heated  until  it 
just  begins  to  boil.  It  is  then  cooled  down  and  given  to  the  child,  lime 
water  being  added  if  required.  Another  plan  is  to  prepare  the  quantity 
necessary  for  24  hours,  divide  it  up  into  the  number  of  feeds,  put  them 
in  separate  bottles,  and  sterilise  in  a  suitable  sterilising  apparatus,  such  as 
Soxhlet's  or  Hawksley's.  After  sterilisation  the  bottles,  stoppered  with 
cotton  wool,  are  kept  in  a  refrigerator  or  cool  cellar  and  used  as  required. 
The  system  of  boiling  milk  when  it  is  first  received,  and  allowing  it  to 
cool  down  gradually,  merely  covered  up  with  muslin  to  keep  off  the  dust, 
is  of  comparatively  little  value,  except  for  destroying  infective  organisms. 
Such  milk  goes  sour  almost  as  quickly  as  if  unboiled,  and  many  deleterious 
organisms,  or  their  spores,  escape  destruction  and  multiply  as  the  milk  cools. 

The  proper  kind  of  bottle  to  use  is  a  boat-shaped  one,  as  simple  as 
possible,  with  a  glass  stopper  and  valve  at  one  end  and  a  large  mouthpiece 
at  the  other,  for  the  attachment  of  a  simple  rubber  teat  which  can  be 
turned  inside  out  for  cleaning.  Bottles  with  long  rubber  tubes  must 
never  be  used,  because  of  the  difficulty  of  keeping  the  tubes  clean  ;  even 
glass  tubes  are  objectionable  for  the  same  reason.  A  further  advantage 
of  the  boat-shaped  bottle  is  that  each  feed  must  be  supervised  by  the 
mother  or  nurse. 

The  temperature  of  the  food  must  be  about  100°  F.,  ascertained  by 
the  thermometer,  and  not  by  taste  or  dipping  in  the  little  finger.  Neglect 
of  this  point  is  a  common  source  of  failure  in  artificial  feeding.  Frequently 
the  food  is  allowed  to  get  cold  before  it  is  finished.  The  food  can  be 
warmed  by  standing  the  bottle  containing  it  in  a  vessel  half  full  of  hot 
water,  or  by  means  of  one  of  the  food  warmers  in  the  market. 

The  child  should  be  fed  while  half  reclining  on  the  nurse's  lap,  with 
the  head  and  back  supported.  The  food  must  be  given  slowly,  and  the 
teat  kept  full,  to  prevent  air  being  swallowed.  Each  feed  should  occupy 
from  10  to  20  minutes.  The  hole  in  the  teat  must  be  of  sufficient  size  to 
allow  the  food  to  pass  through  slowly,  without  undue  exertion  in  sucking. 
After  being  fed,  the  baby's  mouth  is  gently  wiped,  especially  the  corners, 
and  the  child  put  quietly  in  its  cot  and  allowed  to  sleep.  Sucking  at  an 
empty  bottle,  or  at  one  of  those  abominations  known  as  "  Job's 
Comforters,"  should  not  be  permitted  ;  the  latter  may  lead  to  dirt  or 
organisms  being  conveyed  to  the  child's  mouth,  and  both  are  sources  of 
flatulence  and  indigestion. 

All  milk  should  be  fresh  and  kept  in  sweet  smelling,  cool  places, 
such  as  a  cellar  or  refrigerator,  or  in  a  tightly  corked  bottle  in  cold  or 
iced  water.     It  must  not  be  kept  in  a  nursery  or  bedroom,  or  where  it  can 


56  Chapter  III. 

be  contaminated  by  smells  from  drains,  housemaid's  sinks,  or  decomposing 
food.     A  window  ledge  with  a  north  aspect  is  often  a  convenient  place. 

Each  bottle,  after  use,  must  be  washed  out  thoroughly  in  hot  water 
and  then  in  soda  and  water,  a  bottle  brush  being  used.  It  is  then  rinsed 
out  several  times  in  clean  boiled  water  and  put  in  a  basin  of  clean  cold 
water  or  boric  acid  solution,  one  drachm  to  the  pint,  until  next  required. 
Before  use  it  is  again  rinsed  out  in  pure  boiled  water.  The  teats  are 
thoroughly  cleaned  and  kept  in  a  similar  way.  All  the  surroundings  of  the 
child — the  nursery,  the  cot,  and  the  nurse — must  be  kept  scrupulously  clean. 

Bacteriology. — Fresh  milk  possesses  a  certain  inhibitory  power  over 
the  growth  of  organisms.  According  to  Myer  Coplans  (1907)  breast-milk 
inhibits  bacterial  growth  absolutely  for  one  hour  and  almost  absolutely 
in  the  second  hour,  the  milk  being  digested  in  the  stomach  in  the  mean- 
time. Growth  is,  therefore,  inhibited  both  by  milk  and  gastric  juice. 
New  cow's  milk  possesses  inhibitory  powers  for  6  hours,  but  during  the 
next  6  hours  bacterial  growth  rapidly  takes  place.  The  only  alternative 
to  breast-milk  in  preventing  infantile  diarrhoea  is  new  milk,  kept  at  32°  F. 
immediately  after  milking.  Even  at  the  end  of  24  hours  half  its  inhibitory 
power  remains  ;  while  at  blood  heat  this  power  only  persists  for  1-2  hours. 
Under  ideal  conditions  cow's  milk  has  only  one-fourth  of  the  inhibitory 
power  of  human  milk.  Preservatives  damage  this  property  as  well  as 
restrain  microbial  growth.  It  is  completely  destroyed  by  boiling.  Hence, 
the  growth  and  destruction  of  organisms  in  the  stomach  depend  partly 
on  the  inhibitory  properties  of  the  milk  and  partly  on  the  gastric  juice. 

Milk,  as  it  reaches  the  consumer,  contains  organisms  varying  in  number 
from  J  to  10  or  more  million  per  c.c,  according  to  the  external  temperature, 
the  cleanliness  and  purity  of  the  milk,  and  the  care  devoted  to  its  manage- 
ment. In  America  certified  milk  can  be  obtained  containing  not  more 
than  30,000  germs  per  c.c,  4  per  cent,  fat,  and  0-02  per  cent,  acidity. 
The  longer  milk  is  kept  the  greater  is  the  liability  to  changes  due  to 
microbial  growth  and  the  further  is  it  removed  from  its  character  as  a 
living  fluid. 

The  chief  groups  of  organisms  are  those  that  give  rise  to  lactic  acid, 
butyric  acid,  and  peptonisation.  Lactic  acid  fermentation  is  the  common 
cause  of  milk  turning  sour,  and  is  due  to  numerous  types  of  lactic  acid 
bacilli.  The  degree  of  acidity  is  a  fair  test  of  the  number  of  organisms 
present.  The  lactic  acid  bacilli  are  comparatively  harmless,  and  beneficial 
by  crowding  out  and  preventing  the  growth  of  other  organisms.  Sour 
milk  is  obviously  no  longer  fresh,  and  to  delay  the  process  of  souring, 
by  the  addition  of  preservatives,  pasteurisation,  or  other  methods,  simply 
gives  oth'er  and  more  dangerous  organisms  a  better  chance  of  development. 
Sour  milk  does  not  go  putrid  for  a  long  time.  There  is  also  evidence 
that  lactic  acid  bacilli  and  lactic  acid  prevent  the  growth  of  injurious 
intestinal  flora  and  act  as  intestinal  antiseptics. 


Diet    and    Nutrition.  57 

The  organisms  of  diphtheria,  cholera,  specific  fevers,  and  tuberculosis 
are  readily  destroyed  by  heat,  as  in  pasteurisation,  boiling,  and  sterilisation. 
In  pasteurisation  milk  is  heated  to  158°  F.  for  20-30  minutes.  Boiling 
raises  it  to  a  temperature  somewhat  above  that  of  boiling  water  ;  and  in 
sterilisation  it  is  subjected  to  the  influence  of  superheated  steam  for  20-30 
minutes.  Apparently  heat  will  destroy  organisms,  but  not  the  products 
of  the  organisms  ;  so  the  fresher  the  milk  is  when  it  is  heated  the  less  is 
the  risk  of  the  presence  of  toxins.  Unfortunately,  though  these  tempera- 
tures destroy  organisms,  some  of  the  spores  escape  destruction ;  for 
instance,  the  spores  of  the  bacillus  subtilis  are  not  destroyed  by  6  hours' 
exposure  to  a  temperature  of  212°  F.,  and  those  of  the  bacillus  enteritidis 
sporogenes,  a  cause  of  infective  diarrhoea,  are  not  destroyed  by  more 
prolonged  exposure  at  an  even  higher  temperature. 

Pasteurisation  is  generally  a  measure  of  safety,  and  does  not  seriously 
change  the  character  of  the  milk,  nor  affect  its  taste  and  smell.  Rapid 
cooling  after  exposure  to  the  heat  is  an  important  part  of  the  process. 
Commercial  pasteurised  milk  is  often  an  unsafe  article  of  diet. 

Boiling  alters  the  taste  and  smell  of  the  milk,  rendering  it  objectionable 
to  many  infants.  During  cooling  a  thick,  tenacious  scum  forms  on  the 
surface  ;  it  is  composed  of  casein,  albumin,  fat,  and  salts.  The  milk  is 
devitalized,  and  is  possibly  more  indigestible  and  less  nutritious. 

Sterilisation  should  be  carried  out  as  soon  as  the  milk  is  received, 
by  means  of  one  of  the  various  sterilisers  in  the  market.  Properly  prepared 
commercial  sterilised  milk  is  better  in  so  far  as  dirt  and  foreign  bodies 
are  removed  by  the  separator,  and  the  milk  is  fresher  when  it  is  sterilised. 
The  risk  is  that  old,  unsound  or  unclean  milk,  imperfectly  sterilised,  may 
be  sold  under  this  name.  It  is  far  removed  from  fresh  milk,  and  liable  to 
give  rise  to  scurvy  from  prolonged  use. 

Heat  has  important  effects  upon  milk.  Odours  are  expelled.  About 
90  per  cent,  of  the  carbonic  acid  gas  and  50  per  cent,  of  the  oxygen  and 
nitrogen  are  driven  off.  Consequently  the  acidity  falls  and  earthy  phos- 
phates are  precipitated.  Some  of  the  citric  acid  is  precipitated  as 
tricalcium  citrate.  Ferments  are  destroyed,  salts  changed,  and  other 
alterations  in  the  milk  render  it  a  purely  artificial  food  unlikely  to  maintain 
perfect  nutrition.  These  changes  begin  at  140°  F.  The  milk  is  not 
rendered  absolutely  safe  from  bacterial  contamination,  for  Flugge  has 
shown  that  the  spores  of  12  different  kinds  of  aerobic  bacilli  survived  in 
milk  kept  at  boiling  point  for  2  hours  ;  these  organisms  are  liable  to  give 
rise  to  diarrhoea.  The  antiscorbutic  quality  of  the  milk,  highest  when  it 
leaves  the  udder,  diminishes  with  the  age  of  the  milk,  deteriorates  with 
exposure  to  heat,  and  may  be  absolutely  destroyed.  Possibly  this  quality 
is  connected  with  the  citric  acid  present  in  milk.  Heat  is  also  said  to 
render  fat  assimilation  more  difficult,  to  partly  destroy  sugar,  to  convert 
organic   phosphorus  into   inorganic   phosphates,   and  to   destroy  nuclein 


58  Chapter  III. 

and  lecithin.  On  the  whole  it  is  probable  that  no  cooked  milk  is  as 
nutritious  as  uncooked  milk,  and  that  the  nutritive  value  diminishes  in 
proportion  to  the  degree  and  duration  of  heating. 

It  is  unsafe  to  use  unheated  milk,  except  under  special  circumstances 
and  in  cold  weather.  On  the  other  hand,  no  amount  of  heat  will  destroy 
toxins  previously  formed,  nor  will  convert  bad  milk  into  good  milk.  A 
clean  milk  supply  is  of  more  importance  than  methods  employed  to 
counteract  the  defects  of  imperfect  milk.  Unfortunately  such  measures 
are  at  present  necessary.  Hospitals  should  insist  on  a  supply  of  pure 
clean  milk  from  healthy  cows,  cooled  down  to  at  least  60°  F.,  unadulterated, 
not  pasteurised,  free  from  preservatives,  and  containing  3 -25-3 -50  per 
cent,  of  fat. 

It  is  sometimes  important  to  be  able  to  tell  whether  milk  has  been 
cooked.  Some  dairies  send  out  their  milk  pasteurised.  Fresh  unheated 
milk  turns  red  on  the  addition  of  guiacol  and  1  per  cent,  solution  hydrogen 
peroxide,  added  drop  by  drop.  Saul's  test  consists  in  adding  1  per  cent, 
fresh  aqueous  solution  of  ortol  and  one  or  two  drops  of  peroxide  to  10  c.c. 
of  milk.  If  fresh,  the  colour  becomes  a  vivid  red.  Milk  heated  above 
158°  F.  does  not  give  these  peroxide  reactions  ;  there  is  no  change  in  colour. 

The  Effects  of  Heat  and  Attenuants  on  Curdling. — By  heating  milk  to 
various  temperatures  up  to  120°  C,  for  periods  of  J-l  hour,  and  then 
testing  the  coagulability  with  acetic  acid  and  rennet  ferment,  the  tempera- 
ture of  the  milk  being  first  reduced  to  40°  C,  the  following  results  were 
arrived  at.  It  was  found  that  heat  alone  did  not  render  cow's  milk  similar 
to  human  milk  in  its  reaction  to  acetic  acid.  If  the  exposure  at  a  high 
temperature  was  prolonged,  the  curd  became  more  coherent.  If  the  milk 
were  diluted  with  water,  before  being  heated,  the  size  of  the  curd  depended 
on  the  degree  of  dilution.  The  finest  curd,  very  like  that  of  human  milk, 
was  obtained  by  dilution  with  two  parts  of  water  and  exposure  for  J  hour 
at  100°  C.  Using  weak  barley  water,  thick  barley  water,  and  lime  water, 
similar  results  were  obtained  as  regards  the  degree  of  dilution.  The 
finest  curds  were  obtained  when  thin  barley  was  used ;  they  were 
even  finer  than  with  plain  water.  Up  to  80°  C.  lime  water  did  not  prove 
as  satisfactory  a  diluent  as  thin  barley  water.  Above  that  temperature 
the  milk  was  altered  in  colour  by  the  action  of  heat  on  the  lime  water, 
and  the  results  were  of  no  value. 

One  drop  of  rennet  coagulated  fresh  milk  in  two  minutes,  but  if  the 
milk  were  thoroughly  sterilised  by  exposure  to  100°  C.  on  3  successive  days 
for  1  hour  daily,  it  required  a  large  quantity  of  rennet  to  produce  coagulation. 
Even  at  the  end  of  45  minutes  only  a  soft  curd  was  produced.  More 
rennet  is  required  to  curdle  heated  milk,  and  the  amount  increases  with 
the  height  of  the  temperature  and  the  duration  of  the  exposure.  If  the 
milk  were  diluted,  as  well  as  heated,  the  softness  and  degree  of  coherence 
of  the  curd  depended  chiefly  on  the  degree  of  dilution,  rather  than  on 


Diet    and   Nutrition.  59 

the  amount  of  heat  applied.  Barley  water  did  not  appear  to  have  any 
more  effect  than  plain  water  on  rennet  curdling,  but  the  addition  of 
alkalies  lessens  this  coagulability. 

These  experiments  tended  to  show  that  the  essential  factor  in  rendering 
cow's  milk  like  human  milk  consists  in  simple  dilution  with  water  to  such 
an  extent  as  to  reduce  the  percentage  of  casein  to  that  present  in  human 
milk.  They  also  clearly  prove  that  heat  modifies  caseinogen,  possibly 
by  action  on  the  lime  salts,  to  such  an  extent  that  it  is  less  coagulable 
by  rennet.  Alkalies  produce  a  similar  effect,  e.g.,  the  addition  of  a 
grain  of  citrate  of  soda  to  each  ounce  of  milk.  More  may  be  added.  It  is 
generally  stated  that  citrate  of  soda  precipitates  some  of  the  lime  salts  ; 
but,  according  to  Variot  (1905),  it  rather  increases  their  solubility.  Citrate 
of  soda  is  a  neutral  salt,  very  soluble  in  water,  cheaper  and  more  effectual 
than  citrate  of  potash.  A  drop  or  two  of  chloroform  should  be  added  as  a 
fungus  is  liable  to  grow  in  weak  solutions.  It  appears  probable  that  the 
beneficial  effect  of  adding  citrate  of  soda,  or  alkalies,  to  milk  is  the  same 
as  that  produced  by  sterilisation.  By  preventing  the  coagulability  with 
rennet  ferment,  the  milk  does  not  curdle  in  the  stomach,  and  passes  on 
readily  into  the  small  intestine.  Gastric  digestion  is  relieved  and  replaced 
by  pancreatic  digestion. 

Subsidiary  Methods  of  Feeding. — Mechanical  attenuants  include 
decoctions  of  barley,  oatmeal  and  rice.  Egg  albumin,  gelatine  and 
dextrinized  foods  are  sometimes  used.  Oatmeal  is  the  richest  of  the 
cereals  in  fat,  and  is  somewhat  laxative.  Bice  is  practically  devoid  of  fat. 
Sometimes  the  milk,  whole  or  separated,  is  curdled,  and  the  curd  broken  up 
mechanically  with  a  fork  and  squeezed  through  muslin  or  a  fine  hair  sieve, 
thus  breaking  up  the  casein  particles,  which  do  not  again  become  blended 
into  coherent  masses  in  the  stomach.  For  curdling  the  milk,  junket  tablets 
or  various  preparations  of  rennet  can  be  used.  The  latter  are  variable  in 
strength,  made  with  glycerine,  and  may  not  be  pure.  Beauchamp  Hall 
recommends  the  use  of  tablets  containing  purified  and  standardised  rennet 
sufficient  to  curdle  |  pint  of  milk.  Each  tablet  is  made  up  with  sod.  bicarb, 
gr.  1£,  calcii.  phosphat.  gr.  ^,  and  lactose  gr.  5.  Ten  ounces  of  milk  yield 
seven  of  whey. 

Whey. — As  the  curd  contracts  it  squeezes  out  the  fluid  portion  or 
whey.  This  is  consequently  devoid  of  casein,  practically  fat  free,  and 
contains  about  the  same  amount  of  sugar  and  salts  as  the  original  milk. 
It  contains  on  an  average  0-85  per  cent,  of  albumin.  If  the  curd  is  squeezed 
through  muslin,  some  of  the  casein  and  fat  globules  pass  through,  and  the 
fluid  is  thereby  enriched.  Whey  is  an  easily  digested,  weakly  nutritive 
fluid,  useful  as  a  temporary  food  and  in  the  early  months  of  life.  Used  as 
a  diluent  of  milk,  it  is  a  valuable  means  of  increasing  the  amount  of  albumin, 
without  increasing  the  caseinogen.  A  mixture  of  cream  and  whey  is 
more  valuable,  in  that  it  contains   much  more  fat.     The    addition    of 


60  Chapter  III. 

1  dr.  of  cream,  16  per  cent,  fat,  to  2  oz.  of  whey  is  equivalent  to 
adding  1  per  cent,  of  fat.  When  either  cream  or  milk  is  added  to  whey, 
the  whey  must  be  first  heated  to  a  temperature  of  150°  F.  to  destroy 
the  rennet  ferment.  This  is  not  absolutely  necessary  when  only  small 
quantities  of  cream  are  added,  or  if  rich  centrifugal  cream  is  used. 

T art-rated  whey  is  recommended  by  Still  and  Myers  as  a  cheap  substitute. 
Eight  grains  of  tartaric  acid  are  added  to  milk  which  has  been  brought 
to  a  boil,  and  it  is  then  kept  simmering  for  5  minutes  and  is  strained  through 
butter  muslin.  Its  specific  gravity  is  1030  ;  protein  0-58  per  cent.,  fat 
1-2  per  cent.,  and  it  is  only  faintly  acid  to  litmus.  It  can  be  added  to 
milk  without  causing  further  curdling. 

Still  also  advises  the  use  of  a  cheap  cooking  sherry,  about  Is.  per 
bottle,  in  the  making  of  White  Wine  Whey,  because  it  contains  more  acetic 
and  tartaric  acid  and  less  alcohol  than  the  better  wines.  Ten  ounces  of 
milk  are  brought  to  a  boil,  2 J  oz.  of  sherry  added,  and  heat  again  applied 
until  the  mixture  begins  to  boil  up.  It  is  then  removed  from  the  fire 
and  allowed  to  stand  3  minutes  and  strained  through  butter  muslin. 
One  ounce  of  this  whey  is  about  equivalent  in  alcoholic  strength  to  25  drops 
of  brandy. 

Citric  Acid  Whey  is  made  by  boiling  a  pint  of  milk  with  2  teaspoonfuls 
of  lemon  juice. 

Peptonised  or  predigested  milk  is  prepared  by  means  of  Fairchild's 
zymine  powders,  or  the  Allenbury  peptonising  powders.  Directions 
for  making  it  are  given  with  the  powders.  The  milk  is  diluted  with  one- 
fourth  part  of  water,  and  the  duration  of  peptonisation  varies  from  10  to 
20  minutes,  after  which  the  mixture  is  boiled  to  prevent  further  digestion. 
If  the  process  is  carried  on  until  peptonisation  is  more  complete,  the 
mixture  becomes  bitter.  Curdling  during  peptonisation  is  probably 
due  to  the  use  of  stale  powders.  Fairchild's  peptogenic  milk  powder  is 
also  used  for  this  purpose.  It  consists  of  pancreatin,  bicarbonate  of 
soda,  and  milk  sugar.  A  mixture  of  milk  2  oz.,  cream  1  oz.,  water  2  oz., 
and  peptogenic  milk  powder  1  measure,  is  heated  slowly,  with  constant 
stirring,  so  that  it  is  brought  to  a  boil  at  the  end  of  10  minutes  ;  or  is  heated 
quickly  to  100-140°  F.  for  6  minutes.  The  resulting  fluid  is  often 
called  humanised  milk.  According  to  Leeds'  analysis  it  contains 
protein  2-0,  fat  4*5,  sugar  7-0  per  cent. ;  and  the  proteins  are  in  a  minutely 
coagulable  and  digestible  form.  Partial  predigestion  does  away  with  the 
need  of  other  methods  of  attenuating  the  curd,  though  it  may  be  advisable 
to  lower  the  percentage  of  proteins  by  dilution  with  water.  By  gradually 
reducing  the  duration  of  the  exposure  to  heat,  the  amount  of  predigestion 
can  be  reduced  and  a  return  to  the  ordinary  milk  diet  effected.  Or  one 
feed  of  unpeptonised  milk  may  replace  one  of  the  peptonised,  and.  if 
this  is  digested,  the  other  feeds  can  be  gradually  replaced  in  the  same 
way.      Used  reasonably  and  for  not  too  long,  say,  not  more  than  3  or 


Diet    and   Nutrition.  Gl 

4  months,  it  apparently  does  not  injure  the  digestive  capacity  of  the  child. 
It  is  chiefly  valuable  for  delicate  or  wasted  children  with  digestive  powers 
weakened  or  lost ;  for  young  infants  who  cannot  digest  modified  cow's 
milk;  and  in  febrile  disorders  interfering  with  digestion.  When  ordering 
peptonised  milk  full  directions  must  be  given  about  the  process  of  pre- 
paration and  amount  of  each  feed,  and  the  number  of  feeds  to  be  given 
in  24  hours. 

Various  kinds  of  dried  milk  are  occasionally  useful.  Some  of  them 
are  preparations  of  pure  casein,  e.g.,  biogene,  casumen,  plasmon,  protene, 
and  tilia.  Casein  is  combined  with  ammonia,  as  eucasin  ;  with  sodium, 
as  nutrose  ;  with  sodium  glycerophosphate,  5  per  cent.,  as  sanatogen  ; 
with  albumose,  20  per  cent.,  as  sanose.  Dried  casein  is  a  nutritious  food 
on  a  par  with  cheese  made  from  skimmed  milk,  and  is  a  valuable  addition 
to  a  diet  deficient  in  protein. 

Desiccated  whole  milk  is  sold  under  the  names  of  glaxo  and  lacvitum, 
and  desiccated  skimmed  milk  as  lacumen.  Glaxo  contains  nrotein  22-2 
per  cent.,  fat  274,  sugar  41-0,  ash  3-4,  water  6-0  (Guy's  Hospital  Gazette). 
Lacvitum  contains  protein  28  and  fat  29  per  cent.  Suitably  diluted, 
these  preparations  are  useful  as  temporary  foods  in  hot  weather,  but 
must  not  be  long  continued  because  of  their  liability  to  cause  scurvy, 
as  well  as  on  account  of  the  deficiency  in  fat. 

Condensed  milk  is  widely  used,  and  a  valuable  food  when  travelling, 
in  hot  weather,  in  marasmic  conditions,  and  if  good  cow's  milk  is  not 
obtainable.  There  are  two  main  varieties  :  (1)  simple  condensed  milk, 
and  (2)  condensed  milk  with  added  cane  sugar.  They  are  prepared  from 
skimmed  milk,  whole  milk,  or  whole  milk  with  added  cream,  and  evaporated 
down  to  one-third  or  one-fourth  of  their  bulk.  Unsweetened  condensed 
milk,  such  as  the  Ideal,  First  Swiss,  Viking  and  Hollandia  brands,  contain 
protein  8-11  per  cent.,  fat  9-12,  and  lactose  13-18.  Of  these  the 
Ideal  is  the  richest  in  fat.  They  are  useful  in  the  treatment  of  infantile 
diarrhoea  and  other  alimentary  disorders  in  which  a  large  amount  of  cane 
sugar  is  contra-indicated.  They  must  be  diluted  with  water,  and  cream 
and  milk  sugar  added  in  order  to  bring  their  composition  up  to  that  of 
human  milk.     The  milk  soon  turns  sour  when  the  tin  is  opened. 

Of  the  sweetened  condensed  milks,  Nestle's  and  the  Milkmaid  brands 
are  reliable,  and  are  prepared  under  satisfactory  conditions  of  purity 
and  general  cleanliness.  Similar  brands  are  the  Rose,  Full  Weight, 
Anglo-Swiss  and  Peacock.  All  these  contain  approximately  protein  10, 
fat  10,  sugar  60  per  cent.  They  must  be  diluted  with  eight  times  their 
bulk  of  water,  often  more,  and  the  addition  of  cream  is  necessary  to  raise 
the  percentage  of  fat.  Condensed  milk  is  given  much  too  diluted,  and  is 
popular  on  account  of  its  easy  digestibility  and  absorption,  and  because 
it  is  so  easy  to  prepare.  Its  weakness  is  compensated  for  by  the  greater 
quantity  taken,   but  the  usual  defects  arising  from  insufficient  protein 


62 


Chapter  III. 


and  fat  and  excess  of  sugar  are  likely  to  occur  (pp.  31-32).  Babies  fed 
on  condensed  milk  almost  always  develop  rickets.  Often  they  are  very 
fat,  are  liable  to  bronchitis  and  gastro-intestinal  derangements,  and  possess 
little  vital  resistance  to  disease.  Used  under  medical  advice,  excellent 
results  are  obtained,  and  the  lives  of  many  marasmic  infants  are  saved 
by  this  diet.  Extra  protein  can  be  given  in  the  form  of  egg  albumin, 
fat  in  the  form  of  cod-liver  oil  emulsion,  and  the  tendency  to  scurvy 
counteracted  by  means  of  fruit  juice.  Only  those  milks  condensed 
from  whole  milk,  or  from  whole  milk  with  added  cream,  should  be  allowed 
in  infant  feeding,  and  even  they  must  not  be  continued  as  a  permanent 
diet  for  more  than  a  few  months. 

Ass's  milk  is  very  useful  as  a  temporary  food,  and  can  be  obtained 
from  Welford's  Dairy  Company,  in  London  ;  but  is  somewhat  costly, 
3s.  per  pint.  It  is  supplied  in  sealed  glass  bottles.  One  ass  supplies 
enough  milk  daily  for  three  infants  under  3  months  of  age,  two  during 
the  fourth  and  fifth  months,  and  one  only  after  this.  The  milk  is  simply 
warmed  to  a  temperature  of  100°  F.  The  composition  is  shown  in  the 
following  table  : — 


The   Composition  of   Ass's  Milk. 


Dujardin- 
Beaumetz. 

Ellenberger. 

Cheadle. 

Wynter  Blyth. 

Peligot. 

Protein    . . 

! 

1-23 

i 

1-6 

1-7 

1-89 

1-95 

Fat 

3-01 

0-9 

1-4 

1-02 

1-02 

Sugar 

6-93 

i 

5-6 

6-4 

5-50 

6-48 

According  to  most  analyses  it  is  very  deficient  in  fat,  but  contains 
about  the  same  amount  of  both  kinds  of  protein  and  of  sugar  as  human 
milk.  Babies  do  well  on  it  for  a  short  time  only.  It  must  not  be  given 
for  more  than  two  or  three  months,  and  it  is  an  advantage  to  add  cream 
to  it.  Its  laxative  properties  are  counteracted  by  lime  water  and  destroyed 
by  boiling. 

Goafs  Milk  is  said  to  be  more  digestible  than  cow's  milk,  but  judging 
by  various  analyses  it  is  closely  allied  to  it.  Sometimes  it  has  a  strong 
odour  and  unpleasant  taste,  if  the  animal  is  ill,  fed  on  garlic,  ivy,  &c,  or 
milked  into  dirty  pails.  Its  chief  advantage  lies  in  the  fact  that  any 
one  with  a  small  plot  of  grass  can  keep  a  goat,  feed  it  carefully  and  obtain 
fresh  pure  milk. 

Kephir,  Matzoon  and  Koumiss  are  modifications  of  the  milk  of  the 
cow,  goat,  mare,  or  ass,  prepared  by  fermentation  by  means  of  yeast  or 
Kephir  grains.     They  are   quite  unnecessary.     It  is  preferable  to  give 


Diet    and   Nutrition.  63 

alcohol,  when  required,  in  simpler  forms  and  more  accurately  measured 
doses. 

Buttermilk  is  useful.  It  is  made  from  sour  cream  or  milk,  and  should 
be  less  than  24  hours  old.  It  contains  protein  2-3,  fat  0-25-1-5,  sugar 
3-0-3-5  per  cent.,  the  decrease  in  sugar  being  due  to  the  lactic  acid 
fermentation.  Its  acidity  is  about  0-5  per  cent,  and  calorie  value  9-12  per 
ounce.  In  the  process  of  preparation  the  calcium  casein  is  transformed 
into  calcium  lactate.  It  should  be  made  from  sour  milk  previously 
skimmed.  One  pint  is  churned  in  a  glass  churn,  holding  one  quart,  for 
15  minutes,  and  at  a  temperature  of  60-70°  F.  It  is  not  often  taken 
raw,  but  usually  sweetened  and  sterilised.  Add  1  teaspoonful  of  wheaten 
flour  and  4  of  granulated  sugar  to  a  quart  of  buttermilk,  with  constant 
stirring,  and  heat  to  boiling  point  in  a  double  saucepan.  If  heated  too 
much  it  will  curdle,  unless  constantly  stirred  or  made  slightly  alkaline 
by  the  addition  of  carbonate  of  soda.  It  must  be  cooled  rapidly  and 
kept  in  bottles.  It  contains  numerous  lactic  acid  bacilli,  if  unheated, 
and  a  considerable  amount  of  lactic  acid.  A  condensed  buttermilk, 
"  Nutricia,"  can  be  obtained. 

Lactobacilline  Milk  is  analogous  to  buttermilk,  and  is  prepared  from 
milk  by  inoculating  it  with  huge  numbers  of  lactic  acid  bacilli.  It  is  then 
sweetened  and  sterilised,  or  given  unheated  if  it  is  desired  to  give  large 
quantities  of  lactic  acid  bacilli  as  well  as  lactic  acid.  These  foods  are  useful 
in  enteritis  and  colitis,  and  are  supposed  to  limit  intestinal  putrefaction. 

Proprietary  Foods. — In  most  of  the  proprietary  foods  there  is  a  large 
quantity  of  carbohydrates,  frequently  in  the  form  of  starch.  In  some 
the  starch  is  partially  changed  into  dextrins,  dextrose,  and  maltose.  Others 
contain  much  cane  sugar.  Many  have  a  basis  of  condensed  milk.  Seeing 
that  there  is  no  substance  like  starch  in  milk,  it  is  unlikely  to  be  a  suitable 
food  for  young  infants.  The  amylolytic  ferment  in  saliva  is  secreted  in 
very  small  quantities  in  the  early  months  of  life.  It  is  found  in  the  sub- 
maxillary and  parotid  glands,  and  in  the  pancreas  of  newborn  infants, 
even  if  premature.  Possibly  a  small  amount  of  starch  can  be  digested 
by  this  ferment,  as  well  as  by  heat  and  moisture,  even  in  the  youngest 
infant ;  but  salivary  secretion  is  very  scanty  and  rarely  appreciable  before 
the  age  of  2  or  3  months.  During  the  third  month  secretion  is  much 
more  rapid,  and  its  activity  fully  develops  by  the  end  of  the  first  year. 
The  action  of  the  ferment  depends  partly  on  the  variety  of  starch,  and  is 
greater  when  the  starch  is  boiled.  The  pancreatic  secretion  exerts  a 
much  more  powerful  action.  We  may  conclude  that  a  weak  solution  of 
starch  can  be  used  as  a  diluent  after  the  second  month  of  life,  but  that 
any  excess  may  be  injurious,  because  undigested  starch  is  liable  to 
fermentation.  Many  infants  do  better  on  milk  and  water  than  when 
barley  is  used  as  a  diluent,  and  it  is  often  advisable  not  to  commence 
the  use  of  starch  before  the  age  of  6  months. 


64  Chapter  III. 

Many  objections  can  be  raised  against  the  use  of  proprietary  foods 
in  infancy.  A  child  can  be  brought  up  on  suitably  modified  cow's  milk. 
Extra  fat  can  be  given  in  the  form  of  cream,  olive  oil,  cod-liver  oil,  butter, 
or  margarine.  Extra  protein  can  be  given  by  using  whey  or  egg  albumin 
water  as  a  diluent,  or  by  adding  one  of  the  casein  preparations.  Carbo- 
hydrate can  be  added  in  the  form  of  milk  sugar,  cane  sugar,  maltose,  or 
honey.  After  the  age  of  6  months  the  common  starchy  foods  are  at  our 
disposal.  An  excess  of  carbohydrates  in  the  foods  containing  altered 
starch  produces  fatness  rather  than  health  and  strength.  The  mortality 
among  infants  brought  up  on  artificial  foods  is  enormous.  Some  infants 
digest  these  foods  with  impunity,  and  even  with  advantage,  but  they  are 
exceptional.  The  magnificent  babies  of  manufacturers'  advertisements 
only  exist  in  imagination,  or,  when  seen  in  the  flesh,  are  simply  fat  and 
rachitic.  Rickets  and  scurvy  are  undoubtedly  often  due  to  the  use  of 
these  foods.  Fortunately,  their  disadvantages  are  reduced  by  giving 
them  mixed  with  cow's  milk. 

Many  proprietary  foods  prepared  from  cow's  milk  only  have  been 
already  considered.  The  next  group  consists  of  those  prepared  from 
cow's  milk  with  the  addition  of  carbohydrates,  and  include  : — (1)  Condensed 
milk  with  malted  flour,  e.g.,  Allenbury  No.  2  Food,  Horlick's  Malted  Milk, 
and  John  Bull  No.  1  Food.  These  are  practically  devoid  of  starch. 
(2)  Condensed  milk  with  partly  malted  flour,  as  in  Manhu  food,  Milo  food,, 
and  Theinhardt's  Infantina.  (3)  Condensed  milk  with  unchanged  flour, 
as  in  Anglo-Swiss,  Franco-Swiss,  and  American-Swiss  food.  The  foods  in 
group  (1)  only  differ  from  sweetened  condensed  milk  in  containing  maltose 
instead  of  cane  sugar.  Those  containing  starch  are  unsuitable,  except  in 
very  small  amounts,  before  the  sixth  month  of  life. 

Benger's  Food  must  be  included  in  this  group,  for  it  is  a  mixture 
of  cooked  wheaten  meal  and  extract  of  pancreas,  and  is  prepared  with 
milk.  The  ferments  partially  peptonise  protein  and  partially  convert  the 
starch  into  soluble  dextrins  and  sugars.  The  fat  is  unaffected.  It  is 
valuable  for  marasmic  infants  after  the  sixth  month  of  age,  and  can  be 
used  in  small  quantities  of  ^-1  teaspoonful  in  each  feed  as  early  as  the 
fourth  month  of  life.  The  addition  of  a  small  half  teaspoonful  to  each 
feed  is  about  equivalent  to  using  thick  barley  water,  instead  of  water,  as 
a  diluent,  and  has  the  additional  advantage  of  partly  digesting  the  food. 
Care  must  be  taken  that  the  food  is  not  increased  in  quantity  at  the  expense 
of  the  essential  cream  and  milk.  CarnricFs  Soluble  Food  is  made  of 
desiccated  milk,  malt  and  wheat  flour,  lactose,  and  extract  of  pancreas. 
It  is  comparable  with  the  foods  made  from  condensed  milk  and  partly 
malted  flour,  and  is  much  inferior  to  Benger's  Food,  seeing  that  it  is  not 
made  with  fresh  milk. 

The  next  group  consists  of  the  pure  Carbohydrate  Foods,  and  may 
be  subdivided  into  three  classes  : — 


Diet    and   Nutrition.  65 

(a)  The  Starch  practically  unchanged. — Neaves',  Ridge's,  Opinus, 
Albany,  Robinson's  Patent  Barley  and  Groats,  Scott's  Oat  Flour, 
Chapman's  Flour,  &c. 

(b)  Partly  Malted  Foods. — Allenbury  No.  3,  Cheltine  Infants' 
Food,  Coomb's  Malted  Food,  Hovis  No.  2,  John  Bull  No.  2,  Moseley's, 
and  Savory  and  Moore's  Food. 

(c)  Completely  Malted  Foods. — Mellin's,  Horlick's,  Paget's  Malted 
Farina,  and  Hovis  Babies'  Food.  Others  of  a  like  nature  are  Cheltine 
Maltose  Food,  Diastased  Farina,  and  Racia. 

The  completely  malted  foods  can  be  given  at  an  early  age  in  small 
quantities  and  in  preference  to  cane  sugar,  provided  that  they  are  not 
unduly  laxative  and  are  not  given  instead  of  cream  and  milk.  It  may  be 
advisable  to  use  the  partly  malted  foods  before  the  end  of  the  sixth  month, 
but  those  composed  of  unchanged  starch  are  never  really  necessary. 
If  it  is  desired  to  gradually  train  the  child  in  the  digestion  of  starch,  we 
can  begin  with  a  purely  malted  food,  as  Mellin's,  pass  on  to  a  partly  malted 
one,  such  as  Savory  and  Moore's,  and  then  give  one  of  unaltered  starch. 
It  is  simpler  and  generally  quite  as  satisfactory  to  begin  with  thin  barley 
water  and  gradually  make  it  thicker  and  thicker. 

The  Meat  Preparations  include  various  brands  of  meat  teas,  extracts, 
juices  and  jellies,  peptones  and  peptonoids,  and  meat  powders.  Most 
of  them  consist  of  extractives,  of  no  nutritive  value,  possibly  stimulating 
the  digestive  functions  and  throwing  an  extra  strain  on  the  liver  and 
kidneys.  The  high  proportion  of  salts  and  extractives  is  liable  to  cause 
thirst  and  diarrhoea.  Some  of  the  meat  jellies,  though  expensive  and 
innutritious,  have  a  pleasant  flavour,  are  taken  by  a  feverish  infant  who 
refuses  other  food,  and  may  encourage  appetite.  Similarly  hot  fluids,  like 
beef  tea,  are  pleasant  to  the  febrile  tongue  and  in  disordered  digestion. 
In  small  quantities  they  do  no  harm,  and  comfort  an  anxious  mother 
who  fears  her  child  will  die  of  starvation,  and  has  a  profound  faith  in  the 
nutritive  value  of  these  preparations.  As  ordinary  articles  of  an  infant's- 
diet  they  must  be  condemned,  for  they  are  apt  to  spoil  the  appetite  for 
the  simpler  milk  and  carbohydrate  foods.  If  given  in  any  quantity  they 
set  up  an  irritable,  neurotic  state  and  a  tendency  to  night  terrors.  There 
is  no  serious  objection  to  giving  home-made  chicken  tea,  mutton  broth,, 
and  similar  foods  in  the  last  quarter  of  the  first  year  of  life,  especially 
if  it  is  desired  to  reduce  the  nutritive  value  of  the  diet.  A  daily  feed  of 
chicken  broth,  thickened  with  pounded  vegetables  and  some  cereal,  i& 
useful  for  fat,  plethoric,  overfed  babies,  who  have  been  brought  up  on  an 
excess  of  malted  foods,  cream  and  milk.  It  reduces  the  total  calorific 
value  of  the  diet,  and  gives  the  stomach  less  work  to  do. 

Of  the  proprietary  meat  preparations  commonly  used,  Liebig's  Extract 
is  free  from  protein  and  fat ;  Bovinine  appears  to  be  a  mixture  of  blood 
and  glycerine  ;   Puro  is  apparently  chiefly  made  of  egg  albumin  ;   Vinsip 

F 


6G  Chapter  III. 

is  a  mixture  of  blood,  boric  acid,  and  alcohol ;  and  Valentine's  meat  juice 
is,  according  to  Chittenden,  most  innutritious  and  contains  only  0*55  per 
cent,  of  coagulable  protein  and  gelatine.  Bovril  appears  to  be  the  most 
trustworthy  and  nutritious.  No  meat  preparation  containing  alcohol 
or  kola  should  be  given  to  infants. 

Though  not  really  necessary,  proprietary  foods  are  often  of  very 
great  value,  more  especially  the  malted  foods,  if  they  are  used  with 
discrimination  as  additions  to  the  diet,  and  not  as  substitutes  for  cream 
or  milk.  It  is  important,  therefore,  to  be  acquainted  with  their  compo- 
sition, or  one  is  likely  to  be  led  into  errors  of  selection  and  fatal  dietetic 
calamities.  Unfortunately  the  evil  results  of  erroneous  methods  of  feeding 
may  not  develop  for  some  months,  and  are  constantly  ascribed  to  other 
causes.  A  skilled  acquaintance  with  the  use  of  cream,  milk,  various 
kinds  of  sugar,  and  starchy  foods,  renders  one  independent  of  recourse  to 
patent  foods. 

Diet  after  Weaning. — In  the  process  of  weaning,  during  the  tenth 
month  of  life,  the  diet  is  changed  to  one  of  cream,  milk,  barley  water, 
and  sugar,  according  to  the  methods  recommended  under  the  head  of 
artificial  feeding.  Instead  of  barley  water,  barley  jelly,  oatmeal  jelly, 
or  a  thin  gruel  made  with  cornflour,  ground  rice,  fine  oatmeal,  or  arrowroot 
may  be  added  to  the  milk  and  well  boiled.  The  next  step  is  the  addition, 
of  one-half  to  one  whole  nursery  rusk  or  Robb's  biscuit,  to  one  or  two 
feeds  a  day  of  milk  two  parts  and  water  one  part,  or  equal  parts.  If  the 
child  is  at  all  anaemic  or  rachitic,  it  is  advisable  to  give  from  one  to  two 
teaspoonfuls  of  yolk  of  egg,  raw  or  lightly  boiled,  in  two  of  the  daily  milk 
feeds,  or  the  yolk  of  egg  and  raw  meat  juice  on  alternate  days.  The 
drawbacks  to  meat  juice  are  that  it  is  difficult  to  get  quite  fresh,  meat, 
that  it  keeps  badly  in  hot  weather,  and  the  slight  risk  of  the  child  acquiring 
tapeworm.  It  is  best  prepared  by  means  of  a  meat  press,  such  as  the 
Hercules  meat  press,  but  can  be  made  by  mincing  meat,  pounding  it  up 
in  a  mortar  with  a  pinch  of  salt,  and  standing  it  in  a  clean  cup,  with  just 
enough  cold  water  to  cover  it,  for  2-3  hours,  and  then  squeezing  it  through 
muslin.  It  must  be  kept  in  a  closed  bottle  surrounded  by  ice  in  a  re- 
frigerator. This  diet  can  be  continued  till  the  end  of  the  first  year,  or 
amplified  in  the  last  month  by  the  addition  of  custard  or  plain  milk  pudding. 
Five  or  six  meals  a  day  are  sufficient. 

Diet  from  12  to  18  months  of  age. — The  simple  milk  and  carbohydrate 
diet  may  be  continued,  if  the  child  and  mother  are  satisfied.  The  milk 
must  be  still  diluted  with  one-third  its  bulk  of  diluent.  Often  a  more 
mixed  diet  is  desired,  and  can  be  drawn  up  on  the  following  lines  : — 

First  Meal,  at  6  to  7  a.m.  : — 

Six  ounces  of  boiled  milk,  hot  or  cold. 

A  slice  of  stale  bread  or  a  rusk  broken  up  and  soaked  in  the  milk, 
or  a  slice  of  thin  bread  with  dripping  or  butter. 


Diet    and  Nutrition.  67 

Second  Meal,  at  8.30  to  9.30  a.m.     One  of  these  daily  :— » 
A  small  basin  of  bread  and  milk. 
A  little  fine  oatmeal  porridge,  with  cream  or  milk. 
A  basin  of  thick  milk  gruel. 

A  cup  of  thin  cocoa  made  with  milk,  and  a  little  thin  bread  and 
butter. 

Third  Meal,  at  1  p.m.  : — 

First  Course  ;  one  of  the  following  : — 
Mashed  baked  old  potato  moistened  with  milk,  chicken  or  mutton 
broth,  the  red  gravy  of  undercooked  meat    or    meat    juice 
(1-3  oz.). 
Lightly  boiled  or  poached  yolk  of  egg  mixed  up  with  stale  bread 

crumbs  or  mashed  potato  and  gravy. 
Stale  breadcrumbs  soaked  in  gravy  or  meat  juice. 

Second  Course  ;  one  of  the  following  : — 

A   large    tablespoonful    of    custard,    tapioca,    cornflour,    ground 

rice,  or  semolina  pudding,  blancmange  or  junket. 
Cold  boiled  water,  or  milk  and  water,  to  drink. 

Fourth  Meal,  at  5  p.m.  : — - 

The  same  as  the  first  meal,  or  thin  cocoa  with  bread  and  butter. 

Fifth  Meal,  at  9  p.m.  : — 

A  large  cupful  of  milk  gruel  made  with  rice,   sago,  tapioca,  or 
hominy,  or  a  rusk  or  sponge  finger  soaked  in  milk. 

Many  other  foods  can  be  given  at  this  age,  especially  those  of  a  carbo- 
hydrate nature,  preparations  of  egg,  and  small  quantities  of  jellies  and 
fruits,  such  as  baked  apple,  the  pulp  of  grape  and  oranges,  and  even  mashed 
banana  if  it  is  thoroughly  ripe.  If  the  child  is  healthy  and  strong  a  small 
portion  of  pounded-up  fish,  chicken,  or  meat  may  be  given  at  the  midday 
meal,  when  15  months  old. 

During  the  next  period  from  the  eighteenth  month  to  the  middle 
of  the  third  year  of  life,  a  somewhat  similar  diet  is  given,  including  meat, 
fish,  vegetables  and  fruit. 

Diet  from  the   Age  of  18-30  months. 

First  Meal,  6.30  to  7.30  a.m.  :— 

A  large  cupful  of  milk,  with  rusk,  stale  bread,  or  milk  biscuit 
broken  up  and  soaked  in  it,  or  some  bread  and  butter. 

Second  Meal,  at  8.30  to  9.30  a.m.  ;  one  of  the  following  : — 
A  basin  of  bread  and  milk. 

Oatmeal  porridge,  with  cream,  milk,  or  golden  syrup. 
A  basin  of  hominy  grits  or  Quaker  Oats,  and  milk. 
Boiled  milk  or  cocoa,  with  bread  and  butter. 
Boiled  milk,  a  lightly  boiled  egg,  and  bread  and  butter  or  dripping. 


68  Chapter  III. 

Third  Meal,  at  1  p.m.  : — 

First  Course  ;  one  of  the  following  : — 
Mutton,  undercooked  beef,   chicken,  turkey,  or  fish,  minced  up 
finely,  pounded  up  in  a  mortar  into  a  paste  for  the  younger 
children  ;  one  tablespoonful  of  one  of  these  mixed  up  with 
mashed  old  potato  or  stale  breadcrumbs  and  gravy  :  vege- 
tables, such  as  spinach,  young  green  peas,  young  asparagus 
tips,  &c. 
Lightly  boiled  or  poached  egg,  with  mashed  potato  or  stale  bread- 
crumbs and  gravy. 
A  large  cupful  of  broth  or  soup  (puree)    with  mashed  potato  or 
stale  breadcrumbs. 
Second  Course  ;  one  of  the  following  : — 

Custard  or  plain  milk  pudding,  blancmange,  cornflour  or  ground 
rice  mould,  plain  sweetened  jellies,  baked  apple  and  junket. 
Fourth  Meal,  at  5  p.m.  : — 

A  large  cupful  of  milk,  with  bread  and  butter,  rusks,  milk  biscuits, 

or  sponge  fingers. 
A  cup  of  thin  cocoa,  made  with  milk,  and  bread  and  butter  or 

honey. 
A  small  basin  of  milk  gruel  or  bread  and  milk. 
Fifth  Meal,  at  9  p.m.,  if  the  child  wakes  for  it  : — 

A  cup  of  boiled  milk,  with  a  biscuit  or  piece  of  bread  soaked  in 
it,  or  a  cup  of  milk  gruel. 
Other  vegetables,  such  as  broccoli,  cabbage,  turnip  tops  and  cauli- 
flower, may  be  given,  if  passed  through  a  sieve.  Carrots,  potatoes,  and 
artichokes  maybe  allowed  in  the  form  of  vegetable  purees,  providing  they 
are  thoroughly  well  cooked.  Water  should  be  taken  as  a  drink  at  dinner 
time,  arid  either  water  or  barley  water  given  frequently  in  small  quantities 
between  meals  to  relieve  thirst  and  in  hot  weather.  Tea,  coffee,  and 
stimulants  may  not  be  permitted. 

When  all  the  milk  teeth  are  cut,  four  meals  a    day   are   required, 
distributed  as  follows  : — 

Diet  after  the   Age  of  1\  years. 
Breakfast,  at  7.30  to  8.30  a.m.  : — 

Either  bread  and  milk,  porridge   with  milk  or  golden  syrup,  or 
hominy  grits  or  other  cereal  food  and  milk  ;    egg    boiled, 
poached,  or  scrambled  ;  bread,  with  butter,  dripping,  or  fruit 
jelly  ;  milk  or  cocoa  to  drink. 
After  the  Age  of  4  ;  second  course  : — 

Eggs ;  plain  omelette ;  a  little  fat  bacon  or  ham ;  a  little  fish ; 
fresh  potted  meat. 
Lunch,  at  11  a.m.  :— 

A  cupful  of  milk,  and  a  slice  of  bread  and  butter  or  a  plain  biscuit. 


Diet    and  Nutrition.  69 

Dinner,  at  1  p.m.,  of  two  courses,  selected  from  : — 

Vegetable  purees,  minced  beef,  mutton,  chicken  or  turkey ;  boiled 
fish ;  poached  egg  ;  brains  ;  sweetbread ;  mashed  potatoes 
and  pounded-up  vegetables ;  macaroni.  Milk  puddings, 
blancmanges,  farinaceous  moulds,  stewed  fruits,  jellies. 

Tea,  at  5  p.m.  : — 

A  basin  of  bread  and  milk,  milk  gruel,  hominy  and  milk  ;  a  cup 
of  milk  with  bread  and  butter,  biscuit,  or  bread  and  potted 
meat  or  fish  ;  fruit  jellies  may  also  be  allowed. 

Supper,  at  9  p.m.,  if  required  : — 
A  cup  of  milk  and  biscuit. 

After  the  age  of  4  years  meat  need  not  be  minced  if  the  child  eats 
slowly  and  masticates  thoroughly.  Rabbit  and  veal  must  be  well  boiled, 
minced,  and  pounded.  Red  meat  should  not  be  given  more  frequently 
than  three  times  a  week,  because  of  its  stimulating  effects  on  metabolism 
and  nervous  tissues.  If  the  diet  is  plain,  and  the  child  eats  slowly,  it 
may  eat  as  much  as  it  wants.  After  the  age  of  5  years  three  meals  a  day 
are  generally  sufficient,  but  in  addition  milk  and  biscuit  or  some  fruit 
may  be  allowed  in  the  middle  of  the  morning,  and  more  milk  and  biscuit 
at  bedtime.  Eating  between  meals  must  not  be  encouraged,  as  it  leads 
to  loss  of  appetite.  Highly  seasoned  made-up  dishes,  fried  foods,  and 
indigestible  foods  such  as  pork,  tough  steak,  duck,  goose,  nuts,  candied 
fruits,  and  pineapple  should  be  avoided.  If  not  too  new  or  decayed, 
cheese  can  be  given.  Salt  should  be  the  only  condiment.  Fruit  must  be 
ripe,  not  over-ripe,  and  not  allowed  in  unlimited  quantity. 

Diet  during  School  Life. 

The  diet  must  be  liberal  in  protein  and  fat,  contain  a  due  supply  of 
vegetables,  and  above  all  the  food  must  be  fresh.  The  child  should  have 
a  cup  of  milk  or  cocoa*  with  biscuit  or  bread  and  butter,  if  there  is  a 
morning  lesson  or  morning  chapel  before  breakfast. 

Breakfast  should  consist  of  two  courses  : — (1)  A  cereal  food,  such  as 
porridge,  Quaker  Oats,  etc.,  with  salt,  milk,  cream,  or  golden  syrup,  or  bread 
and  milk  ;  (2)  eggs  in  some  form,  fish,  bacon,  ham,  tongue,  meat  rissoles, 
etc. ;  and  fruit,  lettuce,  or  radishes  when  in  season.  Cocoa,  milk,  or  weak 
tea  should  be  given,  and  a  liberal  supply  of  bread,  rolls,  toast,  and  butter. 

In  the  middle  of  the  morning  milk  and  biscuit  or  fruit  can  be  given. 
This  is  important  in  cold  weather  and  for  delicate  children. 

At  dinner  each  child  should  be  given  a  sufficient  portion  of  meat, 
potatoes,  and  green  vegetables.  Fish  may  be  allowed  once  a  week,  preceded 
by  a  vegetable  puree.  Any  kind  of  simple  pudding  is  suitable  for  the 
next  course,  especially  those  that  contain  suet,  jam,  or  fruit.  In  addition, 
plain  cheese,  bread  and  butter  should  be  eaten  if  wanted.     Cheese  is  a 


70  Chapter  III. 

valuable  addition  to  a  diet  deficient  in  protein.  Water,  barley  water, 
oatmeal  water,  or  lemonade  are  the  usual  drinks. 

Tea  should  be  given  at  6  p.m.,  and  consist  of  unlimited  bread  and 
butter;  various  kinds  of  jams  or  marmalade;  freshly  potted  meat  or  fish; 
sardines ;  egg,  cress,  or  tomato  sandwiches ;  plain  cakes  and  biscuits,  with 
milk,  cocoa,  or  weak  tea : — if  sufficiently  liberal,  supper  is  unnecessary. 
Older  children,  who  do  not  go  to  bed  till  10  or  10.30  p.m.,  should  have 
more  protein  food  at  tea,  such  as  fish,  meat  rissoles,  calves'  head,  or  eggs. 
If  not,  milk  and  biscuit  may  be  allowed  at  9  p.m.,  but  no  late  meal  of 
bread,  beer,  and  cheese.     Alcohol  is  quite  unnecessary  during  school  life. 

Fats,  nitrogenous  foods,  and  milk  are  of  the  utmost  importance. 
A  child  requires  from  J-l  lb.  of  nitrogenous  food  daily,  and  1-li  pints  of 
milk.  Animal  proteins  must  not  be  replaced  by  vegetable  ones,  and  no 
tinned  foods  are  permissible  except  sardines.  The  proteins  and  fats 
must  be  distributed,  and  neither  given  mainly  at  only  one  meal. 

Girls  require  just  as  liberal  a  diet  as  boys,  if  they  get  as  much  exercise. 
This  is  especially  necessary  during  the  period  of  rapid  growth,  which  takes 
place  two  years  earlier  in  girls  than  in  boys,  namely,  from  11-16  years  of 
age.  Refusal  of  food  indicates  a  visit  to  the  tuck  shop,  a  hamper  from 
home,  lack  of  variety  in  the  diet,  ill-cooked  or  badly  served  meals,  tainted 
food  or  illness. 

Diet  during  Illness. 

So  great  is  the  importance  of  diet  in  the  treatment  of  disease  in 
children,  that  it  often  takes  precedence  of  every  other  measure.  Many 
ailments  depend  upon  improper  food  or  overfeeding.  In  the  treat- 
ment of  all  gastric  and  intestinal  affections  the  diet  must  be  carefully 
regulated ;  in  babies  according  to  the  methods  already  discussed. 
After  the  first  year  of  life  it  may  be  advisable  to  precede  the  treatment 
by  temporary  starvation.  The  diet  is  of  special  importance  in  lung 
affections,  for  over-distension  of  the  stomach  by  food  or  gas  due  to 
fermentation  presses  up  the  diaphragm,  interferes  with  the  action  of  the 
heart,  and  is  often  the  cause  of  a  fatal  issue.  The  general  principles  of 
feeding  sick  children  consist  in  giving  regular  meals  of  suitably  prepared 
food  appropriate  for  the  particular  age  of  the  child  and  in  quantities 
suitable  to  its  requirements.  The  child  in  bed  does  not  need  quite  as 
liberal  a  diet  as  one  who  is  actively  running  about,  but  unless  there  are 
special  reasons,  such  as  fever  or  alimentary  disturbance,  it  may  have 
much  the  same  as  a  similar  child  in  health.  Sometimes  it  is  necessary 
to  give  greater  variety  and  predigested  foods.  In  acute  illness  the 
digestive  capacity  is  weakened,  and  it  is  easier  to  set  up  alimentary 
disturbance  than  to  cure  it.  Anorexia  and  vomiting  are  the  infant's 
method  of  showing  it  does  not  require  food.  Allow  a  liberal  supply  of 
water  in  fever.     Gavage  is  sometimes  needed. 


Chapter  IV. 

THERAPEUTICS. 

Nursing — Hydrotherapy — Local  Applications  of  Heat — Counter-irritation 
—  Cupping  —  Bleeding  —  Pharmacotherapy  —  Cutaneous  Therapy  — 
Rectal   Therapy — Fever — Collapse — Vaccine   Therapy — Anaesthesia. 

The  treatment  of  disease  is  not  limited  to  the  administration  of  drugs, 
which  are  by  no  means  always  necessary.  Indeed,  drugs  are  constantly 
the  least  important  factors  in  obtaining  good  results,  though  they  can 
be  frequently  used  with  the  greatest  advantage,  and  are  often  imperatively 
needed.  Many  infantile  ailments  are  cured  by  dietetic  and  hygienic 
measures.  Bear  in  mind  that  the  natural  tendency  of  many  diseases 
is  to  end  in  recovery,  and  that  the  outlook  is  often  more  favourable  in 
the  child  than  in  the  adult,  because  of  its  greater  powers  of  regeneration. 
Infants,  too,  in  particular,  have  abnormally  sensitive  alimentary  and 
nervous  systems,  rendering  their  efficient  treatment  by  diet  and  drugs 
more  delicate  and  difficult. 

Nursing. — A  sick  child,  often  a  healthy  one,  requires  one  or  two 
nurses.  The  doctor  is  very  dependent  on  the  attendants  and  surroundings, 
if  the  full  benefit  is  to  be  derived  from  the  measures  which  he  advises. 
The  bed  should  be  warm,  hot  bottles  used  when  needed,  and  the  position 
of  the  child  one  of  comfort.  Clothing  must  be  warm,  light,  and  non- 
irritating.  The  room  must  be  properly  ventilated,  yet  the  child  protected 
from  draughts.  Linoleum  on  the  floor  is  better  than  any  kind  of  carpet, 
for  it  is  easily  kept  clean.  Dusting  should  be  done  with  a  damp  cloth, 
moistened  with  a  disinfectant  in  infective  cases.  A  sweating  child  requires 
the  clothes  changed,  so  that  it  does  not  get  chilled,  and  the  body  should 
be  sponged  with  warm  water.  Cleanliness  of  the  mouth,  teeth,  skin, 
hands,  and  body  as  a  whole  must  be  ensured.  Care  must  be  taken  to 
prevent  bed  sores  by  rubbing  the  skin  with  a  weak  spirit  lotion,  by  pro- 
tecting it  from  irritation  due  to  crumbs,  etc.,  in  the  bed,  by  padding,  air 
cushions,  and  such-like.  Intertriginous  ulceration  is  guarded  against 
by  cleanliness,  drying  with  soft  warm  towels,  dusting  powders  and  mild 
ointments.  The  exhaustion  due  to  crying  can  be  prevented  by  kind 
and  tactful  management. 

Hydrotherapy. — Water  and  soap  are  used  for  cleanliness  and  the 
prevention  of  ill-health,  due  to  the  inefficient  removal  of  dirt  from  the 


72  Chapter  IV. 

skin  interfering  with  elimination  and  liable  to  set  up  local  or  general  cuta- 
neous mischief.  Distilled,  rain,  or  river  water  is  the  best.  Hard  water  is 
disadvantageous,  in  that  it  necessitates  the  use  of  much  more  soap,  which 
may  perchance  be  of  an  irritating  variety.  Such  water  can  be  softened 
by  adding  bran  or  oatmeal,  in  a  bag  if  preferred  on  aesthetic  grounds. 
It  should  not  be  softened  by  adding  borax,  soda,  or  ammonia,  for  these 
chemicals  combine  with  and  saponify  the  fat  of  the  skin,  making  it  harsh 
and  dry.  Glycerine  and  water,  or  glycerine  of  starch,  applied  after 
washing,  keeps  the  skin  moist,  and  may  prevent  chapping,  but  renders 
the  epidermic  cells  abnormally  sensitive.  Frequent  hot  baths  increase 
exfoliation  of  the  skin  and  favour  imperfect  cornification,  besides  being 
somewhat  enervating. 

Soaps  should  be  superfatted  to  the  extent  of  3-5  per  cent.,  and  should 
not  contain  cocoanut  oil.  The  best  soaps  are  neutral  ones  made  from 
pure  fats.  Free  alkali  in  a  soap  dissolves  out  the  natural  protective  fat  of 
the  skin.  Free  fatty  acids  are  irritating  and  readily  absorbed.  Glycerine 
or  resin,  a  cheap  substitute  for  good  fat,  is  not  to  be  recommended. 
Transparency,  due  to  the  presence  of  sugar  instead  of  glycerine,  renders 
such  a  soap  injurious  in  eczema.  Disinfectant  soaps  contain  sanitas, 
tar,  izal,  carbolic  acid,  etc.  Therapeutic  soaps  are  made  to  contain  about 
10  per  cent,  of  such  substances  as  ichthyol,  anthrasol  (colourless  tar),  and 
balsam  of  Peru  with  sulphur. 

The  First  Bath  is  given  at  a  temperature  of  100°  F.,  after  well  oiling 
the  body  to  remove  the  vernix  caseosa,  using  a  pure  castile,  Icilma,  or 
Vinolia  soap.  After  this  a  Daily  Bath  is  given  ;  sponging  only  until  the 
cord  has  separated.  Up  to  3  months  of  age  the  water  should  be  at  98°  F.  ; 
then  it  may  be  reduced  to  95-90°  F.  during  the  first  year,  and  5  or  10 
degrees  lower  in  the  second  year.  The  bath  should  be  given  in  a  warm 
room,  before  an  open  fire,  out  of  a  draught,  and  for  about  5  minutes. 
The  child  must  be  rapidly  dried  with  a  soft  warm  towel,  avoiding  vigorous 
friction  during  infancy,  and  dusting  powder  applied.  Use  little  soap, 
and  that  a  superfatted  one.  If  the  bath  causes  blueness  and  coldness 
of  the  extremities,  the  child  should  only  be  sponged. 

The  Bath  after  the  First  Dentition. — A  daily  sponge  bath,  at  a 
temperature  of  60-70°  F.,  is  a  useful  tonic  to  the  vascular  and  nervous 
systems,  and  diminishes  the  liability  to  catarrhal  affections.  A  good 
large  tub  or  bath  is  necessary,  and  a  large  sponge  or  flannel.  The  child 
is  rapidly  sponged  all  over  and  then  quickly  dried  with  a  rough  towel, 
dressed  and  given  breakfast.  It  may  be  preceded  by  shampooing  for 
5  or  10  minutes.  Many  young  children  cannot  stand  such  stimulating 
and  vigorous  treatment,  remaining  chilly  and  blue  afterwards,  getting  no 
healthy  reaction.  Such  children  should  be  washed  in  warm  water,  and, 
while  sitting  in  it,  have. a  cold  douche  at  about  70°  F.  applied  with  a  large 
sponge  or  from  a  jug  to  the  shoulders  and  spine,  followed  by  immediate 


Therapeutics.  73 

drying.  After  the  age  of  4  years  the  child,  if  strong  and  vigorous,  may 
have  a  cold  plunge  bath,  a  cold  sponge  bath,  a  spinal  douche,  or  a  hot  bath 
followed  by  a  cold  douche  or  shower.  In  addition,  children  should  have 
a  hot  bath  once  or  twice  a  week,  ten  minutes'  duration,  at  bedtime,  to 
thoroughly  cleanse  the  skin.     A  daily  cold  bath  is  insufficient. 

The  Temperature  of  the  Bath. 

Hot  Bath.—  98-100°  F.,  or  95°  F.  and  raised  to  105°  F.,  and  in  some 

circumstances  up  to  110°  F. 
Warm  Bath.— 30-98°  F.  ;  usually  90°  F. 
Tepid  Bath.— 70-90°  F.  ;  usually  80°  F. 
Cold  Bath.— 60-70°  F. 

The  Hot  Bath  is  not  contra-indicated  by  fever.  It  should  last  from 
3-5  minutes,  if  at  a  high  temperature,  5-15  minutes  at  the  ordinary 
temperature,  and  be  followed  by  a  blanket  and  hot  bottle.  It  is  stimulant, 
useful  for  collapse,  and  induces  sweating.  Hot  packs  are  sometimes 
more  readily  applicable.  A  towel  or  sheet  is  wrung  out  in  hot  water 
and  wrapped  round  the  child  ;  then  a  blanket  is  wrapped  round,  a  hot 
drink  given,  and  the  child  left  in  the  pack  for  15-20  minutes.  A  hot 
compress  or  fomentation,  changed  every  10  minutes,  is  useful  for  raising 
the  temperature  in  babies.  Vapour  baths  and  hot-air  baths  are  sometimes 
needed.  A  woollen  blanket  is  put  under  the  child  and  the  nightdress 
kept  on.  The  bed-clothes  are  raised  above  the  patient  by  a  wire  screen, 
and  the  air  can  be  heated  by  an  arrangement  of  electric  lights,  or  moist 
air  provided  from  a  steam  kettle,  or  by  wrapping  stone  bottles,  filled 
with  boiling  water,  in  very  wet  towels  and  then  in  flannel. 

Hot  packs  and  hot  bottles,  applied  for  too  long  a  time,  may  cause 
hyperpyrexia.  Baths  can  be  made  more  stimulating  by  the  addition 
of  sea  salt,  1-3  per  cent.  Sea  baths  have  a  similar  effect.  Carbonated 
salt  baths  are  used  in  cardiac  dilatation,  and  can  be  prepared  in  the  home 
from  the  Zana  Carbonated  Effervescent  Bath  Powders.  Salt  must  not 
be  used  unless  the  skin  is  healthy. 

Sitz  baths,  at  85-95°  F.,  for  3-10  minutes,  are  of  value  in  pelvic 
affections,  and  at  the  onset  of  the  catamenia.  Cold  water  is  used  for 
therapeutical  purposes  in  a  variety  of  ways.  The  cold  bath  or  pack,  and 
modifications  thereof,  are  of  value  for  the  reduction  of  high  temperature, 
restlessness  and  delirium,  the  heat  of  the  body  being  withdrawn  by  con- 
duction. The  child  should  sit  in  water  at  90-95°  F.  up  to  the  level  of 
the  lower  ribs.  The  water  is  applied  gently  to  the  chest  and  head,  and 
then  the  child  is  immersed  and  the  temperature  of  the  bath  is  cooled 
down  to  60-75°  F.  by  adding  cold  water  or  ice.  Keep  the  patient  in  for 
10-30  minutes,  or  until  the  temperature,  which  should  be  taken  every 
few  minutes  in  the  rectum,  is  reduced  to  101-100°  F.  Then  remove  to  a 
hot  blanket  with  a  hot  bottle  to  the  feet.     If  the  child  gets  blue,  faint,  or 


74  Chapter  IV. 

exhausted,  remove  from  the  bath,  wrap  up  in  hot  blankets,  and  give 
stimulants.  Strictly  speaking,  the  above  is  a  warm  bath  gradually  cooled. 
It  is  not  so  efficacious,  but  is  less  alarming  than  the  cold  bath  given  at  a 
temperature  of  about  70°  F.  For  babies  the  temperature  of  the  bath 
should  be  95°  F.  at  first,  and  can  be  reduced  10  degrees.  The  baby  should 
be  gently  massaged,  kept  in  5-10  minutes,  finally  wrapped  up  in  a  hot 
blanket  and  given  a  hot  bottle.  It  is  advisable  to  give  an  initial  dose  of 
stimulant  before  a  cold  bath  or  pack.  Keep  the  head  cool  by  ice,  towels 
wrung  out  in  cold  water,  or  Leiter's  coil.  Remember  that  the  temperature 
continues  to  fall  after  removal  from  the  bath  or  pack.  If  the  child  is 
alarmed,  a  large  Turkish  towel  or  an  old  blanket  can  be  spread  over  the 
bath,  the  child  placed  on  this  and  allowed  to  sink  in  gently. 

The  cold  pack  is  less  alarming  than  the  bath,  and  often  quite  as 
efficacious.  It  can  be  applied  in  two  ways: — (1)  Wrap  the  child  in  a  sheet 
or  Turkish  towel  wrung  out  in  cold  water,  60-70°  F.,  apply  a  cold  compress 
or  ice  to  the  head,  and  cool  the  body  still  further  by  rubbing  with  ice, 
or  cover  with  an  old  blanket  and  leave  in  for  5-15  minutes.  The  bed 
should  be  protected  by  a  rubber  sheet.  (2)  Wrap  the  child  up  in  a  sheet 
dipped  in  warm  water,  and  then  in  another  sheet  wrung  out  in  cold  water. 
Apply  cold  water  or  ice,  with  gentle  friction  as  needed,  for  5-15  minutes  ; 
then  dry  briskly  until  the  skin  is  glowing.  The  brandy  pack  is  a  modification 
of  the  cold  pack,  the  sheet  being  wrung  out  in  a  mixture  of  1  part  of  brandy 
or  Eau  de  Cologne  to  6-10  of  water  at  60°  F.,  and  the  child  is  then  wrapped 
up  in  the  blanket  and  left  in  for  3  hours.  In  the  cross  pack  a  linen  bandage 
is  wrung  out  in  cold  water  and  applied  in  a  figure  of  eight  fashion  to  the 
back  and  front  of  the  chest  and  across  under  the  armpits.  It  is  next 
covered  in  a  like  manner  with  a  thick  single  flannel  bandage,  and  is  left 
on  all  night.  On  removal,  rub  the  chest  with  a  cold  wet  towel  and  dry 
thoroughly.  It  is  unsuitable  for  infants.  Cold  is  also  applied  in  the 
form  of  compresses  and  fomentations.  Several  layers  of  gauze  are  wrung 
out  in  water  at  the  room  temperature,  and  applied  to  the  throat,  thorax, 
etc.,  and  covered  with  rubber  or  oiled  silk.  Unless  renewed  every  15-30 
minutes  it  becomes  a  hot  compress.  Or  a  thick  Turkey  towel  is  wrung 
out  in  tepid,  cold,  or  iced  water,  and  applied  from  the  top  of  the  chest 
to  the  pubes,  covered  with  flannel,  and  changed  every  10  minutes.  This 
is  useful  when  it  is  undesirable  to  move  the  patient.  It  may  be  applied 
to  the  abdomen  only  for  2  hours  twice  a  day,  being  renewed  every  15-30 
minutes.  Ice  bags  relieve  local  pain,  and  can  be  applied  directly  or  on  a 
cold  compress.  They  have  been  strongly  advocated  in  the  treatment  of 
pericarditis,  pneumonia,  and  pleurisy,  but  I  am  not  often  in  favour  of 
them.  If  applied  in  pericarditis,  see  that  the  right  auricle  is  not  over- 
distended,  and  that  the  extremities  are  warm. 

Leiter's  tubes  can  be  used  for  the  application  of  either  hot  or  cold 
water  to  the  head  and  other  portions  of  the  body.     The  cold  compress  is 


Therapeutics.  75 

useful  in  many  local  affections  for  the  reduction  of  local  heat  and  inflam- 
mation, and  must  be  kept  cool.  A  hydropathic  one  is  applied  lukewarm, 
allowed  to  get  warm  and  to  produce  local  congestion.  Cold  is  further 
applied  by  simply  bathing  with  cold  water^e.g.,  the  throat,  for  colds, 
and  the  feet,  for  cold  feet. 

In  the  reduction  of  fever  the  first  measure  commonly  adopted  is 
sponging  hourly  with  water  at  60-90°  F.  for  5-10  minutes,  and  the  loss  of 
heat  by  evaporation  is  encouraged  by  adding  brandy,  Eau  de  Cologne, 
rectified  spirit,  or  vinegar.  The  child  should  have  a  rubber  sheet  on  the 
bed,  be  wrapped  up  in  a  blanket,  and  sponged  limb  by  limb,  not  completely 
exposed  at  once.  Subsequently  it  can  be  put  to  bed,  covered  with  a 
sheet,  and  the  bed-clothes  raised  over  a  wire  screen,  open  at  the  bottom 
end  to  allow  the  free  circulation  of  air. 

Mustard  is  a  powerful  cutaneous  stimulant  in  the  form  of  a  bath  or 
pack,  and  is  valuable  for  convulsions,  prostration  with  cold  extremities 
and  pallor  of  the  skin,  and  collapse.  The  mustard  bath  is  prepared  by 
adding  a  tablespoonful  of  ground  black  mustard  to  about  3  gallons  of 
water  at  85-105°  F.  The  action  of  the  mustard  is  reduced  by  temperatures 
over  85°  F.  In  this  the  child,  with  a  cold  compress  on  the  head,  and  well 
covered  in  at  the  neck,  is  immersed  for  5-15  minutes,  and  then  wrapped  up 
in  hot  blankets.  The  strength  of  the  bath  should  be  such  that  the  forearm 
of  the  nurse  can  be  kept  in  for  a  minute  without  more  than  tingling. 
Stronger  baths  are  made  by  adding  1-4  oz.  to  each  gallon.  The  mustard 
can  be  made  into  a  paste  with  cold  water,  and  stirred  in  gradually  or 
suspended  in  a  linen  bag  in  the  water.  A  mustard  pack  consists  of  a  sheet, 
towel,  or  several  folds  of  muslin,  wrung  out  in  a  quart  of  tepid  water,  to 
which  a  tablespoonful  of  mustard  has  been  added.  This  is  wrapped 
round  the  thorax  or  body,  covered  with  a  blanket,  and  left  on  for  5-15 
minutes,  or  until  the  skin  is  reddened.  If  applied  to  the  chest,  a  cotton 
wool  jacket  should  be  put  on  afterwards.  A  stronger  pack  is  made  by 
wringing  out  the  towel  in  a  liquid  paste  of  1  lb.  of  mustard  to  3  pints  of 
cold  water.  It  is  applied  for  5-15  minutes,  and  the  child  then  washed 
in  warm  water  and  wrapped  in  hot  blankets. 

A  large  variety  of  medicinal  baths  are  available,  chiefly  for  skin 
affections.  The  administration  of  drugs  by  this  means  is  uncertain  in 
degree  and  unsatisfactory,  although  absorption  is  rather  more  marked 
in  the  young.     We  may  classify  these  baths  : — 

Palliative. — Bran,   gelatine,  or  starch  (1   oz.  to  2  gallons),  milk  and 
water  ;  useful  for  itching  affections. 

Alkaline. — Borax,  carbonate  of  soda,  soft  soap  (1  oz.  to  30  gallons)  ; 
if  the  skin  is  irritated  and  thickened. 

Astringent. — Decoction  of  oak  bark  ;  for  moist  eruptions. 

Disinfectant. — Permanganate  of  potash. 


76  Chapter  I  V. 

Antiparasitic. — Potassium  sulphide  or  sulphurata  (1-4  oz.  to  30 
gallons)  ;  or  sulphaqua  if  the  bath  is  a  metal  one.  It  can  be 
used  also  in  dry  eczematous  conditions. 

Tar  Bath. — Add  oil  of  cade  or  liquid  carbonis  detergens  (from  a 
teaspoonful  to  2  tablespoonfuls  per  gallon). 

Mud  and  Peat  baths  are  recommended  for  affections  of  the  lymphatic 
system,  and  are  best  carried  out  at  health  resorts. 

Spa  treatment  generally  consists  of  salt  and  brine  baths,  and  is  not 
as  useful  or  available  for  children  as  for  adults. 

Sea  bathing  can  be  begun  after  the  sixth  year.  The  best  time  is  in 
the  morning  before  breakfast,  after  a  glass  of  hot  milk  and  a  biscuit,  or 
2-3  hours  after  a  meal,  but  not  while  chilly  or  sweating.  The  head  should 
be  immediately  wetted.  Duration  15-20  minutes.  It  should  be  followed 
by  food  and  exercise.     Otorrhoea  is  a  contra-indication. 

Physical  methods  include  simple  rubbing  of  the  skin,  massage, 
abdominal  massage,  passive  and  resisted  movements,  and  muscular  exercise 
in  bed.  These  are  only  applicable,  with  certain  exceptions,  after  early 
childhood.  After  the  fourth  year  we  can  make  use  of  games,  exercises 
and  gymnastics,  drill,  fencing,  running,  rowing,  and  swimming.  School 
life  should  begin  in  the  eighth  year.  Summer  camps  deserve  more  culti- 
vation than  they  receive  in  this  country.  Rest  cures  are  occasionally 
needed. 

Local  Applications  of  Heat  are  generally  made  by  means  of  hot 
bottles,  preferably  indiarubber  ones,  bran  bags,  fomentations,  flannel  or 
spongiopiline  wrung  out  in  hot  water,  changed  frequently  ;  or  by  poultices 
of  bread,  linseed,  starch,  etc.  They  cause  an  active  local  hyperemia, 
increased  local  leucocytosis,  and  the  rapid  removal  of  deleterious  products 
or  pus  formation.  Applied  to  an  acutely  inflamed  surface,  or  an  unbroken 
boil,  a  poultice  affords  very  considerable  relief,  besides  protecting  it  from 
injury  and  infection.  In  its  action  it  is  comparable  with  that  of  Bier's 
cupping  apparatus,  and  leads  to  cure  by  local  auto-inoculation.  Its 
mental  effect  on  the  patient  and  friends  is  considerable,  and  undoubtedly 
it  often  affords  relief.  Although  somewhat  messy,  it  is  easier  to  manage 
than  a  series  of  hot  fomentations,  wets  the  bed  less,  and  retains  its  heat 
and  moisture  longer,  especially  if  covered  with  guttapercha  tissue.  Certain 
varieties  are  worthy  of  mention. 

The  sugar  poultice  or  fomentation  consists  of  a  hot  10  per  cent,  solution 
of  cane  sugar,  to  which  1  per  cent,  of  citrate  of  potash  is  added.  Lint  or 
flannel  is  wrung  out  in  the  mixture,  applied  every  4  hours,  and  covered 
with  guttapercha  and  wool.  It  is  cheap,  handy,  and  painless.  The  sugar 
acts  as  an  osmotic,  attracting  the  lymph  to  the  surface,  and  the  citrate 
prevents  local  coagulation  on  the  surface.  Such  a  poultice  is  very  useful 
for  boils  and  carbuncles,  after  incision.     Creolin  or  boric  acid  can  be  added. 


Therapeutics.  11 

Starch  Poultice. — Mix  a  teaspoonful  of  boric  acid  and  a  tablcspoonful 
of  best  white  starch  with  cold  water,  and  then  add  a  pint  of  boiling  water, 
stirring  well.  A  thick  mucilaginous  mass  is  formed.  Spread  the  jelly, 
when  cold,  thickly  on  cotton,  and  cover  it  with  a  piece  of  muslin.  Put 
it  on  at  night  and  remove  next  morning.  It  is  very  useful  for  cleaning 
the  skin,  especially  in  affections  of  the  scalp. 

Local  applications  of  heat,  applied  to  the  feet  and  back  of  the  head, 
relieve  headache.  They  are  valuable  in  colic,  toothache,  neuralgia,  croup, 
sore  throat,  rheumatism,  pleurisy,  peritonitis,  congestion  of  the  lungs, 
and  other  affections.  In  applying  a  poultice  to  babies  it  should  be  large 
enough  for  the  infant  to  lie  in,  and  not  extend  on  to  the  front  of  the  chest. 

Counter-Irritation. — The  severe  methods  of  blistering  and  vesication, 
of  escharotics  to  create  sloughs  or  ulcers,  and  setons  are  almost  never 
required.  Blistering  with  cantharides  is  liable  to  set  up  nephritis.  Methyl 
iodide,  sprinkled  on  bibulous  paper  and  applied,  is  stated  by  Causson  (1906) 
to  be  cleaner  and  more  powerful  than  cantharides,  and  not  to  cause 
nephritis.  Usually  it  is  quite  enough  to  use  simple  measures,  enough  to 
produce  rubefaction  of  the  skin,  and  even  they  must  be  used  with  caution, 
for  the  skin  is  very  delicate  and  the  nervous  system  very  sensitive  to 
impressions.  The  local  effects  are  dilatation  of  the  blood  vessels,  stimu- 
lation of  the  sensory  nerve  endings  and  pain,  and  reflex  stimulation  of 
the  vaso-motor  system  and  consequent  contraction. 

Electra  cloth,  impregnated  with  Chillie  paste,  and  the  mustard  leaf 
poultice,  pack,  or  bath  are  the  best  counter-irritants.  The  leaf  is  simple, 
clean,  easily  applied,  and  easily  controlled  in  its  effects.  It  can  be  cut 
to  the  required  shape,  requires  no  special  preparation,  and  can  be  applied 
in  almost  any  place  and  for  any  length  of  time.  The  poultice  is  made  of 
1  part  of  mustard  and  8  of  linseed  or  flour.  The  mustard  is  rubbed  up  in 
cold  water  and  well  mixed  with  the  boiled  meal.  A  temperature  above 
85°  F.  or  so  weakens  the  action  of  the  mustard.  Put  on  a  pad  of  cotton 
wool  afterwards.  The  pack  and  bath  are  described  under  the  section  on 
Hydrotherapy.  Counter-irritation  can  be  applied  by  rubbing  in  camphor- 
ated oil  or  turpentine  liniment,  or  by  turpentine  stupes,  a  towel  wrung 
out  in  a  quart  of  hot  water  to  which  turpentine  (1-8  drs.)  has  been 
added. 

Dry  Cupping  is  useful  in  nephritis  and  congestion  of  the  bases  of 
the  lungs.  A  modified  form  is  much  used  nowadays  in  the  treatment  of 
various  diseases,  under  the  name  of  "  passive  hyperaemia"  induced  by 
Bier's  suction  cups.  These  are  glass  cups  attached  to  rubber  balls,  whereby 
suction  can  be  exerted.  The  method  is  useful  for  the  production  of  local 
congestion  and  auto-inoculation  in  the  treatment  of  boils,  carbuncles, 
enlarged  glands,  sinuses,  and  tuberculous  affections. 

Bleeding. — Infants  do  not  stand  the  loss  of  blood  well,  and  older  children 
not  so  well  as  adults.     Local  bleeding,  by  one  or  more  leeches,  relieves 


78  Chapter  IV. 

the  pain  of  acute  otitis,  the  headache  of  meningitis  and  the  pain  of  pleurisy. 
Applied  below  the  right  nipple  the  loss  of  blood  is  beneficial  in  the  cardiac 
dilatation  of  bronchitis,  pneumonia,  acute  pericarditis  and  myocarditis, 
and  mitral  stenosis.  A  leech  to  the  septum  nasi  may  possibly  arrest 
the  onset  of  fits  due  to  cerebral  congestion.  Bleeding  is  also  usefid  in 
ursemic  fits  and  infantile  eclampsia.  Two  leeches  are  sufficient  for  an 
infant  and  3-6  for  an  older  child.  General  bleeding,  with  the  abstraction 
of  not  more  than  3  or  4  oz.  of  blood,  is  sometimes  judicious  in  the  severe 
cyanosis  of  pneumonia  from  dilatation  of  the  right  heart.  Wet  cupping 
must  be  avoided. 

.  Pharmacotherapy. — In  estimating  the  value  of  treatment  it  must  be 
remembered  that  tissue  metabolism  is  much  more  active  in  children  than 
in  adults.  A  judicious  scepticism  is  imperative  or  undue  importance 
will  be  ascribed  to  drugs.  No  medicine  should  be  given  without  a  definite 
object.  If  a  placebo  is  given,  let  it  be  palatable.  Never  give  an  un- 
palatable medicine  if  it  can  be  replaced  by  one  pleasant  to  take.  Give 
drugs  in  small,  frequent  doses,  rather  than  in  large,  occasional  ones. 
Disguise  the  taste  of  nauseous  ones  as  far  as  possible,  and  give  all  medicine 
in  such  a  form  as  to  be  swallowed  easily.  Fluids  are  taken  better  than 
pills  or  powders.  The  dose  should  be  1  teaspoonful  for  infants  and  2  for 
older  children.  A  measure  glass  should  always  be  used  for  domestic 
spoons  vary  greatly  in  size.  In  infants  it  is  of  the  greatest  importance 
to  avoid  drugs  liable  to  cause  anorexia,  nausea,  or  gastric  disturbance. 
Flatulent  distension  of  the  stomach  and  bowels  is  a  serious  complication, 
for  instance,  in  pulmonary  troubles,  and  is  liable  to  be  set  up  by  rash 
medication.  Choose  by  preference  simple  solutions,  concentrated  tinc- 
tures, fluid  extracts,  alkaloids  and  their  salts.  Bitters  are  generally 
disliked,  unless  well  diluted,  and  are  not  often  needed.  Agreeable  pre- 
parations are  syrups,  chocellae,  and  tablets  or  tabloids,  dissolved  in  water 
for  infants. 

Take  into  consideration  the  child's  age  and  mental  calibre,  the 
character  of  the  parents,  the  dose  required,  the  relationship  to  meals  and 
sleep,  and  the  frequency  of  administration.  For  instance,  phosphorus 
is  given  once  daily,  opiates  according  to  their  effect,  and  salicylates  in 
full  and  frequent  doses.  Drugs,  such  as  chloral,  bromides,  and  mercury, 
are  well  borne  by  infants,  but  opiates  must  be  used  with  great  caution. 
Belladonna,  digitalis,  and  quinine  are  also  well  borne  by  the  young.  The 
dose  may  be  estimated  in  accordance  with  the  age  and  size  of  the  child. 
If  by  weight,  the  dose  for  an  infant  is  one-fifteenth  that  for  an  adult. 
If  by  age,  take  the  age  of  the  child  at  its  next  birthday  as  the  numerator 
and  the  age  plus  12  as  the  denominator  of  the  fraction  necessary.  Thus, 
if  the  adult  dose  is  1  gr.,  the  dose  for  a  child  in  its  third  year  is  £^qr^  or 
\  gr.  A.nother  method  is  to  divide  the  age  of  the  child  at  its  next 
birthday    by  24,   giving    a   child   of   3   years  a    dose  of  \   gr.      Under 


Therapeutics.  79 

one  year  of  age  let  the  dose  be  equivalent  to  one-twelfth  of  that  suitable 
at  one  year  for  each  month  of  life. 

The  chief  cathartics  are  castor  oil,  calomel,  sodium  and  magnesium 
sulphate,  sodium  phosphate,  citrate  of  magnesia,  calcined  magnesia, 
milk  of  magnesia,  rhubarb,  manna,  cascara,  senna,  and  aloes.  Epsom 
salts  may  be  given  in  the  form  of  a  saturated  solution,  with  the  addition 
of  1  dr.  of  aromatic  sulphuric  acid  to  4  ozs.,  in  doses  of  1  or  2  drs.  with  a 
little  water. 

Diuretics. — Acetate  of  potash,  liquor  ammon.  acetat.  (Mindererus 
spirit),  bitartrate  of  potash  (cream  of  tartar)  grs.  1-10.  Imperial  drink  : 
1  dr.  of  cream  of  tartar  added  to  boiling  water  and  a  little  lemon  juice, 
given  cold.     Diuretin. 

Diaphoretics. — The  spirit  of  nitrous  ether,  pilocarpin. 

Febrifuge,  and  as  a  pleasant  drink  in  stomachic  disorders. — Use  an 
effervescing  mixture  made  by  mixing  in  equal  quantities  citric  acid 
3  drs.  to  water  6  oz.,  and  bicarbonate  of  potash  2  drs.  to  water  6  oz.,  the 
alkali  not  being  completely  neutralised. 

Antacids. — Bicarbonate  of  soda,  sal  volatile,  milk  of  magnesia. 

Stomachics  and  Carminatives. — Aromatic  water  of  dill,  caraway, 
cinnamon,  aniseed,  and  peppermint. 

Expectorants. — Wine  of  ipecacuanha  and  antimony,  chloride  of 
ammonia,  liquorice,  tolu,  senega,  squills.  The  addition  of  bicarbonate 
of  soda,  liquor  potassae,  or  iodide  of  potash,  helps  by  making  the  secretions 
more  liquid. 

Pulmonary  Sedatives  and  Disinfectants.  —  Heroin  gr.  2I50  ^°  A 
terpene  hydrate,  creosote  and  carbonate  of  creosote  (creosotal),  guiacol 
and  its  carbonate  (duotal). 

Intestinal  Astringents. — Chalk  mixture  ;  carbonate,  subnitrate  and 
salicylate  of  bismuth;  kino,  catechu  and  tannin  rarely.  Turpentine  in 
the  form  of  emulsion,  e.g.  01.  Terebinth,  drs.  iii,  Pulv.  Acacise  J  oz.,  Sacch. 
alb.  I  oz.,  Sp.  Lavandulae  co.  drs.  iii,  Aquas  ad  6  oz.     Dose,  dr.  i-ii  t.d.s. 

Intestinal  Antiseptics  are  considered  under  the  treatment  of  diarrhoea] 
affections  and  Anthelmintics  in  the  chapter  on  worms. 

Urinary  Antiseptics. — Urotropin,  well  diluted  with  water  ;  salol  and 
benzoate  of  ammonia.  Large  doses  of  citrate  of  potash  render  the  urine 
alkaline  and  do  good  in  colon  infections  of  the  bladder,  for  the  bacillus 
will  not  grow  in  an  alkaline  medium.     Acid  sodium  phosphate. 

Antispamodics. — Bromides  and  various  combinations  thereof,  bromo- 
form,  pertussin  (an  extract  of  thyme),  belladonna  and  its  alkaloids. 

Alkalies  are  valuable  in  moderate  doses  in  all  catarrhal  and  ulcerative 
affections  of  the  mucous  membranes,  and  as  a  local  application.  The 
sodium  compounds  are  less  depressant  than  the  potassium  salts.  They 
reduce  the  acidity  of  the  blood  and  urine.     When  given  before  meals  they 


80  Chapter  IV. 

dissolve  mucus,  and  in  efficient  doses  encourage  the  secretion  of  acid. 
After  meals  they  may  be  given  to  reduce  hyperacidity.  The  liquor 
potassse  or  liquor  sodse,  and  other  alkalies,  are  useful  in  acute  bronchitis 
with  viscid  secretion.  Sodium  citrate  added  to  milk  prevents  curdling 
in  the  stomach.  The  bicarbonate  is  of  value  as  a  local  application  in 
eczema,  whitlows  after  incision,  ulcers  (grs.  15  ad  1  oz.)  and  in  toothache. 

Salicyl  compounds  are  used  in  rheumatic  affections,  acute  colds, 
many  febrile  conditions,  and  as  diaphoretics.  Salicylate  of  soda,  salicin, 
salicylic  acid  and  aspirin  (acetyl-salicylic  acid)  are  the  best  preparations. 
Aspirin  cannot  be  combined  with  an  alkali.  It  has  a  more  prolonged 
action  than  the  other  compounds,  for  it  is  not  nearly  as  rapidly  excreted. 
Many  of  these  compounds  are  only  active  because  they  are  converted  into 
salicylic  acid  in  the  body.  Salicin,  aspirin  and  methyl-salicylate,  applied 
locally,  act  in  this  way.  Benzoic  acid  is  a  valuable  anti-rheumatic  remedy, 
but  inferior  to  salicylic  acid.  Large  doses  of  these  drugs  can  be  given  if 
the  bowels  are  kept  open,  and  if  alkalies  are  added  in  large  amounts.  Further 
consideration  of  them  will  be  found  in  the  chapter  on  acute  rheumatism. 
Quinine  can  be  given  in  warm  chocolate,  shaken  up  with  syrup, 
mixed  with  glycerine,  1  gr.  to  the  drachm,  and  given  in  milk ;  in  gelatine 
capsules;  mixed  with  scraped  raw  apple.  An  effervescing  mixture  is 
made  by  adding  sulphate  of  quinine  gr.  i,  citric  acid  grs.  iii,  and  syrup  of 
orange  1  dr.,  to  a  solution  of  bicarbonate  of  soda  in  water.  Or  it 
may  be  given  as  a  tannate  in  powder  or  chocolate  tabloids,  or  as  euquinine. 
It  can  be  rubbed  into  the  skin,  1  dr.  to  the  ounce  of  benzoated  lard  ; 
given  in  suppository;  as  an  enema;  or  subcutaneously,  one  part  of  the 
hydrochlorate  in  four  of  water. 

Iodine  is  rather  difficult  to  administer.  Wingrave  advises  that 
5  gms.  of  iodine  should  be  dissolved  in  76  c.c.  of  90  per  cent,  alcohol,  and 
added  to  8  gms.  of  tannic  acid  and  60  c.c.  syrup.  It  is  heated  without 
boiling  for  20  minutes,  and  more  syrup  added  up  to  a  total  of  150  c.c. 
The  dose  is  from  J-2  teaspoonfuls  in  water  or  wine  before  meals.  It 
contains  2  grs.  of  iodine  in  each  drachm,  and  is  somewhat  similar  to 
"  Vin  Nourry."  Smaller  doses  should  be  given  to  children.  Tincture  of 
iodine  in  drop  doses  is  given  to  stop  vomiting.  Iodine  ointment  contains 
iodine  gr.  i,  pot.  iod.  dr.  i,  vaseline  oz.  i.  It  can  be  made  with  glycerine, 
instead  of  vaseline,  for  application  to  mucous  surfaces.  The  iodides  of 
sodium  and  potassium  are  of  great  value  in  many  diseases. 

Creosote  is  used  as  an  intestinal  disinfectant,  anti-fermentative,  and 
in  pulmonary  affections.  One  part  of  best  creosote,  with  one  part  of  a 
50  per  cent,  solution  of  pure  sodium  salicylate,  and  two  parts  of  concen- 
trated decoction  of  quillaia  (1  in  7),  forms  a  clear  solution.  Or  it  can  be 
given  in  capsules.  In  mixture  the  taste  can  be  disguised  by  spirits  of 
chloroform,  ext.  glycyrrhizse  liq.,  and  inf.  gentian,  co.  ;  by  tinct.  gentian., 
rectified  spirits,  and  sherry  wine ;  or  by  syr.  tolu  and  rum.     As  an  ointment 


Therapeutics.  8 1 

it  is  prescribed  with,  equal  parts  of  lard,  olive  oil,  and  lanolin,  |  dr. 
to  the  ounce. 

Mercury  is  generally  given  in  the  form  of  calomel,  grey  powder,  or 
blue  ointment.  The  immediate  resort  to  grey  powder  in  every  infantile 
ailment  is  by  no  means  to  be  recommended,  but  should  not  be  spoken  of 
contemptuously.  Many  a  time  when  the  so-called  inevitable  dose  of  grey 
powder  has  been  omitted,  it  has  been  to  the  child's  disadvantage.  Its 
use  in  syphilis  is  too  well  known  to  require  comment  further  than  in  the 
section  on  this  disease. 

Cod-liver  oil  is  the  best  of  tonics,  and  a  food  also.  It  can  be  given 
in  innumerable  ways  and  combinations,  as  with  maltine,  syr.  ferri.  phosph. 
co.,  vinum  ferri,  glycerin,  syrup  of  orange,  lime  water,  and  caraway  water  ; 
or  as  : — 

Tinct.  calumbae  m.  v,  ol.  mor.  m.  xxx,  aq.  carui  ad  dr.  i  ; 

01.  mor.,  syr.  calcis  lactophosph.,  aq.  calcis  aa  m.  xviii,  sod.  hypo- 
phosph.  gr.  i,  mucil,  acacise  m.  v,  ol.  cassiee  m.  J  ; 

01.  mor.  oz.  ii,  maltine  oz.  ^,  syr.  calc.  hypophosph.  oz.  \,  glycerine 
drs.  ii,  pulv.  acacia?  drs.  ii,  aq.  cinnamomi  ad  4  oz. 

Iron  is  given  in  the  form  of  organic  compounds,  as  in  yolk  of  egg, 
meat  juice,  potatoes,  spinach  and  other  green  vegetables,  and  various 
preparations  from  blood,  such  as  haematogen.  The  inorganic  salts,  least 
likely  to  upset  the  digestion,  are  the  citrate  of  iron  and  ammonia,  tartrate 
of  iron,  dialysed  iron,  reduced  iron,  and  the  saccharated  carbonate  of  iron, 
in  doses  of  £-5  grs.  The  reduced  iron  does  not  discolour  the  teeth, 
and  can  be  given  in  sandwiches.  A  good  mixture  for  simple  anaemia 
and  debility  contains  the  citrate  or  tartrate  grs.  i-iii,  pot.  cit.  grs.  v,  sp. 
amm.  arom.  m.  v-x,  glycerine  and  inf.  calumbse.  It  is  beneficial  in  chronic 
gastric  catarrh,  an  hour  before  meals,  after  a  course  of  alkalies.  The 
acid  salts,  such  as  the  perchloride  and  the  sulphate,  are  more  powerful, 
and  useful  for  tuberculous  affections,  rickets,  splenic  anaemia,  purpura, 
and  other  blood  dyscrasia.  For  enlarged  glands  a  useful  mixture  contains 
the  tincture  of  the  perchloride  of  iron  m.  v-x,  liq.  hydrarg.  perchlor.  m.  v-xv, 
liq.  arsenici  hydrochlor.  m.  ii-v,  made  up  with  syrup  of  orange  and  chloro- 
form water.  The  perchloride  can  be  pleasantly  given  in  aerated  water 
after  food.  Iron  Lemonade  is  made  of  tinct.  ferri  perchlor.  drs.  ii,  acidi 
phosph.  dil.  oz.  i,  syr.  limonis  oz.  -§-,  syrupi  ad  oz.  vi.  Dose :  1  dessertspoonful 
in  water  after  meals.  A  good  mixture  for  the  convalescent  stage  of  acute 
parenchymatous  nephritis  contains  the  tincture  of  the  perchloride  m.  v, 
liq.  amnion,  acetat,  m.  xv,  ac.  aceti  dil.  m.  ii,  water  ad  drs.  ii,  given  after 
food  in  aerated  water.  The  sulphate  can  be  combined  in  mixtures  with 
the  sulphate  of  magnesia.  During  a  course  of  iron  a  saline  aperient  should 
be  given  twice  a  week  before  breakfast.  Other  compounds  often  used 
are  the  syrup  of  the  phosphate,  the  compound  syrup  of  the  phosphate 
(Parrish's  or  Squire's  Chemical  Food),  and  the  syrup  of  the  iodide,  especially 

G 


82  Chapter  I  V. 

useful  in  tuberculous  affections  and  the  resolving  stages  of  chronic  lung 
affections. 

Arsenic  is  a  valuable  gastric  sedative.  Minim  doses  of  Fowler's 
solution  often  stop  reflex  vomiting,  colic,  or  diarrhoea.  In  doses  of  3-5 
minims  it  is  a  valuable  heematinic.  In  large  doses  it  is  given  for  chorea 
(q.v.),  but  may  give  rise  to  peripheral  neuritis,  skin  pigmentation,  kera- 
tosis, etc.  It  is  generally  contra-indicated  in  acute  skin  affections  and 
valuable  in  chronic  ones.  The  liq.  arsenici  hydrochlor.  must  be  used 
in  acid  mixtures.  The  stronger  preparations  of  arsenious  acid  are  not 
often  used  for  children,  e.g.  the  acid,  the  iodide,  and  soamin  or  atoxyl. 

Coal  Tar  Products. — Phenazone  (antipyrin)  is  used  for  the  reduction 
of  temperature,  the  relief  of  nervous  symptoms,  headache,  convulsions, 
enuresis,  etc.  Phenacetin  is  less  dangerous,  and  almost,  if  not  quite,  as 
efficacious,  especially  for  the  relief  of  headache.  Still,  young  children 
stand  phenazone  very  well.  Antefebrin  is  contra-indicated,  for  it  is 
unnecessarily  powerful  and  dangerous.  These  drugs  are  valuable  nerve 
sedatives. 

Phenacetin  is  not  soluble,  so  is  given  in  powders.  The  combination 
of  1  gr.  with  |  gr.  of  caffein  citrate  is  very  valuable.  Antipyrin  is 
soluble,  but  does  not  taste  nice.  One  grain  doses  in  a  drachm  of  syrup  of 
orange  can  be  given  hourly  at  one  year  of  age.  The  addition  of  \  gr.  of 
codeia  to  2  oz.  of  the  mixture  makes  it  more  efficacious  as  a  sedative  and 
antispasmodic.  As  antipyretics  these  drugs  must  be  used  with  caution, 
and  should  not  be  given  unless  the  temperature  is  persistently  at  or  over 
104°  F.  They  produce  their  results  by  acting  on  the  nervous  and  muscular 
mechanisms  of  the  circulation  and  respiration,  and  are  powerful  depressants. 
It  may  be  necessary  to  give  them  for  the  reduction  of  high  fever  when 
the  attendants  are  stupid  or  ignorant,  and  efficient  nursing  is  not  available. 
In  the  hyperpyrexia  of  acute  rheumatism,  in  enteric  fever,  and  broncho- 
pneumonia they  are  sometimes  permissible  ;  still  more  rarely  in  diphtheria, 
specific  fevers,  and  croupous  pneumonia.  In  all  these  affections  the 
myocardial  degeneration  or  inflammation,  so  apt  to  occur,  makes  them 
dangerous  remedies.  On  the  other  hand,  frequent  small  doses  of  either 
antipyrin  or  phenacetin  are  rarely  injurious,  lessen  the  frequency  of  the 
pulse,  and  often  increase  sweating.  The  use  of  synthetic  drugs  in  fever 
is  based  on  the  false  idea  that  the  malaise  is  due  to  the  fever.  Large 
doses  for  infants  are  unnecessary  and  often  dangerous.  The  smaller 
doses  recommended  act  more  as  nerve  sedatives  and  are  harmless.  Any 
depressant  effect  can  be  counteracted  by  a  few  drops  of  brandy. 

Bromides  can  be  given  freely  at  all  ages,  and  act  simply  as  nerve 
sedatives.  Up  to  4  grs.  for  a  dose  every  2  hours  may  be  given  even  in  the 
first  month  of  life,  but  such  large  doses  are  rarely  needed.  Bromides  are 
useful  in  all  forms  of  nervous  irritability,  convulsions,  reflex  colic,  and 
some  cases  of  enuresis.     Bromural,  a  combination  of  bromine,  valerian, 


Therapeutics.  83 

and  urea,  is  a  harmless  and  mild  hypnotic  in  doses  of  5  grs.  Occasionally 
a  child  shows  a  marked  susceptibility  to  bromides,  and  develops  a  rash, 
which  may  be  extremely  severe  and  disfiguring,  even  though  only  a  few 
grains  have  been  given.  The  liability  to  acne  spots  of  a  mild  type  can  be 
counteracted  by  adding  a  few  minims  of  liq.  arsenicalis  to  the  mixture. 

Chloral  is  without  doubt  the  most  valuable  drug  for  all  kinds  of  infantile 
convulsions.  During  the  first  year  it  may  be  given  in  doses  of  1  gr. 
for  each  3  months  of  life,  combined,  if  desired,  with  double  the  amount  of 
sodium  bromide,  and  given  in  syrup  of  orange.  Under  supervision, 
reducing  the  amount  according  to  the  effect,  it  may  be  given  every  2  hours, 
and  in  even  larger  doses.  If  it  cannot  be  swallowed,  it  can  be  given  by 
rectal  injection  in  doses  of  5-10  grs.  every  6  hours,  dissolved  in  water. 
This  method  is  particularly  valuable  for  a  child  actually  in  convulsions. 
Frequent  small  doses  are  useful  in  severe  chorea,  but  large  doses  seem 
to  be  sometimes  dangerous.  The  syrup  contains  10  grs.  in  each  drachm, 
and  can  be  given  in  soda  water  or  lemonade. 

Hypnotics. — Bromural,  bromides,  and  chloral  meet  the  needs  of 
most  children.  Phenacetin  and  antipyrin  suit  others.  Veronal,  trional, 
and  sulphonal  are  rarely  necessary. 

Opium  and  its  preparations  are  occasionally  absolutely  necessary. 
They  must  be  used  with  great  caution,  not  indiscriminately.  Codeia  is 
often  preferable  to  morphine.  These  drugs  are  specially  valuable  for 
the  relief  of  pain  and  laryngeal  spasm,  the  prevention  of  peristalsis  in 
diarrhoea  after  free  evacuation  of  the  bowels,  and  as  hypnotics.  Small 
doses  must  be  given  during  the  first  year  of  life.  The  dose  of  codeia  is 
gr.  -giro,  morphine  toVoj  Dover's  powder  gr.  ^j,  tincture  of  opium 
m.  ^tfj  paregoric  m.  i.,  per  month  of  life  in  the  first  year,  and  can  be 
given  every  3  or  4  hours. 

Stimulants. — The  most  powerful  cardiac  stimulants  are  given  subcu- 
taneously,  e.g.  strychnine  gr.  4^0  - tiJ  ;  Merck's  digitalin  gr.  xihi -  20  ', 
a  10  per  cent,  solution  of  camphor  in  sterilised  oil  m.  ^-3. 

Alcohol  is  a  useful  and  necessary  medicine  for  infants  and  children, 
but  is  often  given  too  readily  and  in  too  large  quantities.  It  must  be 
looked  upon  as  a  powerful  drug,  and  only  ordered  when  necessary.  It 
should  be  given  well  diluted,  in  small  and  frequent  doses,  e.g.,  3-10  minims 
every  2-3  hours  in  the  first  year  of  life,  and  not  continued  for  long  after 
recovery.  It  is  used  to  tide  a  child  over  a  crisis  in  an  acute  illness,  as  a 
soporific  in  fever,  and  as  a  gastric  stimulant  in  chronic  ailments.  It  is 
beneficial  in  collapse,  in  septic  conditions  of  all  kinds,  and  in  the  cardiac 
asthenia  of  diphtheria,  pneumonia,  typhoid  fever,  scarlatina,  and  measles. 
Generally  speaking,  it  is  contra-indicated  in  cerebral  and  bronchial 
affections.  Epilepsy,  chorea,  and  neurasthenia  have  been  ascribed  to 
the  too  free  use  of  alcohol  in  early  life,  and  the  frequent  stimulation  of 
the  gastric  mucosa  is  said  to  induce  dyspepsia,  gastritis,  and  even  hepatic 


84  Chapter  IV. 

cirrhosis.  Certainly,  acute  gastritis  in  a  baby  has,  in  my  experience,  been 
due  to  champagne,  but  this  was  not  the  result  of  medical  advice.  Brandy 
is  the  most  reliable  form,  diluted  with  water  or  added  to  the  medicine. 
Other  spirits  may  be  used.  Pure  rectified  spirit  never  seems  to  produce 
as  good  results,  probably  because  of  its  lack  of  ethers.  Champagne, 
iced  in  cases  of  vomiting,  good  hock,  and  white  wine  whey  are  useful.  A 
child  generally  prefers  the  non-sparkling  wines.  Burgundy,  port  wine, 
light  ale,  and  stout  are  valuable  in  convalescence.  Malt,  in  the  form  of 
Guinness's  stout,  mixed  with  cream  and  sugar,  is  valuable  in  infantile 
malnutrition.  Another  good  food  is  brandy  and  egg,  made  of  the  yolk 
of  one  egg,  sugar  dr.  i,  brandy  m  x,  cinnamon  water  dr.  i. 

Cutaneous  Therapy. — Simple  massage  of  the  skin  is  useful  to  improve 
the  circulation  and  nutrition.  Precede  it  by  a  bath  at  90-100°  F.  for 
10  minutes.  Dry  by  gentle  rubbing  with  a  hot  rough  towel,  and  then 
rub  with  warm  olive  or  cod-liver  oil  or  benzoated  lard,  and  put  on  a  flannel 
nightdress.  Drugs  may  be  given  in  this  way,  but  the  amount  of  absorption, 
via  the  gland  ducts,  is  uncertain.  The  oleate  of  mercury  and  blue  ointment 
are  commonly  applied  by  this  method,  a  lump  the  size  of  a  large  pea  being 
rubbed  into  the  skin  of  the  abdomen  and  covered  with  a  flannel  binder. 
The  red  iodide  of  mercury  ointment  is  used  for  glandular  enlargements. 
Some  drugs  are  readily  absorbed  by  the  skin,  notably  carbolic  acid,  which 
is  consequently  a  dangerous  drug  in  early  life,  and  salicylic  acid  and  its 
congeners,  especially  methyl  salicylate  and  betul  oil,  a  preparation  con- 
taining this  compound.  Quinine  and  digitalis  can  be  absorbed  in  small 
quantities. 

Endermatics  are  rarely  used.  The  skin  is  removed  by  blistering, 
painting  with  pure  carbolic  acid,  or  moistening  a  watch  glass  with  strong 
ammonia  and  inverting  it  over  the  skin. 

Hypodermic  medication  should  not  be  used  for  children  under  3  years 
of  age,  except  after  great  experience  and  in  serious  collapse.  Dangers 
arise  from  idiosyncrasy.  It  is  not  advisable  for  older  children,  because 
of  the  pain  and  fright,  and  rarely  needful  for  the  relief  of  pain.  If  necessary, 
the  skin  can  be  numbed  by  ethyl  chloride  spray,  ether,  or  rubbing  with  a 
menthol  cone.  The  antitoxin  for  diphtheria  is  the  drug  most  often  given 
in  this  manner.  Morphia,  gr.  -^ho  under  1  year  of  age,  may  be  required 
in  otitis  media,  renal  colic,  uraemia,  and  the  status  epilepticus.  Pilocarpin 
is  sometimes  given  in  daily  or  weekly  doses  to  remove  exudations,  and 
to  induce  sweating  in  uraemia.  It  should  be  preceded  by  a  warm  bath 
and  blanket  wrap,  and  given  at  night.  After  the  sweating  is  over  put  on 
a  warm  nightdress.  Give  it  in  small  doses  tentatively,  for  is  is  quite 
impossible  to  estimate  individual  susceptibility.  Atropin,  in  doses  of 
4tnr-2l5cF  of  a  grain,  counteracts  the  bad  effects,  namely,  weak  pulse, 
vomiting,  coldness,  depression  and  threatened  collapse.  Liquor  strychninse, 
ether,  brandy,  musk,  and  caffein  are  given  for  cardiac  failure.     Ether  is 


Therapeutics.  85 

liable  to  cause  sloughing  of  the  skin.  Adrenalin  solution  is  of  little  or  no 
value. 

Transfusion,  i.e.,  subcutaneous  injection  of  saline  fluids,  is  used  for 
collapse,  shock,  loss  of  blood  after  operations  and  in  haemophilia  etc., 
severe  vomiting  and  diarrhoea,  to  promote  elimination  in  septic  states, 
and  in  coal  gas  poisoning.  Intravenous  injections  have  no  additional 
advantage,  and  are  not  necessary.  The  chief  effects  are  a  rise  of  blood 
pressure  and  stimulation  of  the  kidneys. 

The  apparatus  consists  of  a  glass  cylinder,  such  as  that  of  a  syringe, 
2-4  feet  of  rubber  tubing,  and  a  Dieulafoy's  or  long  hypodermic  needle, 
all  of  which  are  carefully  sterilised.  Disinfect  the  skin  at  the  site  of 
injection.  Insert  the  needle  for  about  2  inches  under  the  skin  of  the 
abdomen,  into  the  side  of  the  thorax  directed  upwards  towards  the  axilla, 
below  the  clavicles,  or  on  the  inner  side  of  the  thighs.  A  pressure  of 
18  inches  is  sufficient  when  once  the  flow  has  started.  Inject  3-4  oz., 
or  less  in  infants.  It  will  flow  in  through  one  puncture  in  about  15-60 
minutes.  Close  the  puncture  with  cotton  and  collodion,  and  massage 
gently.  The  rate  of  absorption  varies.  The  only  complications  are 
subcutaneous  haemorrhage  and  abscess  formation.  Use  for  injection 
normal  saline  0*9  per  cent,  strength  ;  as  a  stimulant,  sod.  chlorid.  2*5, 
caffein.  citrat.  0*75,  sterile  water  300  c.c,  in  doses  of  1-4  drachms  every 
4  hours  ;  or  a  mixture  of  sod.  chlorid.  grs.  180,  potass,  chlorid.  grs.  12, 
sod.  sulphat.  grs.  100,  sod.  carbonat.  grs.  100,  sod.  phosphat.  grs.  8,  in 
8  oz.  of  distilled  water,  made  up  to  2  pints  for  use.  These  fluids  should 
be  sterilised  by  boiling  for  10  minutes,  and  at  a  temperature  of  120°  F. 
when  poured  into  the  cylinder. 

The  subcutaneous  injection  of  nutritive  materials,  such  as  6  per 
cent,  dextrose  solution  and  yolk  of  egg,  is  occasionally  employed. 

Rectal  Therapy. — The  rectum  is  used  as  a  channel  for  the  adminis- 
tration of  water  and  food  for  the  maintenance  of  life,  in  the  reduction  of 
the  body  temperature,  in  the  treatment  of  collapse,  in  the  treatment  of 
local  and  general  diseases,  such  as  colic  and  tenesmus,  abdominal  distension, 
colitis  and  other  diarrhoeal  affections,  haemorrhage,  prolapse  of  the  rectum, 
and  threadworms  ;  and  for  the  introduction  of  drugs  which,  for  various 
reasons,  cannot  be  given  by  mouth  or  subcutaneously.  Rectal  absorption 
includes  absorption  by  the  colon,  for  solids  and  fluids  pass  upwards  into 
the  colon  as  far  as  the  caecum,  and  even  further,  in  consequence  of  reflex 
peristalsis.  Insoluble  substances  may  reach  the  stomach.  Cases  in 
which  rectal  feeding  has  proved  unusually  satisfactory  are  probably 
those  in  which  the  reflex  peristalsis  is  considerable.  The  capacity  for 
absorption  varies  with  the  individual  and  the  nature,  rather  than  the 
percentage  composition,  of  the  nutrient  fluid.  Irrigation  of  the  colon 
is  necessary  for  cleansing,  previous  to  giving  a  rectal  feed,  to  empty  the 
bowel  and  wash  away  the  decomposing  material  left  from  previous  feeds. 


86  Chapter  I  V. 

It  should  be  done  once  in  24  hours.  Irrigation  is  also  valuable  in  the 
relief  of  thirst,  the  reduction  of  fever,  to  counteract  collapse,  and  to  wash 
away  mucus,  toxins,  bacteria,  and  degenerated  epithelium.  It  must  be 
carried  out  by  a  doctor  or  skilled  nurse.  An  inexpert  person  is  liable  to 
cause  damage  or  perforation  of  the  gut.  Use  salt  solution,  1  teaspoonful 
to  the  pint  of  water. 

Place  the  child  on  the  left  side  with  the  hips  raised  on  a  pillow,  on 
the  back  with  the  buttocks  raised,  or  in  the  genupectoral  posture.  The 
best  position  for  a  baby  is  on  the  back  or  the  attendant's  lap,  with  the 
buttocks  raised.  A  rubber  sheet  must  be  so  arranged  that  the  escaping 
fluid  flows  into  a  basin  or  other  receptacle.  Use  a  soft  rubber  catheter, 
No.  9-12,  attached  to  a  rubber  tube  3  or  4  feet  long,  with  a  glass  funnel 
inserted  at  the  free  end.  Oil  the  catheter  well  and  pass  it  upwards  slowly 
and  gently  as  the  fluid  flows  in  and  distends  the  bowel,  opening  out  the 
folds  and  enabling  the  tube  to  be  pushed  steadily  higher.  It  is  infinitely 
easier  to  get  good  results  when  the  fluid  is  injected  into  the  colon.  If  it 
only  distends  the  rectum  it  will  be  evacuated  suddenly  and  forcibly.  Only 
use  moderate  pressure,  holding  the  funnel  at  a  height  of  one  to  two  feet 
above  the  level  of  the  anus.  Gentle  manipulation  of  the  abdomen  assists 
the  flow  up  the  colon.  Normally  some  of  the  fluid  escapes  by  the  side  of 
the  catheter  from  time  to  time.  When  a  sufficiency  has  been  injected, 
compress  the  buttocks  with  the  hand  and  keep  the  fluid  in  for  a  time. 
Then  detach  the  tube  and  allow  the  fluid  to  flow  out  through  the  catheter. 
For  cleansing  purposes  the  water  should  be  lukewarm,  about  80°  F.  The 
colon  will  hold  one  pint  at  six  months  and  double  that  amount  at  two  or 
more  years  of  age.  The  injection  may  be  repeated  several  times  if  the  child 
is  not  distressed. 

Rectal  Feeding  is  an  overrated  means  of  nutrition.  Nutrient  suppo- 
sitories are  useless,  and  nutrient  injections  not  much  better.  What  little 
benefit  there  is,  depends  on  the  fluid  rather  than  the  nutritive  constituents. 
Simple  saline  injections  are  generally  as  beneficial.  Even  as  a  means  of 
giving  the  stomach  a  complete  rest  the  method  is  unreliable,  for  the  intro- 
duction of  nutrient  material  into  the  lower  bowel  will  cause  gastric  secre- 
tion, pain,  and  vomiting.  In  the  colon  cane  sugar  can  be  converted  into 
grape  sugar,  and  a  certain  amount  of  starch  into  dextrin.  The  continuous 
or  drop  method  is  unavailable,  unless  the  child  is  comatose.  Otherwise 
it  will  not  keep  still  enough.  For  injection  we  may  use  plain  water,  normal 
saline  fluid,  dextrose  6  per  cent,  solution,  cane  sugar,  dextrin,  and  peptones. 
Peptones  are  liable  to  set  up  diarrhoea.  Dried  casein,  e.g.,  protein,  plasmon, 
and  sanatogen,  are  little  absorbable,  and  even  egg  albumin  is  not  much 
better  in  this  respect.  Fat  in  the  yolk  of  egg  can  be  fairly  well  absorbed, 
and  emulsified  olive  oil  and  milk  fat  to  a  less  extent.  Unpeptonised  milk, 
starch  and  wines  must  be  avoided.  Brandy  can  be  added.  Salt  is  a  useful 
addition  to  most  mixtures. 


Therapeutics.  87 

The  following  feeds  may  be  tried  :  (1)  One  egg-white,  salt  grs.  x, 
weak  starch  solution,  3  oz.  (2)  Horse  serum,  with  5  grs.  of  salt  per  ounce. 
(3)  Yolk  of  one  egg,  dextrose  drs.  ii,  salt  grs.  x,  water  or  peptonised  milk 
to  5  oz.  (4)  Two  drachms  each  of  somatose,  sanatogen,  or  plasmon,  and  of 
dextrose  or  dextrin,  salt  grs.  x,  and  water  or  peptonised  milk  to  5  oz.  This 
may  be  enriched  by  adding  the  yolk  of  an  egg,  and  10-30  drops  of  brandy. 
Dilute  it,  if  too  thick  or  if  more  fluid  is  needed.  Even  under  the  most 
favourable  conditions  the  method  is  only  a  means  of  delaying  starvation. 
From  1-2  oz.  for  an  infant,  and  2-4  oz.  for  an  older  child  may  be 
injected  every  4  hours  at  first,  and  then  every  6  hours. 

The  reduction  of  fever  is  brought  about  by  irrigation  of  the  colon  with 
a  gallon  of  water  at  95°  F. ;  by  enemata  of  water  at  70-80°  F. ;  by  the 
injection  of  small  quantities  of  cold  or  iced  water  ;  or  by  ice  suppositories. 
It  is  a  useful  means,  if  there  is  not  much  prostration,  in  cases  of  high  fever 
in  infants  and  young  children. 

Collapse  is  treated  by  injecting  water  or  normal  saline  at  105-110°F. 
The  addition  of  \-\  dr.  of  tincture  of  musk  or  of  brandy  makes  the 
injection  more  efficacious.  One  to  three  minims  of  tincture  of  opium 
may  be  added  for  collapse  due  to  severe  pain. 

Tain  and  tenesmus  are  relieved  by  iced  water,  hot  water,  starch  solution 
with  a  few  minims  of  tincture  of  opium,  or  cocaine  suppositories  gr.  J, 
glycerine  enema  and  hot  applications  to  the  abdomen  are  generally  sufficient 
to  relieve  colic. 

Abdominal  distension  is  relieved  and  flatulence  is  evacuated  by  passing 
a  rectal  tube  ;  by  an  enema  of  dill  water,  alone  or  with  an  equal  quantity 
of  chloroform  water  ;  or  of  i-2  drs.  of  tincture  of  assafcetida  in  water  or 
starch  mucilage.  The  treatment  of  constipation  is  discussed  under  that 
head. 

For  irrigation  use  simple  solutions  of  water,  common  salt,  or  bicar- 
bonate of  soda,  a  drachm  to  the  pint.  As  antiseptics  add  to  each  pint  a 
drachm  of  boric  acid,  sod.  salicyl.,  or  sod.  benzoat ;  napthol  3-5  grains  ; 
thymol  5-10  grains.  For  astringents  make  use  of  1  per  cent,  tannin 
lotion  ;  tannic  acid  i  dr.  or  ext.  hamamelis  1  dr.  to  the  pint,  or  to 
3  or  4  oz.  if  it  is  to  be  retained ;  argyrol  grs.  1-3,  or  nitrate  of 
silver  gr.  £-1  in  each  ounce.  Silver  nitrate  is  the  best  astringent  in 
chronic  ulcerative  colitis,  more  valuable  than  organic  silver  compounds. 
It  is  preceded,  3  hours  beforehand,  by  an  enema  of  salt  and 
bicarbonate  of  soda.  From  i-1  pint  of  the  silver  solution  is  injected. 
If  it  causes  much  pain,  give  a  small  dose  of  morphia  or  laudanum. 
The  injection  may  give  rise  to  pain  and  vomiting,  but  never  does  harm, 
though  the  symptoms  may  be  alarming.  Constipation  often  follows,  and 
must  be  relieved  by  a  simple  enema  in  3  days  time.  Not  more  than 
3  or  4  of  these  injections  should  be  given,  at  intervals  of  3  or  4   days, 


88  Chapter  I  V. 

unless  definitely  good  results  are  obtained.  Sedative  injections  consist 
of  decoctions  of  gum  arabic,  starch,  linseed,  and  various  cereals. 

Drugs,  such  as  antipyrin,  creosote,  potassium  iodide,  quinine,  etc., 
can  be  given  in  suppositories,  but  the  method  is  unsatisfactory,  as  it  is 
impossible  to  gauge  the  rate  or  amount  of  absorption.  Chloral  hydrate  in 
watery  solution  is  absorbed  very  readily. 

Objections  to  the  use  of  enemata  and  irrigations: — Mechanical  injuries 
are  not  unknown.  The  continued  use  of  enemata  and  suppositories  is 
liable  to  set  up  catarrh  of  the  mucous  membrane.  The  effect  on  consti- 
pation is  lost  after  a  time,  unless  changes  in  the  kind  of  enema  are  made. 
The  enema  rash  is  an  important  effect.  It  appears  most  commonly  in 
young  patients,  between  6  and  12  years  of  age,  after  an  enema  for  con- 
stipation, as  a  preliminary  to  operation,  or  for  the  cure  of  thread  worms. 
It  is  not  due  to  soap,  for  it  may  follow  the  injection  of  plain  water.  Prob- 
ably, it  is  caused  by  the  absorption  of  dissolved  faecal  material.  The  rash 
is  symmetrical;  consisting  of  slightly  raised  patches  of  erythema  which 
run  into  blotches,  confluent  like  that  of  scarlatina,  sometimes  urticarial. 
It  appears  in  3-48  hours  ;  on  the  front  of  the  knees,  extensor  surfaces  of  the 
elbows  and  the  buttocks  ;  spreads  to  the  cheeks  and  chin,  the  outer  sides 
of  the  thighs,  but  not  to  the  palms  or  soles.  It  may  come  out  first  on  the 
buttocks,  spreading  upwards  and  downwards.  It  does  not  itch,  and 
rarely  desquamates.  There  is  occasionally  a  little  fever.  The  erythematous 
rash  disappears  in  less  than  24  hours,  but  the  urticarial  one  may  last  2 
or  3  days.    No  treatment  is  needed. 

Fever,  its  Causation  and  Treatment. — The  body  temperature  of  infants 
and  children  is  very  unstable.  Fever  is  easily  induced  during  the  first 
6  months  of  life,  and  up  to  puberty  the  temperature  rises  on  slighter 
provocation  than  in  later  fife.  This  is  due  to  the  rapidity  of  the  circula- 
tion, oxidisation  and  growth,  and  the  instability  of  the  nervous  system. 
Mere  fright  may  raise  a  baby's  temperature  several  degrees.  A  rise  of 
temperature  is  due  to  increased  production  or  diminished  loss  of  heat, 
or  a  combination  of  the  two  factors.  It  may  result  from  the  application  of 
external  heat,  e.g.,  by  the  continuous  hot  pack  or  by  hot  bottles,  if  the 
means  of  elimination  are  restricted.  Protection  from, loss  of  heat  is  one  cause 
of  the  maintenance  of  fever.  It  is  imperative  that  for  the  reduction  of 
fever  the  clothing  should  be  light,  and  the  room  well  ventilated.  Patho- 
logically a  rise  in  temperature  is  ascribed  to  increased  oxidation,  set  up 
by  a  combination  of  toxins  with  antibodies  ;  varying  with  the  virulence 
of  the  organism  and  the  reaction  of  the  host.  Toxins  produced  in  the 
tissues  of  the  body  or  in  the  food,  before  or  after  ingestion,  may  directly 
affect  the  heat  regulating  nervous  mechanism. 

The  temperature  of  the  newborn  babe  is  the  same  as,  or  slightly 
higher  than,  that  of  the  mother,  but  soon  falls  to  or  below  normal  from 
exposure,  bathing,  and  lack  of  food.     It  may  reach  the  normal  level  in 


Therapeutics.  89 

24  hours,  or  not  for  3  or  4  days,  and  then  ranges  from  98-99-4°  F.,  being  a 
fraction  higher  in  the  evening  than  in  the  morning.  An  occasional  rise 
for  a  few  hours  has  no  special  significance,  but  a  daily  rise,  or  the  persistence 
of  a  temperature  one  degree  above  normal,  requires  investigation  of  its 
cause.  A  rise  of  temperature  is  indicative  of  mischief,  but  may  occur 
without  any  evident  cause  or  sign  of  illness.  It  is  often  overlooked,  for  the 
temperature  is  not  systematically  taken  unless  the  child  is  ill.  Half  the 
cases  are  due  to  infection,  one-fourth  to  gastro-enteric  disturbance,  a  few 
to  inflammation  of  the  lungs  and  serous  membranes,  and  in  the  residue 
the  cause  is  doubtful. 

Inanition  or  Thirst  Fever  is  a  name  given  to  cases  of  fever  during  the 
first  few  days  of  life,  on  the  assumption  that  sepsis  rarely  produces  fever 
before  the  fifth  day,  and  because  the  fever  has  subsided,  sometimes 
quite  abruptly,  on  the  free  administration  of  water  or  a  plentiful  supply  of 
breast-milk.  These  infants  show  no  sign  of  illness,  though  the  fever  may 
last  for  3  or  4  days.  Seeing  that  insufficient  food  generally  causes  fall 
in  temperature,  it  is  much  more  probable  that  the  fever  in  these  cases  is 
due  to  mild  sepsis,  to  the  absorption  of  abnormal  intestinal  products,  or  to 
intestinal  or  renal  irritation. 

In  investigating  the  sources  of  fever,  examine  for  teething  and  local 
affections  of  the  mouth,  throat,  and  naso-pharynx.  Sore  throats  are  often 
overlooked,  for  a  child  may  not  complain  of  pain,  while  chronically 
enlarged  and  pitted  tonsils  may  give  rise  to  fever  through  the  decom- 
position of  food  and  secretions  retained  in  the  crypts  or  infective  organisms 
entangled  therein.  Causes  liable  to  be  overlooked  are  intestinal  infections 
and  toxaemias,  enteric  fever,  rheumatism,  and  pyelitis  in  girl  babies. 
Acute  coryza  is  obvious,  except  in  the  very  early  stages,  but  true  influenza 
is  often  unrecognised,  and  still  more  often  diagnosed  on  insufficient  grounds. 
In  making  a  diagnosis  it  is  necessary  to  examine  the  patient  for  the  onset 
of  a  specific  fever,  cerebrospinal  meningitis,  acute  anterior  poliomyelitis, 
pneumococcal  infections,  loculated  empyema,  osteomyelitis,  otitis  media, 
gastritis,  and  all  possible  causes  of  sepsis.  Constipation  alone  may  be  the 
cause,  and  faecal  impaction  may  exist  though  the  bowels  act  daily.  Neurotic 
children  are  particularly  liable  to  fever  from  excitement,  undue  exertion, 
and  overfeeding.  Chill  and  insufficient  clothing  are  sometimes  to  blame, 
and  at  times  one  can  ascribe  the  condition  to  heat  stroke,  malaria,  tuber- 
culosis, osteo-arthritis,  or  even  hysteria. 

Hyperpyrexia  may  occur  in  sepsis  neonatorum,  heat  stroke,  malaria, 
infective  endocarditis,  specific  fevers,  towards  the  end  of  meningitis,  and, 
rarely,  in  rheumatism  and  chorea. 

Occasionally  fever  persists  for  months,  without  any  apparent  cause 
and  ending  in  recovery.  Thus,  a  girl  of  12  years  had  an  irregularly  hectic 
temperature,  sometimes  up  to  104°  F.,  and  only  coming  down  to  normal 
in  the  course  of  five  weeks  ;    twice  she  had  mild  rigors.     Puberty  was 


90  Chapter  IV. 

beginning,  and  possibly  the  fever  was  in  some  way  connected  with  this.  In 
another  instance  the  fever  persisted  for  about  2  years.  I  saw  the  girl  at 
the  age  of  6  years  for  a  hectic  fever  of  2  months  duration,  with  loss  of  flesh 
and  occasional  epistaxis,  and  a  history  of  cough  and  malaise  for  4  months. 
Even  at  the  end  of  2  years,  though  plump  and  looking  healthy,  she  was 
not  entirely  free  from  fever.  A  third  girl,  in  her  fourth  year,  of  neurotic, 
artistic,  and  rheumatic  parentage,  was  subject  to  attacks  of  fever  of  about 
2  hours  duration,  her  temperature  rising  to  103°  or  104°  F.,  and  followed 
by  excitement  and  a  kind  of  epileptic  fit.  She  was  a  mischievous  and 
destructive  child,  but  no  cause  for  the  fever  could  be  found,  except  the 
unstable  state  of  the  nervous  system.  In  a  fourth  case,  also  that  of  a 
girl,  fever  persisted  for  10  months,  as  a  sequel  of  mild  typhoid  fever,  and 
ended  in  death  from  marasmus.  In  such  a  case  there  is  most  probably  a 
chronic  blood  infection. 

In  practice  cases  of  obscure  fever  are  a  source  of  great  anxiety.  High 
fever  with  little  general  malaise  is  less  serious  than  the  temperature 
suggests.  More  importance  should  be  attached  to  the  general  state  of  the 
child  than  the  actual  height  of  the  fever.  Prolonged  irregular  fever 
necessitates  repeated  thorough  examination  to  exclude  all  possible  causes. 
Either  a  definite  or  the  probable  cause  is  found,  or  the  patient  gets  well. 
The  prognosis  must  be  guarded,  for  it  is  clearly  impossible  to  say  in  early 
stages  that  nothing  beyond  the  fever  will  develop.  It  is  wiser  to  state  to  the 
relatives  that  there  is  no  discoverable  cause,  that  they  must  wait  with 
patience,  rather  than  to  jump  at  a  doubtful  diagnosis  or  make  alarming 
suggestions  of  malignant  endocarditis,  tuberculosis,  or  other  deadly 
complaint. 

General  Treatment. — The  reduction  of  fever  does  not  necessarily 
shorten  disease.  It  is  unusual  and  unnecessary  to  reduce  the  temperature, 
unless  its  height  is  such  as  to  have  an  unfavourable  result  on  the  system  as 
a  whole,  and  the  course  of  the  disease  in  particular.  Unfavourable  indica- 
tions are  drowsiness,  delirium,  convulsions,  a  rapid  and  weak  pulse, 
restlessness,  and  sleeplessness.  The  treatment  depends  on  the  height  of  the 
temperature,  the  duration  of  the  fever,  the  nature  of  the  disease,  and  its 
probable  course.  Severe  remedies  are  not  needed  for  high  fever  in  a  pneu- 
monic attack  near  its  crisis,  but  are  imperative  in  hyperpyrexia  due  to 
rheumatism.  Hydro  therapeutic  measures,  such  as  cradling,  sponging, 
cold  fomentations,  cold  packs,  and  a  cold  bath,  lessen  the  intensity  of  the 
chemical  activity  by  which  the  febrile  temperature  is  produced,  probably 
by  increasing  leucocytic  activity.  If  there  are  cerebral  symptoms  apply 
ice  or  Leiter's  coils  to  the  head,  or  let  it  rest  on  a  cold  water  rubber  bag 
as  a  pillow.  Rectal  irrigation  with  ice-cold  water  is  useful  for  infants  and 
young  children,  if  there  is  not  much  prostration. 

Elimination  is  encouraged  by  saline  purgatives,  diaphoretics,  and 
diuretics.     The  use  of  synthetic  drugs,  coal  tar  products  (p.  82),  is  based 


Therapeutics.  91 

on  a  false  idea  that  the  malaise  is  due  to  the  fever.  For  infants  they  are 
unnecessary  and  often  dangerous.  Phenacetin  is  the  most  harmless. 
Tincture  of  aconite,  m.  £-1  hourly  for  8  doses  is  sometimes  used,  but  is 
undoubtedly  depressant.  Salicylate  of  soda  and  quinine  or  euquinine  are 
the  best  remedies.  Quinine,  in  doses  of  1  gr.  per  year  of  life,  is  very  useful 
in  late  stages  of  broncho-pneumonia  with  a  hectic  type  of  fever  and  a 
failing  heart.  Dover's  powder  is  given  for  irritability  and  restlessness. 
Alcohol  may  be  used  as  a  stimulant,  and  strychnine  if  there  is  depression. 
The  diet  should  be  light,  liquid,  and  cool. 

Treatment  of  Collapse. — Collapse  is  usually  associated  with  a  subnormal 
temperature,  but  the  latter  may  occur  without  collapse.  A  subnormal 
temperature  is  due  to  exposure  to  cold,  prematurity,  malnutrition  and 
inanition,  fluxes  and  haemorrhages ;  sometimes  to  heart  disease,  and 
frequently  is  a  sequel  of  acute  disease,  such  as  specific  fevers  and  pneumonia. 
In  some  instances,  e.g.,  infantile  cholera,  the  collapse  is  very  analogous 
to  shock,  and  may  possibly  be  due  to  the  action  of  toxins  on  the  splanchnic 
area  ;  or  it  may  be  due  to  cardiac  failure,  or  the  severe  pain  of  colic,  and 
the  passage  of  calculi.  In  its  mildest  form  it  is  treated  by  hot  bottles, 
fomentations,  packs  or  bath,  and  stimulants  by  the  mouth.  For  great 
prostration,  with  cold  extremities  and  pallor  of  the  skin,  give  a  mustard 
bath,  or  apply  a  mustard  leaf  or  hot  fomentations  to  the  prsecordium. 
A  hot  or  mustard  bath,  with  hot  whisky  and  water  internally  and  strychnine 
(s.o.s.)  subcutaneously,  is  the  best  treatment  for  subnormal  temperature 
due  to  cold  and  inanition.  Subcutaneous  injection  of  adrenalin  m.  1-5 
(1  in  1000)  is  said  to  raise  blood  pressure,  but  is  probably  useless  unless 
given  intravenously.  It  acts  as  a  direct  stimulant  of  the  heart  and  peri- 
pheral vessels,  causing  contraction,  and  an  excessive  dose  may  cause  rigor 
of  the  heart. 

Vaccine  Treatment. — The  vaccine  treatment  of  tuberculosis  is  similar 
in  character  to  that  of  all  microbial  infections.  According  to  recent  views 
there  is  present  in  the  serum  a  substance,  called  opsonin,  which  combines 
with  the  microbes  and  prepares  them  for  ingestion  by  the  leucocytes. 
Hence,  phagocytosis  varies  directly  as  the  amount  of  opsonin.  This 
substance  is  destroyed  by  heating  at  60°  C.  for  10  minutes. 

Leucocytes  washed  free  from  serum  have  no  phagoc}Ttic  action  on 
bacteria.  Their  phagocytic  power  remains  constant.  This  is  shown  by 
taking  washed  leucocytes  from  a  normal  and  a  phthisical  person,  mixing 
them  with  serum  from  another  normal  person  and  an  emulsion  of  tubercle 
bacilli,  and  incubating  them.  An  equal  phagocytosis  results  in  each  case. 
To  obtain  the  opsonic  index,  mix  an  equal  quantity  of  washed  leucocytes, 
microbial  emulsion,  and  the  serum  from  a  normal  person  and  the  patient. 
Incubate  at  37°  C.  for  15  minutes,  and  make  blood  films.  Count  the 
number  of  organisms  taken  up.  The  opsonic  index  is  the  relative  pro- 
portion of  the  numbers  in  the  two  cases.     Thus,  if  100  microbes  are  taken 


92  Chapter  1  V. 

up  by  100  cells  in  normal  serum,  and  only  70  in  the  patient's  serum,  the 
patient's  opsonic  index  is  0*7.  The  opsonic  index  is,  therefore,  the  measure 
of  the  resistance  of  the  blood  serum  to  microbic  invasion.  Raise  it  and  the 
resistance  to  infection  is  raised. 

The  opsonic  index  to  tubercle  bacilli  varies  between  0-8  and  1*2  in 
normal  individuals.  It  is  lower  in  the  infant  than  the  mother.  In  localised 
tuberculous  infections  it  is  below  normal,  and  in  unlocalised  ones  it  fluctuate  3 
from  high  to  low.  In  slight  early  cases  it  is  above  normal ;  in  chronic  case  3 
it  is  below  normal ;  and  in  acute  cases  it  fluctuates  greatly  from  day  to 
day.  A  high  index  may  mean  auto-inoculation.  This  can  be  induced  by 
exercise,  by  manipulation  of  the  affected  part,  and  by  suction  cups,  because 
of  the  increased  blood  supply.  It  is  important  to  estimate  the  index 
before  and  after  exercise  to  ascertain  whether  auto-inoculation  is  taking 
place,  and  to  rest  during  treatment. 

Mode  of  Treatment. — Isolate  and  cultivate  the  infecting  organism. 
Estimate  the  patient's  opsonic  index  for  that  organism.  Raise  the  index 
by  inoculating  with  vaccine,  i.e.,  with  dead  organisms  in  salt  solution. 
Re-inoculate  during  the  maximum  height  or  the  fall  of  the  positive  phase, 
but  not  during  the  rise  or  in  the  negative  phase.  Each  inoculation  is 
followed  by  a  negative  phase,  i.e.,  a  drop  in  the  opsonic  index,  which  lasts 
for  a  few  days,  and  is  quite  short  in  the  healthy.  In  tuberculosis  a  negative 
j)hase  may  last  from  a  few  hours  up  to  14  days  ;  and  it  may  be  preceded  by 
a  short  rise,  the  pre-negative  phase.  By  the  positive  phase  is  meant  the 
gradual  rise  of  the  index  to  a  maximum,  immediately  after  the  end  of 
the  negative  phase.  It  remains  there  for  a  time  and  then  slowly  falls.  There 
is  little  or  no  rise  of  temperature  unless  big  doses  are  used.  Injection  during 
the  negative  phase  causes  a  further  drop  in  the  opsonic  index  and  diminished 
resistance.  Negative  phases  can  be  accumulated  one  on  another  ;  not  so 
the  positive  phases,  but  one  positive  phase  can  be  followed  by  another  with 
only  a  short  and  slight  intervening  negative  phase. 

In  treating  tuberculosis  in  children  a  dose  of  yoioo  -  ioooo  nig. 
is  injected,  and  repeated  in  increased  strength  every  10-11  days  ;  the 
patient  must  be  kept  quiet  for  a  day  or  two  afterwards.  The  injection  is  of 
very  little  value  if  the  index  is  already  high.  No  injection  should  be  given 
during  intercurrent  acute  illness.  The  effects  can  be  estimated  by  taking 
the  opsonic  index  in  24  hours,  72  hours,  7  days,  and  14  days,  to  determine 
the  phases.  Clinical  experience  shows  that  the  injections  can  be  given 
about  every  14  days  with  safety,  without  troubling  to  estimate  the  opsonic 
index. 

This  treatment  may  be  considered  as  still  on  its  trial.  It  is  spoken  of 
favourably  in  cases  of  tuberculous  adenitis,  dactylitis  and  joint  affections. 
The  best  results  are  obtained  in  staphylococcal  infections,  such  as  acne, 
multiple  boils,  and  abscesses.  At  least  6  doses  are  required,  often  more, 
at  intervals  of  17-21  days. 


Therapeutics.  93 

Anaesthesia. — Anaesthetics  must  be  given  with  as  much  precaution  as 
in  adults.  Bear  in  mind  the  small  size  and  compressibility  of  the  thorax 
in  infants,  and  the  effect  of  fear  in  older  children.  Examine  the  mouth  for 
loose  teeth,  sweets,  and  other  foreign  bodies.  As  a  rule  operations  should 
be  done  at  the  time  of  the  evening  or  midday  meal,  for  children  are  not  in 
such  a  good  condition  as  adults  after  a  night's  fast.  In  light  ancesthesia 
dangers  arise  from  shock  and  laryngeal  spasm.  In  deep  ancesthesia  suffoca- 
tion may  be  due  to  the  tongue  falling  back  into  the  pharynx.  The  selection 
of  the  anaesthetic  depends  on  the  condition  of  the  child,  and  nature  of  the 
operation,  and  its  probable  duration.  Nitrous  oxide  gas,  ethyl  chloride, 
A.C.E.  mixture,  ether,  and  chloroform,  are  the  usual  anaesthetics,  and 
are  mentioned  in  the  order  of  safety.  Ethyl  chloride  and  chloroform 
can  be  given  during  sleep.  Chloroform  is  generally  taken  extremely  well 
by  babies.      Children  she  old  be  anaesthetised  on  the  operating  table. 

Nitrous  oxide  gas  is  unsuitable  for  young  children,  especially  if  nervous, 
as  the  apparatus  is  alarming.  They  are  frightened,  and  take  it  badly.  It  is 
suitable  for  short  and  trivial  operations,  such  as  tooth  extraction,  and  as  a 
preliminary  to  ether  administration,  in  older  children.  It  may  cause 
inconvenient  rigidity,  jactitation,  and  involuntary  evacuations.  Being 
often  followed  by  screaming  and  struggling  it  is  unsuitable  if  a  wound  has 
to  be  dressed. 

Ethyl  chloride  has  largely  replaced  nitrous  oxide,  but  is  more  dangerous, 
and  is  more  often  followed  by  vomiting,  headache,  and  restlessness.  It  is 
pleasant,  simple,  easy  to  give,  and  does  not  irritate  the  air  passages.  The 
mode  of  administration  is  not  alarming.  Somnoform  is  a  mixture  of  ethyl 
chloride  60  parts,  methyl  chloride  35  parts,  and  ethyl  bromide  5  parts. 
It  has  no  special  advantages  over  the  pure  ethyl  chloride,  and  is  more 
expensive.  Ethyl  chloride  can  be  given  as  a  preliminary  to  ether  or 
chloroform.  It  prevents  the  struggling  and  excitement  induced  by  ether. 
If  followed  by  chloroform,  the  latter  must  be  given  slowly,  as  its  effect 
cannot  be  appreciated  while  the  patient  is  under  the  influence  of  ethyl 
chloride. 

The  patient  should  be  prepared  in  the  usual  manner.  For  babies  and 
young  children  J-l  c.c.  is  sprinkled  on  lint  and  held  over  the  mouth  and 
nostrils.  It  must  be  given  quickly.  For  older  children  a  Clover's  inhaler  can 
be  used,  so  that  recourse  can  be  had  at  once  to  ether  if  the  operation  is 
prolonged  or  the  patient  weak.  A  gag  should  be  inserted  for  mouth 
operations,  and  the  chin  held  well  forward  to  allow  air  to  enter  freely. 
Consciousness  is  lost  in  10-15  sees.  The  breathing  becomes  slow  and  deep, 
the  pupils  usually  dilate,  and  the  muscles  are  relaxed,  except  the  masseters. 
In  deep  anaesthesia  the  muscles  become,  if  possible,  more  relaxed,  the  face 
flushed  and  perhaps  covered  with  sweat,  the  corneal  reflex  sluggish  or 
absent,  and  an  external  squint  often  develops.  There  is  no  cyanosis  or 
venous  congestion.     Unconsciousness  lasts  from  1-2  minutes.    Becovery  is 


94  Chapter  IV. 

rapid  ;    preceded  by  a  dreamy  state  and  slight  mental  confusion.     An 
overdose  is  followed  by  headache,  excitement,  nausea,  and  vomiting. 

This  anaesthetic  is  not  absolutely  safe,  for  the  rapidity  with  which 
anaesthesia  is  induced  increases  the  liability  to  overdose  and  death  from 
syncope  or  asphyxia.  McCardie,  in  1906,  collected  21  deaths,  of  which  only 
3  were  children,  showing  its  comparative  safety  for  children  to  whom  it  is 
so  often  given.  It  is  especially  suitable  for  short  operations,  such  as  the 
removal  of  teeth,  tonsils,  adenoids,  circumcision,  and  the  opening  of 
abscesses.  It  must  not  be  used  for  long  operations,  except  as  a  preliminary. 
For  the  removal  of  tonsils  and  adenoids  it  can  be  given  in  the  sitting 
position,  but  if  either  the  operator  or  the  anaesthetist  be  inexpert  the  child 
may  come  round  too  soon,  or  too  large  a  dose  may  cause  danger  from 
abolition  of  the  cough-reflex  or  muscular  rigidity. 

Ether  is  an  admirable  anaesthetic  for  long  operations  provided  plenty 
of  air  is  given.  Babies  take  it  well.  It  has  been  credited  unduly  with 
safety,  and  insufficient  importance  attached  to  the  subsequent  bronchitis 
and  pneumonia  to  which  it  may  give  rise.  Fatal  cases  are  generally  due 
to  one  of  these  sequels.  It  is  contra-indicated  in  the  presence  of  respiratory 
troubles,  and  for  operations  on  the  abdomen  or  brain. 

Chloroform  can  be  given  safely  by  the  open  method,  if  plenty  of  air 
is  allowed,  although  the  percentage  of  vapour  to  air  varies  within  wide 
limits,  from  1-10  per  cent.  With  care  the  former  percentage  is  the  usual 
amount.  For  safety  it  should  be  continuously  given  in  1-2  per  cent,  strength, 
but  the  various  inhalers  used  for  this  purpose  are  likely  to  alarm  the  child. 
Begin  gradually  with  a  few  drops,  and  increase  steadily  by  adding  more  at 
definite  intervals.  Methylated  chloroform  is  not  inferior  to  the  ethylic 
variety,  and  is  much  cheaper.  If  it  is  not  pushed  beyond  the  stage  of 
complete  anaesthesia  the  percentage  of  drug  within  the  blood  is  one  within 
the  limits  of  safety. 

In  the  first  stage  there  may  be  some  preliminary  agitation.  Then 
sensation  and  voluntary  movements  are  suppressed,  while  reflex  and  auto- 
matic ones  are  preserved.  The  corneal  reflex  is  present.  The  pupils  are 
usually  a  little  contracted,  but  may  remain  dilated  to  the  end  of  this  stage  ; 
they  react  to  light.    This  is  called  Light  Anaesthesia. 

In  the  second  stage,  that  of  Deep  Anaesthesia  or  Surgical  Anaesthesia, 
the  reflex  movements  are  suppressed  and  the  corneal  reflex  abolished. 
Finally  the  automatic  respiratory  movements  cease,  and  are  quickly 
followed,  within  60  sees.,  by  stoppage  of  the  heart,  and  death. 

The  corneal  or  lid  reflex  is  elicited  by  touching  the  centre  of  the  cornea 
or  the  conjunctiva,  and  feeling  and  seeing  the  responsive  closure  of  the 
upper  lid.  The  lid  reflex  may  be  absent,  but  the  cornea  give  a  slight  re- 
sponse. As  long  as  the  latter  is  present  and  the  breathing  is  free  the 
patient  is  in  a  satisfactory  state.  It  is  not  necessary  to  abolish  the  corneal 
reflex,  and  some  anaesthetists  regard  its  disappearance  as  indicative  of  the 


Therapeutics.  95 

stage  of  dangerous  anaesthesia.  It  is  unreliable  in  children,  and  on  the 
whole  the  pupils  are  a  better  guide,  for  damage  may  be  done  to  the  cornea 
by  frequently  touching  it  with  the  finger,  especially  if  wet  with  chloroform. 
The  pupils  should  be  contracted  and  react  sluggishly  to  light.  Dilatation 
may  indicate  reflex  irritation  at  the  wound,  the  onset  of  vomiting  or 
danger.  It  may  be  present,  extreme  and  fixed  in  some  patients  during 
deep  anaesthesia,  without  danger  if  the  breathing  is  satisfactory.  If  the 
pupils  begin  to  dilate  and  the  lid  reflex  returns,  it  indicates  too  little 
anaesthetic.  A  dilating  pupil  with  loss  of  corneal  reflex  is  generally  a  sign 
of  danger.  On  the  other  hand  the  contracted  pupil  is  not  an  absolute  sign 
of  security  against  respiratory  failure.  It  is  important  to  watch  the 
respiration  rather  than  the  pulse.  Breathing  becomes  shallow,  irregular, 
and  imperceptible  from  an  overdose  of  the  drug,  while  the  pulse  may  be 
strong  and  regular,  or  may  fail  about  the  same  time.  A  preliminary 
injection  of  atropin  has  been  said  to  reduce  the  risk,  but  Webster's  recent 
experiments  on  dogs  contra-indicate  this. 

Chloroform  and  Ether,  and  A.C.E.  mixture  are  pleasant,  and  safer 
than  chloroform  alone.  They  are  given  gradually  and  unconcentrated. 
An  overdose  is  indicated  by  dilatation  of  the  pupils  and  respiratory  failure. 

Anaesthetic  deaths  may  occur  before  true  anaesthesia  is  established,  and 
the  operation  begun.  Similar  deaths  occurred  from  fright  in  pre-anaesthetic 
days.  They  are  unavoidable,  but  care  should  be  taken  not  to  alarm  the 
child  and  to  acquire  its  confidence.  Apart  from  status  lymphaticus  (q.v.), 
death  during  operation  is  never  quite  sudden,  and  is  due  to  gradual  failure 
of  respiration  or  circulation,  from  the  action  of  the  poison  on  the  medulla. 
After  operation  death  may  take  place  within  10  minutes  as  a  result  of 
continued  toxaemia,  or  from  vomiting  and  aspiration  of  food  into  the 
larynx.  Later  on  occur  the  cases  of  delayed  chloroform  poison  described 
subsequently. 

Treatment  of  impending  calamity. — At  once  try  and  restore  respiration. 
Rub  the  lips  briskly  with  a  dry  towel,  insert  a  gag,  and  pull  forward  the 
tongue.  Rhythmical  tongue  traction  is  sometimes  used,  and  is  a  somewhat 
barbarous  method,  as  tongue  forceps  are  needed.  Lower  the  head  and 
raise  the  feet ;  babies  can  be  held  head  downwards.  Try  artificial  respira- 
tion combined  with  inhalation  of  oxygen.  Give  a  hypodermic  injection  of 
strychnine  or  ether.  Apply  heat  in  the  form  of  hot  blankets  and  bottles  to 
the  limbs,  and  hot  towels  to  the  praecordium.  If  there  is  much  shock  inject 
strychnine  subcutaneously  and  saline  infusion  into  the  median  basilic  vein, 
and  bandage  the  limbs  from  below  upwards  (auto-transfusion).  For 
cyanosis  with  good  heart  sounds,  give  inhalations  of  oxygen  or  amyl 
nitrite.  Acupuncture  and  massage  of  the  heart  are  the  last  and  most 
desperate  remedies.    Faradism  can  be  tried. 


CHAPTER    V. 

PREMATURE    INFANTS. 

An  infant  born  only  a  week  or  two  before  term  requires  no  special 
care  or  diet,  provided  it  is  well  developed  and  weighs  over  6  lbs.  It  is  the 
infants  born  at  an  earlier  period  of  gestation  that  are  difficult  to  rear,  and 
the  difficulty  increases  in  proportion  to  the  diminution  in  maturity.  Few 
born  before  the  twenty-eighth  week  of  intra-uterine  life  survive.  Villemin 
reared  one,  who  was  born  at  f>\  months,  or  on  the  most  liberal  computation 
at  6  months,  and  weighed  less  than  2  lbs.  In  estimating  the  chance  of 
life  of  a  premature  infant  the  degree  of  development  is  of  more  importance 
than  the  actual  age,  even  if  this  could  be  ascertained.  A  premature  infant 
is  not  always  a  weakling.  No  matter  how  small  and  delicate,  an  attempt 
must  be  made  to  preserve  its  life. 

The  premature  infant  is  under  weight,  breathes  and  eats  imperfectly, 
has  incompletely  formed  organs,  and  ill-developed  functions.  The  cry  is 
feeble.  The  muscles  are  weak  and  the  child  may  be  absolutely  inert,  quite 
motionless  and  in  a  kind  of  torpor,  and  perhaps  unable  to  suck  on  account 
of  the  muscular  debility.  The  skin  is  soft  and  delicate,  bright  red  in  colour, 
loose  and  movable,  with  little  subcutaneous  fat  and  plentiful  lanugo. 
After  the  seventh  month  the  skin  is  not  so  brightly  red.  Hair  may  be 
present  on  the  scalp.  The  nails  may  be  absent,  or  thin,  small,  and  not 
projecting  beyond  the  finger  tips.  The  centres  of  ossification  of  the  lower 
end  of  the  femur  and  upper  end  of  the  tibia  are  usually  absent.  The  head 
is  large,  face  small  and  wizened,  belly  protuberant,  and  the  lower  limbs 
less  developed  than  the  upper  limbs.  The  brain  is  soft  and  ill-differentiated  ; 
the  lungs  anaemic,  and  presenting  patches  of  atelectasis  ;  the  foramen 
ovale  and  ductus  arteriosus  patent ;  and  the  ductless  glands  large. 
Digestion,  absorption,  and  assimilation  are  defective. 

These  babies  are  liable  to  sepsis,  cerebral  hemorrhage  and  affections 
of  the  nervous  system,  gastro-enteritis,  asphyxia,  atelectasis,  and  pneu- 
monia ;  hemorrhages,  because  of  deficient  blood  coagulability  ;  abrasions 
of  the  skin  ;    umbilical  hernia,  urinary  infarcts,  and  sclerema. 

Warmth,  diet,  and  protection  are  the  main  essentials  in  treatment. 
Daily  weighing  is  the  only  available  indication  of  progress,  and  until  there 
is  a  regular  progressive  increase  in  weight  we  cannot  be  certain  that  the 
child  wiJ]  live.     The  loss  of  weight,  from  1-14  oz.,  during  the  first  3  days 


Premature  Infants. 


97 


depends  upon  the  amount  of  urine  and  meconium  passed,  and  the  amount 
of  water  and  food  given.  It  may  bear  a  much  higher  percentage  ratio  to  the 
total  weight  than  in  a  full-time  child,  and  is  more  serious,  for  it  continues 
longer  and  is  more  slowly  regained.  The  mortality  is  greatest  during  the 
period  of  loss  or  stationary  weight.  The  child  who  attains  its  birth  weight 
in  2  or  3  weeks  does  very  well. 

The  weight  is  no  measure  of  prematurity,  for  it  varies  in  infants  at 
the  same  period  of  gestation  just  as  it  does  in  infants  at  term.  The  daily 
increase  should  bear  some  proportion  to  the  original  weight,  and  be  greater 
in  the  heavier  infants.  At  20  weeks  the  average  weight  of  the  foetus  is 
39  oz.  (Hecker  and  Lusk),  and  the  daily  gain  in  order  to  attain  the  same 
rate  of  development  as  in  utero  should  be  0-75-1  per  cent,  of  its  weight. 
The  mortality  rapidly  diminishes  with  the  increase  in  the  period  of 
gestation. 


Potel's  Statistics. 

Percentage  Mortality. 

Average  daily  gaiu 
in  weight. 

At  6£ 

months  11  survived  out 

of    56 

80-4 

9  "4  gms. 

At  7 

55 

»    131 

58'1 

11-5      „ 

At  7i 

36 

„     53 

31-0 

13-8      „ 

At  8 

„        71 

„  no 

355 

22-8      „ 

Nearly  50  per  cent,  of  the  350  survived.    Weighing  must  be  conducted  with 
the  greatest  gentleness,  for  the  child  should  be  handled  as  little  as  possible. 

The  gastric  capacity  is  estimated  at  1  per  cent,  of  the  body  weight,  and 
the  composition  of  the  food  is  the  same  as  that  for  ordinary  infants,  but  a 
weaker  quality.  Weakly  babies  must  be  fed  hourly.  Maternal  nursing  is 
often  injurious  as  lactation  is  not  fully  established.  A  wet  nurse,  who  has 
been  confined  at  least  a  month  previously,  is  preferable  to  the  mother  if 
the  child  is  strong  enough  to  nurse.  She  should  nurse  her  own  child  in 
addition,  and  give  the  last  part  of  the  feed  to  the  foster  child.  If  suckling  is- 
out  of  the  question  from  J-l  teaspoonful  of  a  5  per  cent,  solution  of  milk 
sugar  may  be  given  hourly  for  24  hours,  and  then  a  similar  quantity  of  the 
breast-milk  of  a  wet  nurse  added  to  each  feed  and  the  amount  gradually 
increased.  Or  recourse  must  be  had  to  whey,  weak  peptonised  milk,  weak 
condensed  milk,  or  a  laboratory  mixture  containing  casein  0*25,  albumin 
0-25,  fat  TO,  and  sugar  3-0  per  cent.,  one  teaspoonful  being  given  hourly. 
Or  a  mixture  of  cream,  lactose  and  water  can  be  used.  The  quality  and 
quantity  of  the  food  are  increased  according  to  the  way  in  which  it  agrees. 
The  chief  point  in  feeding  these  babies  is  to  give  a  very  weak  fluid,  con- 
taining little  fat,  in  small  feeds  hourly.  This  reduces  the  risk  of  dilatation 
of  the  stomach  and  gastro-enteric  troubles.     Insufficient  diet  is  indicated 

H 


98  Chapter    7. 

by  feeble  continuous  cries.  When  taking  enough,  the  child  sleeps  quietly 
between  each  feed,  but  the  lethargy  due  to  debility  and  inanition  must  not 
be  mistaken  for  contentment.  With  satisfactory  progress  the  interval 
between  the  feeds  can  be  increased. 

If  the  child  is  too  feeble  to  take  an  ordinary  feeding  bottle,  it  should 
be  fed  by  means  of  a  glass  cylinder,  graduated  in  cubic  centimetres  or  half 
drachms,  with  a  sloping  end  to  which  an  ordinary  teat  is  fixed,  an  india- 
rubber  ball  beiDg  attached  to  the  larger  end.  The  warm  food  is  poured  into 
the  cylinder,  the  rubber  ball  fixed  on,  and  the  food  forced  slowly  into  the 
child's  mouth.  This  method  is  especially  suitable  for  a  baby  kept  in  an 
incubator,  for  the  child  need  not  be  handled.  If  the  baby  is  not  able  to 
swallow,  it  must  be  fed  by  means  of  a  tube  passed  into  its  stomach. 

The  temperature  falls  rapidly  to  90°  F.,  or  lower,  unless  special  care 
is  taken,  and  is  subsequently  very  unstable.  It  is  of  the  utmost  importance 
to  maintain  the  temperature  near  the  normal  level,  by  preventing  the  loss 
of  heat  as  well  as  by  diet.  The  child  should  be  wrapped  in  layers  of  cotton 
wool,  covered  with  blankets,  and  kept  in  a  cradle,  containing  2  or  3  hot 
water  bottles  or  1  U-shaped  one,  or  electric  heaters.  The  room  temperature 
must  be  maintained  at  90°  F.,  and  all  changes  of  clothing  made  before  a 
good  fire.  Unfortunately  this  temperature  is  very  trying  to  the  nurse,  that 
of  the  cradle  cannot  be  absolutely  gauged  or  regulated,  and  the  frequent 
changing  of  the  napkins  exposes  the  baby  to  considerable  risk. 

Various  incubators,  hatching  cradles,  or  brooders  have  been  devised, 
and  one  such  apparatus  should  be  attached  to  every  maternity  home  or 
hospital.  A  useful  one  can  be  bought  or  hired  from  Hearson,  Regent 
Street,  London.  An  incubator  should  be  simple,  reliable,  easily  cleaned, 
and  easily  regulated  as  to  the  supply  of  heat,  moisture,  air,  and  light.  If 
the  child  is  very  premature  the  temperature  should  be  kept  up  to  90-95°  F., 
and  gradually  reduced  as  the  child  gets  older  and  heavier,  e.g.,  to  68°  F. 
at  5  lbs.  weight.  A  temperature  of  80°  F.  is  often  high  enough.  In  all 
cases  it  must  be  lowered  if  the  child  sweats,  is  restless,  cyanotic,  breathes 
rapidly,  or  its  temperature  rises.  The  air  supply  should  be  pure  and 
contain  60  per  cent,  of  moisture.  The  incubator  must  be  kept  thoroughly 
clean,  well  ventilated,  and  not  exposed  to  the  direct  rays  of  the  sun. 

Washing  should  not  be  allowed  if  the  child  is  very  weak,  and  even  the 
bath  at  birth  must  be  omitted.  If  the  child  is  rubbed  over  with  warm  oil 
and  kept  in  an  incubator,  washing  may  be  postponed  for  a  couple  of  months. 
If  a  bath  is  given,  the  water  should  be  previously  boiled  and  a  super- 
fatted soap  used.  A  bath  at  blood  heat  and  raised  to  105°  F.  is  a  useful 
means  of  raising  the  temperature,  if  much  subnormal. 

No  clothing  is  necessary  beyond  cotton  wool,  which  should  be  changed 
morning  and  evening.  A  separate  piece  can  take  the  place  of  a  napkin, 
and  be  changed  when  necessary.  Drying  powders  may  be  used  in  modera- 
tion, and  warm  oil  relied  upon  for  cleaning  purposes. 


Premature  Infants.  99 

General  Directions. — Maintain  the  temperature  of  the  child,  and  take 
its  rectal  temperature  regularly.  Carefully  regulate  that  of  the  incubator. 
Give  a  suitable  diet  and  brandy  if  necessary.  Avoid  handling  and  all 
measures  likely  to  cause  exhaustion.  Guard  against  exposure  to  light  and 
noise,  and  infection  of  the  alimentary  or  respiratory  tract.  Nasal  catarrh 
is  a  serious  complication.  Note  the  character  of  the  cry,  the  presence  or 
absence  of  colic,  and  the  character  of  the  stools,  for  the  crying  may  be  due 
to  hunger  or  indigestion.  A  marked  fall  in  temperature,  coldness  of  the 
hands  and  feet,  and  increased  frequency  of  respirations  may  indicate  that 
the  apparatus  of  the  incubator  is  wrong  or  that  the  food  supply  is  deficient. 
A  continuously  low  temperature  is  often  due  to  low  vitality,  and  irregularity 
to  lack  of  control  of  the  heat  regulating  mechanism.  A  sharp  rise  may  be 
due  to  too  high  a  temperature  of  the  incubator,  septic  infection,  and  gastro- 
intestinal or  pulmonary  complications.  Oxygen  gas  is  useful  if  there  is 
cyanosis.  Brandy  is  constantly  necessary,  and  occasionally  recourse  must 
be  had  to  saline  injections. 

Prognosis. — Few  born  before  the  twenty-ninth  week  survive.  Those 
under  2J  lbs.  in  weight  generally  die,  and  those  over  3J  lbs.  usually  survive. 
Even  when  a  child  is  gaining  weight,  death  may  occur  absolutely  suddenly. 
Rapid  loss  of  weight,  overlapping  sutures,  and  a  rectal  temperature  below 
90°  F.  are  very  bad  signs.  A  continued  slow  loss  of  weight,  subnormal 
temperature,  and  apathy  are  unsatisfactory  symptoms.  Breathing  is 
usually  irregular,  imperfect,  and  may  assume  the  Cheyne-Stokes  type. 
Attacks  of  cyanosis  are  the  commonest  cause  of  death,  and  result  from 
atelectasis  or  failure  of  the  respiratory  centre.  Pulmonary  collapse  is 
frequent  and  very  fatal  during  the  first  2  or  3  days,  but  rare  after  the 
tenth  day.  The  longer  the  child  lives,  the  less  severe  are  the  attacks  of 
cyanosis,  and  the  less  likely  are  they  to  be  fatal.  They  may  be  due  to  food 
getting  into  the  trachea.     Sudden  death  is  often  due  to  cardiac  failure. 

General  oedema  is  common  on  account  of  the  feeble  heart,  anaemia,  and 
imperfect  action  of  the  kidneys.  Many  of  these  babies  are  very  anaemic, 
because  of  the  delayed  development  of  haemoglobin  formation.  Nasal 
catarrh,  bronchitis,  and  gastro-enteritis  are  serious  complications. 

The  most  favourable  conditions  are  two  skilled  nurses,  an  incubator, 
a  physician  who  understands  such  cases,  and  parents  who  do  not  interfere 
and  press  for  changes  of  treatment.  Eventually  these  babies  develop  into 
normal  children.  By  the  use  of  the  incubator  and  forced  feeding  the 
mortality  has  been  reduced  50  per  cent,  for  premature  infants  born  at  7| 
months,  and  about  20  per  cent,  for  those  more  premature. 


CHAPTER    VI. 

MOETALITY. 

Intra-uterine  death — Intra-uterine  putrefaction — Rigor  mortis  in  the  stillborn 
—  General  mortality —  Death  from  overlaying — Sudden  death. 

Though  the  incidence  of  life  is  associated  with  the  liability  to  sudden  or 
unexpected  death,  and  the  fragility  of  the  hold  on  life  in  the  first  months  of 
existence  is  great,  the  death  of  a  child  after  this  period  should  be  regarded 
as  unnatural. 

Intra-uterine  death  may  take  place  quite  suddenly,  even  within 
half-an-hour  of  birth.  The  foetal  movements  cease.  It  may  be  due  to 
malformation  of  the  heart  or  main  vessels,  premature  closure  of  the  ductus 
arteriosus,  or  serious  congenital  defect.  The  left  lung  was  absent  in  a  case 
of  Schrader's.  Sometimes  it  is  due  to  disease  or  separation  of  the  placenta, 
or  to  injury.  Occasionally  no  cause  can  be  found.  A  child  born  in  a  state 
of  apparent  death  is  not  necessarily  dead,  so  the  usual  means  of  resusci- 
tation must  be  tried,  viz.,  rhythmical  traction  of  the  tongue,  insufflation,  etc. 

Intra-uterine  putrefaction  is  nearly  always  caused  by  foetal  decom- 
position. In  exceptional  instances  a  live  child  has  been  born,  the  putre- 
faction being  due  to  decomposition  of  the  placenta  or  of  blood  clot. 

Rigor  Mortis  can  occur  in  a  stillborn  child  before  or  very  shortly  after 
birth,  so  it  must  not  be  regarded  as  reliable  evidence  of  live  birth.  Chowne 
published  the  first  ante-natal  case  in  1841,  and  a  good  many  have  been 
recorded  since.  One  of  twins  has  been  affected,  while  the  other  lived 
(Ulrich).  This  ante-natal  rigidity  may  pass  off  before  labour  ;  may  prevent 
labour  until  it  has  passed  off  ;  may  hinder  labour,  and  give  the  sensation 
of  a  half-frozen  child  to  the  examining  finger  ;  may  continue  after  delivery. 
It  may  set  in  during  or  after  confinement,  the  foetus  having  died  in  the 
late  stages.  It  does  not  always  accompany  still-birth.  The  rigidity  varies 
in  degree,  is  most  marked  in  the  upper  limbs,  and  causes  the  body  to 
assume  the  intra-uterine  position.  The  head  is  drawn  forward,  back  some- 
what rounded,  arms  flexed  at  the  elbows  and  bent  on  the  chest,  and  the 
thighs  and  legs  flexed.  More  rarely  the  body  is  fully  extended  and  rigid 
"  like  a  soldier  at  attention,"  in  the  cadaveric  position,  and  in  this  form 
it  has  even  caused  fatal  injury  from  rupture  of  the  uterus,  due  to  the  feet 
passing  through  its  wall.      Usually  the  cadaveric  position  in  rigor  mortis 


Mortality.  101 

implies  that  the  child  has  had  a  separate  existence,  and  the  intra-uterine 
position  implies  still-birth.  This  must  not  be  accepted  as  universally  true. 
Ante-natal  rigor  mortis  may  be  associated  with  haemorrhage.  It  does  not 
return  after  passing  off. 

General  Mortality. — The  death  rate  of  infants  is  lowest  among  the 
British  Peerage,  and  the  fisherpeople  of  the  Faroe  Islands.  It  is  lowest 
in  the  breast-fed,  except  in  places  like  Bavaria,  where  the  infants  are  taken 
by  their  working  mothers  to  the  fields  and  exposed  to  cold  and  wet.  It  is 
highest  in  the  bottle-fed  infants  in  manufacturing  centres,  where  the 
mothers  work  in  factories.  It  is  greater,  for  instance,  in  the  northern  than 
the  southern  parts  of  Staffordshire,  for  the  latter  is  a  mining  district,  and 
the  women  remain  at  home,  while  in  the  former  the  women  work  in  factories 
as  potters.  Infantile  mortality  depends  on  defective  viability  of  the  child 
through  ante-natal  conditions  affecting  the  mother,  such  as  insufficient 
food,  anaemia,  alcohol,  overwork,  lead  and  other  poisons,  insanity,  and 
constitutional  disease.  It  may  be  due  to  injury  at  birth,  asphyxia,  or 
intracranial  haemorrhage  ;  or  it  results  from  post-natal  conditions,  many 
of  which  are  indirectly  due  to  ante-natal  causes,  such  as  debility,  inanition, 
atrophy,  marasmus,  and  convulsions  ;  prematurity  ;  asphyxia,  atelectasis, 
syphilitic  pneumonia,  and  congenital  defects. 

The  number  of  premature  infants  has  shown  a  considerable  increase 
in  recent  years,  the  cause  of  which  is  uncertain.  Perhaps  it  is  due  to  the 
survival  of  the  delicate  up  to  parental  age  under  the  improved  environment 
of  modern  life  ;  to  the  use  of  drugs  and  other  means  to  procure  abortion  ; 
or  to  artificial  measures  adopted  to  prevent  conception,  leading  to  minor 
effects  on  the  endometrium.  Both  prematurity  and  still-birth  are  more 
frequent  in  boys  than  girls,  and  in  the  illegitimate  than  the  legitimate, 
except  where  illegitimacy  is  not  considered  a  disgrace. 

Infantile  mortality  is  very  high  in  the  first  month,  sinking  to  less  than 
half  in  the  second  month,  and  progressively  decreasing  with  each  successive 
month  during  the  first  year.  It  decreases  with  every  day  of  advancing  life, 
for  the  younger  the  infant  the  greater  are  the  effects  of  ante-natal  debility, 
of  injury  at  birth,  and  of  congenital  defects,  and  the  more  active  are  the 
processes  of  disease. 

Death  during  the  first  year  is  ascribed  to  congenital  weakness  in  15  per 
cent.,  infections  in  5  per  cent.,  and  respiratory  diseases  in  10-20  per  cent. 
One-third  may  be  put  down  to  disorders  of  the  digestive  organs,  and  one- 
third  to  various  other  causes.  Alimentary  affections  are  the  chief  cause 
among  the  poor,  increasing  in  frequency  with  the  poverty  of  the  parents, 
and  comparatively  rarely  fatal  among  the  well-to-do.  In  the  second  year 
of  life  about  three-fifths  of  the  deaths  are  due  to  respiratory  and  one-fifth 
to  alimentary  troubles.  A  marked  rise  or  fall  in  the  atmospheric  tem- 
perature increases  the  mortality.  Especially  is  this  the  case  with  a  high 
summer  temperature  and  diarrhceal  affections  in  large  towns.    Cold  lowers 


102  Chapter    VI. 

the  vitality,  and  leads  to  fatal  affections  of  the  respiratory  organs.  The 
neglect  of  suckling  is  one  of  the  chief  causes  of  death  in  infancy. 

Poverty,  leading  to  the  dependence  of  the  child  on  the  maternal  milk 
supply,  reduces  infantile  mortality.  No  woman  should  be  allowed  to  return 
to  any  work,  which  interferes  with  regular  nursing  of  her  infant,  until 
3  months  after  confinement. 

Death  from  Overlaying. — Nearly  1,500  infants  are  killed  yearly  in 
England  and  Wales  through  being  overlaid  by  one  of  the  parents.  Death 
results  from  suffocation  by  the  pressure  of  the  arm  or  body.  Occasionally 
it  is  due  to  the  pressure  of  another  child,  the  domestic  cat  or  dog,  or  of 
clothes.  Or  the  child  may  turn  on  its  face,  and  bury  the  mouth  and  nostrils 
in  the  pillow.  In  most  instances  this  avoidable  cause  of  death  must  be 
ascribed  to  carelessness,  reckless  indifference,  or  culpable  neglect,  almost 
amounting  to  manslaughter  or  murder.  Drunkenness  in  the  parent,  and 
the  lack  of  a  cot  or  cradle  for  the  child  are  the  two  most  important  factors. 
A  padded  soap  box  or  a  hammock  would  be  quite  sufficient.  No  child  should 
be  permitted  to  sleep  in  the  same  bed  as  a  parent  until  2  years  of  age. 

Drunken  parents  who  cause  the  death  of  their  offspring  in  this  way 
should  be  severely  punished.  More  than  three-fourths  of  these  babies  are 
under  3  months  of  age.  After  6  months  of  age  comparatively  few  succumb, 
and  over  1  year  the  child  is  generally  strong  enough  to  protest. 

Examination  of  the  body  may  show  marks  of  pressure,  e.g.,  a  flattened 
nose,  or  merely  signs  of  suffocation.  Asphyxia  occurs  from  other  causes, 
so  cannot  be  accepted  alone  as  proof  of  death  from  overlaying.  Usually 
there  are  found  bluish  lips  and  livid  face,  reddened  eyeballs,  punctiform 
conjunctival  haemorrhages,  sometimes  a  protruded  and  discoloured  tongue, 
and  froth,  often  bloodstained,  in  the  mouth  or  nostrils.  The  lividity  of  the 
complexion  may  soon  pass  off.  The  limbs  are  flexed,  the  hands  clenched,  and 
the  nails  blue.  The  blood  is  dark  and  liquid,  the  right  ventricle  distended 
with  soft  clot  and  the  left  contracted  and  empty.  The  mucous  membrane 
of  the  trachea  is  reddened.  The  lungs  are  congested,  sodden,  and  cedematous, 
containing  much  frothy  fluid,  but  yielding  no  microscopical  evidence  of 
inflammation,  in  contra-distinction  to  that  of  acute  pneumonic  congestion. 
Minute  petechias  are  found  on  the  serous  membranes.  The  brain  and 
meninges  are  congested. 

Sudden  Death  is  of  frequent  occurrence,  and  requires  special  study  in 
connection  with  those  cases  which  do  not  lead  to  the  child  being  placed  under 
medical  care.  Strictly  it  must  be  ascribed  either  to  failure  of  the  circulation, 
or  of  respiration,  but  it  will  be  more  convenient  to  discuss  it  under  the 
headings  of  syncope,  asphyxia,  convulsions,  intestinal  disorders,  and 
toxaemia.  Some  of  these  are  organic,  others  apparently  functional  in 
origin.  An  unexpected  death,  in  the  course  of  a  disease  which  seems  to  be 
running  a  harmless  course,  is  also  a  sudden  death,  lamentably  so  from  the 
parent's  point  of  view  unless  the  possibility  thereof,  has  been  suggested. 


Mortality.  103 

Syncope  or  heart  failure  is  the  common  termination  of  many  diseases, 
especially  prolonged  wasting  affections.  Many  a  marasmic  infant  dies 
suddenly  from  this  cause,  with  or  without  slight  agonal  convulsive  move- 
ments. Sometimes  the  cause  is  a  myocardial  weakness  dependent  on  fever, 
a  cloudy  degeneration,  a  fatty  change,  atrophy  of  cardiac  muscle,  an 
unsuspected  myocarditis,  or  fibroid  disease.  Death  is  myocardial  in  origin 
when  it  ensues  on  slight  exertion  in  pneumonia,  diphtheria,  influenza,  and 
other  specific  fevers.  The  heart  may  exhibit  severe  myocardial  changes, 
though  to  the  unaided  eye  appearing  normal.  Less  frequent  causes  are 
congenital  and  acquired  heart  disease,  adherent  pericardium,  pericardial 
effusion,  acute  dilatation  of  the  heart  following  extreme  exertion  or 
whooping  cough,  the  displacement  of  the  heart  by  rapid  pleural  effusions, 
and  possibly  the  cumulative  effects  of  digitalis.  Spontaneous  rupture  has 
followed  septic  embolism  and  abscess  of  the  myocardium,  even  in  the 
first  year  of  life. 

Syncope  may  occur  from  a  fit  of  coughing  or  from  violent  pain,  reflex 
action  or  direct  inhibition.  Death  from  fright  or  excitement  is  not  unknown, 
and  is  almost  certainly  due  to  vagus  inhibition  of  the  heart.  Inhibition 
may  be  caused  by  a  slight  blow  or  pressure  on  the  larynx,  a  blow  in  the 
epigastrium  during  digestion,  a  blow  in  the  hypogastrium,  sudden  injury 
in  the  regions  supplied  by  the  trigeminal  nerve,  a  sudden  cold  plunge, 
minor  operations,  e.g.,  circumcision,  puncture  with  a  trocar  or  exploring 
syringe,  the  hypodermic  injection  of  serum,  or  the  sting  of  a  bee.  Death  by 
cardiac  inhibition  is  sudden,  calm,  and  unaccompanied  by  convulsions. 
Cervical  caries,  with  separation  of  the  odontoid  process,  might  cause  it  by 
pressure  on  the  cord.  The  sudden  lowering  of  blood  pressure  by  the 
rapid  escape  of  cerebro-spinal  fluid  may  be  quickly  fatal. 

In  many  of  these  cases  of  sudden  and  fatal  syncope  there  is  another 
important  factor  present,  namely,  the  status  lymphaticus  (q.v.).  It  is 
incredible  that  several  of  the  slight  causes  mentioned  could  produce  the 
fatal  result,  were  it  not  for  the  presence  of  some  peculiarity  of  constitu- 
tion which  renders  the  child  extremely  susceptible  to  the  effects  of 
shock. 

Asphyxial  causes  include  glottic  spasm  from  laryngeal  irritation  by 
foreign  bodies  or  inflammation,  obstruction  in  some  portion  of  the 
respiratory  tract  by  too  large  a  bolus,  or  by  food  regurgitated  and 
inspired  when  the  child  is  on  its  back,  from  a  smack  on  the  back  while  eating, 
during  artificial  feeding,  or  in  post-anaesthetic  vomiting  ;  or  by  various 
foreign  bodies,  a  round  worm,  the  contents  of  a  tuberculous  cavity,  or  a 
caseating  gland  ulcerating  into  the  trachea.  Acute  periglandular  oedema 
and  swelling  may  cause  compression  of  the  trachea  and  death  in  a  few  hours 
from  suffocation. 

Acute  pulmonary  congestion  or  inflammation,  atelectasis,  the  rapid 
effusion  of  a  pleural  effusion  and  laryngospasm  may  all  end  fatally.    Cardiac 


104  Chapter    VI. 

thrombosis  is  an  occasional  cause.     A  thrombus  may  be  carried  into  the 
pulmonary  artery  from  the  lateral  sinus  in  ear  disease. 

Death  from  asphyxia  is  rarely  as  sudden  as  that  from  syncope,  and 
some  of  the  pulmonary  causes  act  rather  through  the  nervous  than  the 
respiratory  system.  Thus  the  so-called  "  inward  convulsions  "  are  often 
due  to  glottic  spasm  of  purely  nervous  origin.  Analogous  spasms  may  be 
due  to  pertussis,  to  laryngeal  papillomata  or  foreign  bodies,  or  the  pressure 
of  enlarged  glands  on  the  vagus  or  its  branches. 

In  asphyxia!  cases,  especially  those  of  acute  capillary  bronchitis, 
the  "  suffocating  catarrh  "  of  Laennec,  liable  to  occur  in  delicate  infants  in 
the  first  6  months  of  life,  froth  is  found  in  the  bronchi.  Portions  of  the 
lung  are  hard,  but  float  in  water,  and  yield  little  rods  of  muco-pus  on 
pressure  ;  and  subpleural  ecchymoses  are  present.  Similar  congestion  may 
occur  in  any  fever,  unsuspected  typhoid  and  tuberculosis. 

Convulsions  are  fatal  from  syncope  or  from  asphyxia,  due  to  spasm 
of  the  respiratory  and  laryngeal  muscles.  Hemorrhage  into  the  cranial 
cavity  is  a  common  cause  at  birth.  Subsequently  it  may  be  due  to  blood 
diseases,  toxemic  affections,  or  rupture  of  a  blood  vessel.  Miliary  aneur- 
isms have  been  found  in  quite  young  children.  Haemorrhage  is  especially 
likely  to  cause  sudden  death  when  it  takes  place  in  large  amount  into  the 
lateral  ventricles. 

Meningitis,  cerebral  tumours,  the  rupture  of  an  abscess,  and  brain 
softening  may  all  cause  fatal  convulsions.  If  there  is  fever  with  convulsions 
the  onset  of  an  exanthem  should  be  suspected.  If  there  is  no  fever,  in  nine 
out  of  ten  cases  the  cause  lies  in  some  affection  of  the  alimentary  system. 

Intestinal  disorders,  causing  sudden  or  unexpected  death,  may  do  so 
through  setting  up  convulsions,  from  profuse  haemorrhage,  profound 
toxaemia,  or  the  very  rapid  loss  of  fluid  in  cholera  and  cholera  nostras. 
Death  takes  place  rapidly  but  rarely  quite  suddenly. 

Toxaemic  states  are  best  illustrated  by  the  rapidly  fatal  issue  in  some 
cases  of  malignant  fevers,  cerebro-spinal  meningitis,  pneumonia,  appen- 
dicitis, pyaemia,  and  others  of  uncertain  origin.  A  rapidly  fatal  disease 
has  been  reported  as  occurring  in  institutions.  Dr.  C.  J.  Macalister  described 
four  such  cases.  A  boy  was  sent  to  bed  on  account  of  an  irritable  cough, 
and  was  found  dead  half-an-hour  later.  Another  had  violent  vomiting 
and  diarrhoea,  soon  became  profoundly  weak,  livid  and  unconscious,  and 
died  in  3  hours.  A  third  complained  of  headache  at  night,  was  very  weak  in 
the  morning,  became  unconscious,  and  died,  with  the  appearance  of 
asphyxia  or  strangulation.  In  a  fourth  child  there  was  vomiting,  a  little 
diarrhoea,  and  a  similar  asphyxial  appearance  after  death.  Probably  the 
exciting  cause  was  a  toxin  acting  on  the  respiratory  centre,  causing  engorge- 
ment, oedema,  and  even  pneumonia  of  the  lungs.  Suprarenal  haemorrhage 
has  been  found  in  cases  fatal  in  a  few  hours  from  vomiting,  diarrhoea, 
lividity,  and  collapse.     It  may  occur  in  healthy  robust  children,  and  is 


Mortality.  105 

probably  toxsemic.  Death  may  follow  the  rapid  cure  of  a  skin  eruption, 
e.g.,  the  so-called  "  eczema  death."  Possibly  in  some  of  these  cases  a 
nephritis  is  set  up,  and  in  others  the  status  lymphaticus  is  present. 

Sudden  death  also  occurs  from  anaesthetic  and  surgical  causes.  Shock 
may  be  due  to  or  accentuated  by  cold  during  an  operation ;  the  rapid 
evacuation  of  a  pleural  effusion  or  psoas  abscess  ;  mere  exploratory  punc- 
ture ;  or  the  washing  out  of  cavities.  Death  may  follow  the  entrance  of  air 
into  veins  or  embolism,  for  instance,  after  the  injection  of  iron  into  a 
nsevus. 


Chapter  VII. 

CONGENITAL  DEFORMITIES  AND  INJURIES  AT  BIRTH. 

Deformities  —  Ante-partum  Injuries  —  Caput  Succedaneum  —  Cephal- 
hcematoma  —  Cranial  Depressions  —  Sterno-mastoid  Tumour  —  Dia- 
phragmatic Hernia. 

Deformities  have  already  been  shown  to  be  in  many  instances  the 
result  of  inheritance,  depending  on  the  direct  transmission  of  some  pecu- 
liarity in  the  male  or  female  germ  cells.  Others  are  due  to  injury,  toxic 
or  microbial  infection,  or  poisons  during  intra-uterine  life  ;  or  to  actual 
intra-uterine  disease,  though  this  is  more  likely  to  cause  abortion.  Many 
defects,  e.g.,  dimpling,  grooving,  and  scarring  of  the  skin,  and  amputation  of 
limbs,  are  ascribed  to  amniotic  adhesions  or  to  strangulation  by  the  cord. 
Malformations  may  affect  every  structure  in  the  body.  Many  of  these 
are  referred  to  in  the  chapters  on  special  diseases.  Here  a  few  of  the  more 
obvious  ones  will  be  described.  Family  deformities  may  be  limited  to  one 
sex.    Some  are  due  to  defects,  others  to  excess  of  normal  development. 

Acephaly  is  a  deformity  incompatible  with  life.  In  the  variety, 
acephalus  monobrachius,  there  is  only  one  upper  extremity.  In  para- 
cephalus  both  upper  extremities  are  absent.  Myacephalus  is  a  shapeless 
mass  covered  with  skin.  Deformities  of  the  limbs  may  be  present.  There 
may  be  no  rudimentary  head ;  no  trace  of  a  cranial  bone  ;  a  soft  nodular 
mass  of  vascular  connective  tissue  ;  or  sometimes  a  circular  line  of  hair 
and  central  depression  at  the  upper  end  of  the  foetus.  The  cerebrum  and 
cerebellum  are  absent.    It  is  due  to  agenesis  in  early  foetal  life. 

Ectromelus  is  ascribed  to  intra-uterine  amputation  of  the  arms  and 
legs.  It  is  most  unlikely  that  the  cord  could  exert  sufficient  pressure  without 
its  circulation  being  stopped.  The  only  case,  which  has  come  under  my 
care,  was  a  boy,  3  months  old,  the  fourth  child  of  apparently  healthy 
parents.  The  mother  stated  that  she  nearly  aborted  after  a  fright  when 
3  months  pregnant.  There  were  no  deformities  in  other  children.  The 
patient  was  born  at  full  time,  and  was  well  grown.  The  right  arm  was  absent 
at  the  elbow,  the  left  at  the  wrist ;  the  right  leg  at  the  ankle,  and  the 
left  at  the  knee.  He  died  in  a  few  days  from  infective  diarrhoea.  Well 
known  cases  are  those,  of  Matthew  Buchinger  and  Arthur  Kavanagh. 
Buchinger  was  born  in  1674  and  died  in  1722.    He  could  play  several  musical 


Congenital   Deformities  and  Injuries  at  Birth.  107 

instruments,  write,  draw,  juggle,  and  stave ;  was  married  four  times,  and  had 
11  children.  Kavanagh  could  write,  draw,  ride,  drive,  shoot,  and  fish,  and 
was  a  member  of  Parliament.  This  deformity  is  not  transmissible  and  not 
incompatible  with  prolonged  life.  All  the  extremities  may  be  almost 
entirely  absent.  Bones  can  be  felt  in  the  stumps.  Cases  in  which  rudimen- 
tary extremities  are  attached  to  abortive  or  shortened  limbs  are  clearly 
of  a  different  type  in  that  they  cannot  be  due  to  intra-uterine  amputation  ; 
they  can  be  produced  by  abnormalities  of  development  of  the  limb  segments. 
There  is  often  no  history  of  shock  or  maternal  impression.  The  extent 
of  the  amputations  vary.  It  may  be  limited  to  one  finger.  Occasionally  it 
is  incomplete,  the  limb  remaining  attached  by  a  fibrous  cord,  or  simply 
marked  by  a  line  of  constriction.  The  remains  of  a  supernumerary  little 
finger  may  be  indicated  by  a  little  nodule  near  the  base  of  the  normal  finger, 
as  if  amputated  in  utero. 

Split  Hand  and  Foot  or  Lobster  Claw  is  a  truly  hereditary  defect.  The 
foot  malformation  is  the  most  constant,  so  Hereditary  Split  Foot  is  the 
best  name.  It  must  be  regarded  in  its  origin  as  a  sport  or  mutation,  though 
it  varies  in  degree  in  different  individuals.  Lewis  and  Embleton  (1908) 
collected  over  180  cases.  In  six  generations  of  one  family  44  were  affected, 
generally  in  all  extremities.  The  hands  were  never  deformed  alone,  nor  one 
foot  alone.  The  feet  showed  three  types  of  deformity :  absence  of  the  second, 
third,  and  fourth  phalanges  and  metatarsals  ;  deformity  of  the  second  toe 
chiefly  ;  malformation  of  the  third  toe.  Syndactyly  of  the  unaffected  toes 
was  common.  The  feet  have  a  cleft  or  bifid  appearance.  In  another 
family  of  87,  28  were  affected  (Robinson  and  Bowen,  1909). 

Possibly  this  is  an  atavistic  reversion.  So,  too,  the  peculiarity  of  an 
extremely  short  first  metatarsal  bone,  inasmuch  as  it  resembles  that  of  an 
anthropoid  ape  in  which  the  big  toe  is  like  a  thumb.  It  may  be  bilateral. 
The  whole  foot  indicates  a  reversion  towards  that  of  the  higher  apes.  In  the 
foetus  the  great  toe  is  apposable,  and  in  childhood  it  is  much  more  movable 
than  in  later  life. 

In  Brachydactyly  the  middle  phalanges  of  the  hands  and  feet  are 
abortive,  sometimes  reduced  to  a  cubical  bone,  generally  ankylosed  with  the 
ungual  phalanx.  The  first  phalanx  of  the  thumb  is  affected,  and  is,  therefore, 
regarded  as  homologous  with  the  middle  phalanx.  In  Matthew's  family 
(1908)  it  occurred  in  12  members  in  five  generations,  was  transmitted  by 
affected  females,  and  rarely  affected  males. 

Polydactyly  is  not  uncommon,  and  may  affect  all  the  extremities. 

Syndactyly,  or  Webbed  Fingers  and  Toes  is  still  more  frequent,  and  often 
associated  with  Polydactyly  or  other  deformity.  Morrish  (1907)  reported 
the  case  of  a  man  with  an  extra  digit  on  each  hand  and  foot,  and  webbing 
of  both  second  and  third  toes.  He  was  an  only  child  and  his  parents  were  un- 
affected. Of  his  seven  children  two  boys  were  normal ;  five  girls  had  extra 
ulnar  digits  on  each  hand,  attached  by  a  pedicle  or  with  bony  union.     Various 


108  Chapter    VII. 

degrees  of  webbing  of  the  toes  were  present,  and  three  children  had  extra 
toes.  Webbing  of  the  fingers,  generally  between  the  third  and  fourth,  is 
the  most  common  malformation  of  the  hand,  and  is  due  to  an  arrest  of 
development.  In  early  f cetal  life  the  fingers  are  bound  together  by  webs  of 
varying  extent.  The  thumb  becomes  detached  in  the  eleventh  week,  and  the 
fingers  separate  later.  Hence  it  is  common  for  the  thumbs  to  remain  free, 
though  all  the  fingers  are  united.  In  three  recorded  instances  the  thumbs 
were  affected.  Syndactylism  of  the  toes  is  similar  in  character.  The 
treatment  is  purely  surgical. 

The  Thumb  and  First  Metacarpal  may  be  absent.  This  rare  deformity 
is  usually  associated  with  defect  or  absence  of  the  radius.  Occasionally  the 
radius  is  normal.  The  trapezium  and  scaphoid  may  be  absent.  An  absent 
radius  may  be  associated  with  club-hand.  Bifurcation  of  the  terminal 
phalanx  of  the  thumb  assumes  two  varieties.  The  bone  may  be  bifid, 
and  the  nail  single,  though  grooved.  Or  both  may  be  bifid  and  united  by  a 
web.  It  may  affect  one  or  both  thumbs,  and  both  big  toes.  Other  ungual 
phalanges  may  show  similar  conditions.  Malcolm  (1908)  records  a  curious 
case  in  which  the  nails  were  absent  on  the  thumb,  first  and  second  fingers, 
and  radial  half  of  the  third.  The  feet  were  affected  in  the  same  way.  It 
had  occurred  in  four  generations.  Absence  of  the  proximal  phalanges,  the 
fingers  ending  in  rounded  stumps,  has  been  transmitted  through  five 
generations  (Lewis  Marshall,  1903). 

Of  the  various  deformities  of  the  leg  we  find  absence  of  the  tibia, 
alone  or  associated  with  other  defects,  such  as  supernumerary  digits  and 
absent  radii.  In  a  case  of  Openshaw's  the  upper  fifth  of  the  tibia  in  the  left 
leg  was  alone  present,  and  the  right  external  malleolus  was  absent.  Both 
the  fibulae  and  certain  toes  may  be  absent ;  or  one  alone,  in  conjunction 
with  the  outer  half  of  the  foot  and  two  outer  toes. 

The  patellae  may  be  absent  causing  genu  recurvatum,  or  congenitally 
dislocated,  producing  genu  valgum.  Possibly  this  is  due  to  weakness 
of  the  vastus  internus  muscle. 

Ante-partum  Injuries  are  comparatively  infrequent  for  the  foetus  is 
well  protected.  Nevertheless  both  slight  and  serious  damage  may  occur, 
even  though  there  is  no  external  evidence  of  violence.  In  rare  cases  the 
child  is  born  with  a  wound  in  process  of  healing,  due  to  an  accidental  or 
intentional  blow  on  the  pregnant  womb.  Sometimes  multiple  fractures  are 
found,  but  these  are  more  likely  to  be  the  result  of  osteogenesis  imperfecta. 

Injuries  at  Birth  are  much  more  frequent,  and  due  to  the  relative  size 
of  the  head  of  the  child,  and  the  bony  outlet  of  the  pelvis ;  deformity  of  the 
pelvis  ;  tumours  ;  injury  by  the  examining  finger  ;  and  to  the  amount  of 
violence,  necessary  or  unnecessary,  used  in  delivering  the  child,  or  to  the 
local  pressure  of  the  forceps.  The  cranial  bones  may  be  fractured  ;  the 
parietal  being  the  most  liable  in  unassisted  labour,  and  the  frontal  if  forceps 
are  used.    Fracture  of  the  vertebral  column  ;    of  one  or  more  bones  of  the 


Congenital   Deformities  and  Injuries  at  Birth.  109 

limbs,  notably  the  humerus,  clavicle,  and  femur  ;  separation  of  a  humeral 
epiphysis  ;  and  single  or  multiple  dislocations  may  all  occur.  Visceral 
haemorrhages  are  sometimes  found.  Thus,  we  may  find  abrasions,  ecchy- 
moses,  wounds,  fractures,  dislocations,  internal  haemorrhages,  rupture  of 
internal  organs,  and  even  avulsion  of  a  limb.  Normally  the  cranial  bones 
overlap,  remaining  so  for  a  few  days,  and  the  skull  is  asymmetrical  in  conse- 
quence of  the  moulding  of  the  head  during  its  birth.  This  asymmetry  is 
often  distressing  to  the  mother,  if  the  child  is  a  girl,  for  it  persists  for  a  long 
time,  and,  indeed,  is  more  or  less  permanent  in  a  very  modified  degree, 
insufficiently  to  be  noticeable  in  later  life.  It  is  always  safe  to  state  that  it 
is  of  no  importance,  and  that  it  will  gradually  improve  as  the  head  increases 
in  size.  No  head  is  truly  symmetrical.  Certain  types  of  deformity  of  the 
skull  will  be  considered  later  for  they  are  not  due  to  injury  at  birth,  but  to 
developmental  errors.  Much  injury,  even  fractures,  may  occur  in  unaided 
labours.  Injuries  found  after  instrumental  labours  are  by  no  means  always 
due  to  the  instruments  used,  and,  even  if  they  are,  they  may  have  been 
unavoidable. 

The  Caput  Succedaneum  is  very  commonly  present.  It  is  situated  on 
the  head,  usually  over  the  posterior  part  of  the  parietal  or  the  mem- 
branous part  of  the  occipital  bone,  but  may  be  found  on  the  nates,  scrotum, 
or  other  presenting  parts.  It  varies  in  size  and  shape  ;  generally  round, 
oval,  or  somewhat  elongated.  The  superjacent  skin  is  unaltered  or  con- 
gested, even  purple,  according  to  the  duration  and  effect  of  the  pressure. 
The  swelling  is  due  to  a  ring-like  compression  of  the  part  first  presenting, 
and  serous  or  sero-sanguineous  transudation  into  the  cellular  tissues.  If 
many  blood  vessels  give  way  the  amount  of  haemorrhage  may  produce  a 
fluctuating  tumour.  It  differs  from  a  cephal-haeniatoma  in  its  doughy  or 
cedematous  swelling,  generally  pitting  ;  its  greater  diffuseness,  not  being 
limited  by  the  sutures  ;  and  its  occurrence  at  birth,  though,  if  due  to 
thrombosis,  it  may  take  1-3  days  to  develop.  Sometimes  two  are  present, 
one  being  due  to  constriction  by  the  neck  of  the  womb,  and  the  other  at  the 
pelvic  outlet.  No  treatment  is  necessary,  unless  the  skin  is  abraded  or 
broken,  or  inflammation  and  suppuration  ensue.  Sloughing  of  the  scrotum 
has  been  recorded.  The  swelling  subsides  in  1-3  days,  and  usually 
disappears  entirely  in  a  week. 

A  Cephal-haematoma  is  a  special  variety  of  tumour  due  to  haemorrhage 
between  the  periosteum  and  the  cranium.  Occasionally  the  term  is  used 
to  include  haemorrhages  between  the  scalp  and  periosteum  (haematoma 
simplex),  between  the  skull  and  dura  mater  (cephal-haematoma  internum), 
and  meningeal  haemorrhage.  On  the  whole  it  is  best  to  reserve  the  name 
for  the  type  here  described.  Shortly  after  birth,  generally  on  the  second 
or  third  day,  a  slight  swelling  is  found  on  the  head,  and  it  gradually  increases 
in  size  for  a  few  days  to  a  week. 

It  is  due  to  bleeding  from  the  subperiosteal  vessels  or  those  passing 


110  Chapter    VII. 

through  bony  foramina,  in  consequence  of  excessive  moulding  of  the 
skull,  injury  by  forceps,  increased  blood  pressure,  constriction  of  vessels 
of  the  scalp  during  labour,  or  asphyxia.  The  periosteum  is  raised  by  the 
haemorrhage.  Dark  fluid  blood  and  some  fibrin  are  found  between  it  and 
the  bone,  with  bony  formation  later.  The  superjacent  skin  is  movable 
over  the  surface  of  the  tumour,  and  usually  not  discoloured.  This  tumour 
is  most  common  in  difficult  or  prolonged  labour,  and  in  vertex  presentations. 
It  may  be  found  after  spontaneous  easy  confinement,  and  in  breech 
presentations.  Eighty  per  cent,  are  said  to  occur  in  primiparae,  elderly  ones 
being  particularly  liable.  Of  six  successive  cases  all  were  in  multiparae  ; 
the  fourth  to  the  fourteenth  labour.  One  was  a  twin.  It  is  twice  as  frequent 
in  boys  as  in  girls,  because  of  the  larger  size  of  the  head.  It  occurs  in  1  per 
cent,  of  all  infants  (Kleinwachter,  04-0-5  per  cent.).  A  similar  hsematoma 
may  result  from  injury  after  birth. 

Though  usually  single,  bilateral  and  even  triple  tumours  are  sometimes 
seen.  The  most  common  situation  is  over  the  right  parietal  bone,  because 
of  the  frequency  of  left  occipito-anterior  presentations.  In  my  experience 
it  is  just  as  common  over  the  left  parietal  bone,  but  is  rare  over  the  occipital. 
In  other  situations  it  is  more  likely  to  be  due  to  injury  by  forceps  than  to 
the  other  causes  mentioned. 

The  swelling  is  soft,  fluid,  fluctuating,  irreducible,  painless,  and  free 
from  heat  and  inflammation.  It  does  not  pulsate,  and  does  not  increase 
in  size  on  cough  or  crying.  In  size  and  shape  it  is  about  that  of  half  a  hen's 
egg  or  a  small  apple,  and  it  contains  about  an  ounce  of  blood.  It  may  be 
much  larger,  and  hold  5  or  6  oz.  Koughly  it  corresponds  with  the  shape  of 
the  bone,  for  it  is  almost  invariably  limited  by  the  attachments  of  the 
periosteum,  and  does  not  extend  on  to  the  sutures  or  fontanelles. 

Though  at  first  it  may  be  tense,  it  is  usually  quite  soft  when  brought 
for  diagnosis.  Gradually  it  hardens  by  coagulation  of  the  blood,  and 
presents  a  soft  central  area  with  a  raised  hard  encircling  ring.  At  the  end 
of  a  week  bony  spicules  and  plates  develop  from  the  inner  layer  of  the 
periosteum,  spread  into  the  encircling  ring  and  over  the  whole  surface, 
giving  rise  to  a  peculiarly  crackling  feel  on  examination.  Sometimes  the 
new  bone  is  only  formed  at  the  edges,  the  fluid  blood  is  absorbed,  and  the 
periosteum  becomes  adherent  again.  Unless  the  effusion  is  quite  small, 
the  ossification  proceeds  until  a  smooth,  sometimes  uneven,  hard,  bossy 
tumour  is  left,  creating  a  certain  degree  of  asymmetry  or  deformity  of  the 
skull.  Ordinarily  the  tumour  is  well  in  1-3  months,  except  for  the  bossing 
which  lasts  for  as  many  years,  eventually  disappearing  and  leaving  no 
trace.  The  absorption  is  due  to  the  ordinary  processes  of  growth  in  the 
periosteal  bones. 

Inflammation  may  result  from  severe  traumatism.  Infection  is  liable 
to  lead  to  abscess  formation,  caries  of  the  underlying  bone,  and  secondary 
purulent  meningitis. 


Congenital   Deformities  and  Injuries  at  Birth.  Ill 

This  head  tumour  must  be  diagnosed  from  caput  succedaneum,  various 
forms  of  meningocele,  dermoids,  and  fractures.  A  caput  succedaneum  is 
not  limited  by  sutures,  has  no  bony  ring,  and  begins  to  disappear  on  the 
second  or  third  day  of  life.  A  meningocele  issues  from  a  fontanelle  or  suture, 
pulsates,  increases  in  size  on  cough  and  crying,  is  partly  reducible,  and  causes 
cerebral  symptoms  when  compressed.  A  cephal-hydrocele  is  associated 
with  fracture  and  pulsates.  Dermoids  in  this  situation  are  very  rare.  The 
most  common  error  is  that  of  ascribing  the  tumour  to  fracture  of  the  skull, 
because  of  the  prominent  hard  ridge  and  soft  centre.  It  is,  however,  a 
tumour,  and  not  a  depression,  and  the  bony  cranium  can  be  felt  on  pressure 
in  the  centre  of  the  swelling.  Occasionally  it  is  associated  with  a  cranial 
depression  or  fracture.  In  one  case  haematoma  of  the  left  parietal  bone  was 
associated  with  a  smaller  subdural  haemorrhage,  a  similar  subdural  haemor- 
rhage on  the  opposite  side,  a  frontal  meningocele,  and  a  myelo-meningocele 
in  the  lumbar  region. 

No  treatment  is  needed,  except  protection  from  pressure  and  injury. 
Painting  with  equal  parts  of  flexile  and  non-flexile  collodion  may  help 
absorption  by  causing  contraction.  Evacuation  by  puncture  and  subse- 
quent compression  are  unsatisfactory,  and  there  is  risk  of  sepsis.  It  may  be 
advisable  to  evacuate  the  blood  if  the  effusion  is  so  great  and  rapid  as  to 
threaten  the  nutrition  of  the  scalp  ;  or  if  the  skin  becomes  red  and  cede- 
matous.  No  such  case  has  come  under  my  notice.  Complications,  such  as 
fracture,  intracranial  haemorrhage,  and  abscess,  require  appropriate 
treatment. 

Injuries  of  the  face  and  head. — Abrasions,  bruises,  and  various  wounds 
may  be  caused  by  the  finger  of  the  accoucheur,  the  pressure  of  forceps, 
other  instruments,  and  falls  during  precipitate  labour.  Occasionally  the 
pressure  may  be  so  severe  as  to  result  in  local  gangrene.  Such  a  case  came 
under  my  notice,  although  premature  labour  was  induced  in  the  eighth 
month  because  of  the  small  size  of  the  maternal  pelvis.  A  patch  of  dry 
gangrene  developed  in  front  of  the  ear.  The  child  showed  remarkably 
little  vitality,  and  died  later  from  sepsis.  Sloughing  of  the  scalp,  more  or 
less  severe  injury  to  the  eye,  facial  palsy,  and  dislocation  or  fracture  of  the 
lower  jaw  have  all  occurred. 

A  Cranial  Depression,  spoon-shaped  or  furrow-shaped,  is  due  to  pelvic 
deformity,  the  head  being  compressed  against  the  sacral  prominence  or 
other  bony  ridge  ;  and  sometimes  to  instruments.  It  can  be  produced  by 
persistent  pressure  with  the  finger  in  an  attempt  to  turn,  or  by  pressure 
against  an  elevated  arm  in  a  breech  presentation. 

It  may  occur  in  more  than  one  child  in  a  family.  The  common  site 
is  the  frontal  or  parietal  region,  especially  the  left  frontal,  near  the  anterior 
fontanelle.  Occasionally  it  is  bilateral.  About  one-third  of  these 
children  are  stillborn.  Some  are  asphyxiated  at  birth.  Some  die  from 
twitching,  convulsions,  and  paralysis. 


112  Chapter    VII. 

The  spoon-shaped  depressions  are  the  more  serious.  Frequently  they 
give  rise  to  no  symptoms  and  disappear  in  a  week  or  two,  leaving  no  ill- 
effects.  Some  are  permanent,  though  producing  no  symptoms  or  merely 
minor  nerve  storms.  Others  cause  pressure  symptoms,  e.g.,  signs  of 
irritation  of  the  motor  area.  The  frontal  ones  are  more  serious  than  the 
parietal.  Out  of  65  cases  of  spoon-shaped  depression  collected  by  Schroeder 
32  died,  22  being  stillborn,  from  the  more  or  less  direct  results  of  the  injury. 
The  depression  may  be  associated  with  fracture,  and  perhaps  subdural 
haemorrhage.  Fracture,  usually  parietal,  may  occur  in  either  spontaneous 
or  assisted  delivery,  even  though  there  be  no  pelvic  disability. 

Many  disappear  spontaneously.  Gentle  manipulation,  as  by  anterior 
and  posterior  compression  of  the  skull,  is  of  assistance.  Possibly  the 
application  of  a  cupping  glass  is  justifiable.  If  there  are  signs  of  compression 
and  irritation,  operation  is  essential.  An  incision  is  made  through  the 
adjacent  bone,  and  the  depressed  portion  is  elevated  by  means  of  a  periosteal 
elevator,  inserted  between  the  bone  and  dura  mater.  Or  a  disc-shaped 
piece  of  bone  is  cut  out  by  the  trephine,  inverted  and  replaced.  It  becomes 
firmly  re-united  in  a  week  or  two.  If  it  is  removed,  new  bone  will  be 
reproduced  in  about  3  months.  Trephining  is  more  reliable  than  elevation, 
for,  unless  the  elevation  is  done  soon  after  delivery,  the  bone  usually  falls 
in  again,  and  has  to  be  removed. 

A  similar  depression  may  be  produced  after  birth,  commonly  in  the 
parietal  region,  by  falls  and  other  injuries.  Localised  fractures  also  occur, 
and  sometimes  rupture  of  the  dura  mater,  remarkably  adherent  in  infants, 
with  escape  of  cerebrospinal  fluid  and  the  formation  of  a  Cephal-hydrocele. 
This  is  a  pulsating  tumour,  which  may  be  translucent.  In  fractures  and 
falls,  whether  at  or  after  birth,  the  injury  to  the  brain  is  greater  than  in 
adults  because  of  the  yielding  character  of  the  bones  and  the  ununited 
sutures.  Yet  the  symptoms  are  slighter ;  cerebral  compression  is  less 
readily  produced. 

Sterno-Mastoid  Tumour. — (Hsematoma  or  Induration  of  the  Sterno- 
Mastoid).  First  described  by  Dieffenbach  in  1830.  Both  sexes  are  equally 
liable.  It  is  most  common  in  first-borns  (9  out  of  14  cases).  The  tumour  is 
found,  usually  accidentally,  in  one  or  other  of  the  sterno-mastoid  muscles 
about  the  second  or  third  week  of  life,  or  even  a  few  days  after  birth. 
Out  of  13  successive  cases  11  were  on  the  right  side.  It  is  rarely  bilateral. 
The  common  situation  is  at  the  junction  of  the  middle  with  the  lower 
third  of  the  muscle,  mainly  on  the  inner  side.  At  first  the  lump  is  soft, 
like  fluid,  but  it  gradually  hardens  and  forms  a  nodular,  ovoid  swelling, 
solid  and  almost  cartilaginous  in  consistency,  about  an  inch  long,  and  of 
the  size  of  a  blackbird's  egg.  It  is  movable,  painless,  and  rarely  tender. 
The  skin  is  unaffected.  The  chin  is  a  trifle  rotated  to  the  opposite  side,  and 
the  head  inclined  towards  the  shoulder  of  the  affected  side.  Out  of  11  cases 
four  were  breech,  and  seven  vertex  presentation,  but  it  is  commonly  stated 


Congenital   Deformities  and  Injuries  at  Birth.  113 

that  three-fourths  of  these  tumours  occur  in  breech  presentations,  and  only 
one-fourth  in  vertex  presentations.  It  occurs  in  non-instrumental  labour, 
especially  if  rapid,  and  must  not  be  ascribed  to  undue  violence.  It  is  most 
frequent  on  the  right  side  because  of  the  common  obstetrical  positions. 

As  a  result  of  twisting  of  the  head  or  stretching  of  the  neck  during  birth 
some  of  the  muscle  fibres  are  ruptured,  and  a  certain  amount  of  blood  is 
effused.  The  tumour  has  been  found  full  of  pure  blood  (hsematoma).  More 
often  there  is  little  blood,  and  the  swelling  is  the  result  of  a  primary  or 
secondary  myositis  and  proliferation  of  connective  tissue.  In  a  case  of 
Volkmann's  the  whole  muscle  became  fibrous,  and  of  almost  cartilaginous 
hardness.  Possibly  this  was  a  syphilitic  myositis,  which  chiefly  affects 
the  sterno-mastoid,  biceps,  and  rectus  abdominis  muscles. 

The  tumour  is  slowly  re-absorbed  and  disappears  in  2  or  3  months, 
occasionally  persists  for  9  months,  leaving  no  permanent  deformity. 
Torticollis  has  ensued,  a  result  more  likely  if  the  myositis  is  syphilitic. 
The  diagnosis  is  easy,  but  the  lump  is  sometimes  mistaken  for  an  enlarged 
gland. 

In  my  experience  no  ill-effects  have  followed  when  no  treatment 
has  been  adopted.  Very  gentle  massage  may  be  used  twice  a  day.  Blue 
ointment  can  be  rubbed  in.  The  muscle  can  be  kept  exercised  and  stretched 
in  the  opposite  direction  to  prevent  contraction.  Too  energetic  measures 
may  increase  the  myositis. 

Diaphragmatic  Hernia. — Over  500  cases  of  diaphragmatic  hernia  are 
on  record,  but  it  is  rarely  diagnosed  during  life.  Eighty  per  cent,  of  481 
cases  were  on  the  left  side  (Paillard,  1903).  Because  of  the  mode  of  develop- 
ment of  the  diaphragm,  which  is  completed  in  the  second  month  of  foetal 
life,  they  are  situated  in  the  posterior  half  and  vary  in  type.  In  the 
Embryonic  form,  called  Complete  or  Incomplete,  according  as  the  whole 
or  part  of  the  dorso-lateral  element  (Pillar  of  Uskow)  of  the  diaphragm 
is  absent,  there  is  no  sac,  for  it  is  developed  before  the  complete  closure  of 
the  pleuro-peritoneal  septum.  In  the  Congenital  or  Foetal  type  this 
septum  is  formed,  but  the  muscular  tissue  is  imperfect,  and  the  hernia  has  a 
sac.  An  Acquired  hernia  is  due  to  protrusion  through  an  unusually  large 
normal  orifice,  such  as  that  for  the  oesophagus.  The  contents,  in  order  of 
frequency,  are  stomach,  transverse  colon,  omentum,  small  intestine,  spleen, 
liver,  pancreas,  kidney,  caecum,  and  appendix. 

Symptoms  may  be  absent.  Sometimes  there  is  no  characteristic  cry 
at  birth,  and  attempts  at  full  inspiration  are  unsuccessful.  Dyspnoea,, 
cyanosis,  recession  of  the  lower  ribs,  and  displacement  of  the  heart  may  be 
present.  Examination  of  the  chest  may  reveal  tympanitic  resonance,  varying 
with  the  distension  of  the  gut  and  its  contents  ;  dulness  due  to  the  liver, 
collapsed  lung,  or  fluid  intestinal  contents.  Attacks  of  distressed  breathing 
may  be  relieved  by  passage  of  flatus.  Sometimes  there  are  gastric  symptoms 
and  uncontrollable  vomiting,  due  to  intestinal  obstruction.    A  female  baby,. 

i 


114  Chapter    VII. 

who  died  at  the  age  of  5  months,  presented  in  sequence  attacks  of  dyspnoea 
and  cyanosis,  recession  of  the  chest  wall,  and  dulness  over  the  right  base  ; 
and  2  hours  later  appeared  in  normal  health  with  resonant  note,  though 
rather  weak  breathing,  at  the  right  base.  Adenoids  were  removed  under 
ethyl  chloride  without  benefit  to  the  breathing.  The  dulness  varied  from 
time  to  time  ;  recession  was  most  marked  on  the  right  side  ;  and  she  died 
during  an  attack  of  collapse.  The  hernia  included  the  large  intestine,  most 
of  the  small  intestine,  the  left  lobe  of  the  liver,  the  gall  bladder,  and  part  of 
the  pancreas.  The  liver  was  rotated  on  its  axis,  and  extended  to  the 
umbilicus.  The  heart  was  not  displaced.  The  middle  and  lower  lobes  of 
the  right  lung  were  unexpanded.  In  another  girl,  aged  10  months, 
apparently  healthy  till  a  fortnight  before  admission,  vomiting  and  shortness 
of  breath  with  displacement  of  the  heart  to  the  right,  dulness  over  the  left 
lower  lobe  behind,  and  absent  breath  sounds,  were  the  chief  symptoms. 
The  breath  sounds  remained  absent,  but  the  note  varied  in  resonance,  some- 
times hyper-resonant.  The  child  suffered  little  distress,  but  died  from 
cyanosis  and  respiratory  failure.  Both  these  cases  were  of  the  embryonic 
type. 

In  the  diagnosis  of  this  condition  chief  stress  must  be  laid  upon  the 
variable  character  of  the  percussion  note,  absent  breath  sounds,  displace- 
ment of  the  heart,  respiratory  difficulties,  and  vomiting  or  signs  of  intestinal 
obstruction.  Some  of  the  milder  degrees  of  the  congenital  type  are  com- 
patible with  prolonged  life.  It  is  liable  to  be  mistaken  for  pleural  effusion, 
pneumothorax,  and  some  form  of  pulmonary  inflammation  or  collapse. 


Chapter  VIII 

ASPHYXIA    NEONATORUM    AND    ATELECTASIS. 

The  stillborn  babe  is  not  necessarily  dead,  though  it  does  not  breatne 
or  cry  and  may  succumb.  Lividity  or  Cyanosis  is  congenital  or  acquired. 
It  may  depend  on  ante-natal  causes,  the  effects  of  labour,  or  post-natal 
factors.  The  maternal  causes  include  death  of  the  mother  ;  interference 
with  placental  circulation  from  prolongation  of  the  second  stage  of  labour  ; 
mechanical  compression  or  stretching  of  the  cord  ;  tetanus  uteri,  and 
asphyxial  conditions.  The  foetal  causes  include  damage  to  the  respiratory 
centre  by  cerebral  pressure  or  intracranial  haemorrhage  ;  respiratory  ob- 
struction during  and  after  birth  ;  the  entrance  of  secretions  into  the  tubes 
and  atelectasis  ;  and  various  forms  of  congenital  heart  disease.  The  ante- 
natal signs  of  asphyxia  are  failing  heart  sounds  and  the  passage  of  meconium. 
The  usual  appearances  of  asphyxia  are  found  post  mortem.  The  condition 
of  the  lungs  depends  on  the  mode  of  treatment  and  causation,  e.g.,  great 
emphysema  following  on  inflation,  or  abnormal  secretions  in  the  air 
passages. 

Two  varieties  are  described,  though  it  is  asserted  by  some  that 
one  of  them  is  due  to  shock.  In  Asphyxia  Livida  muscular  tonicity 
and  cutaneous  sensibility  are  present.  The  head,  lower  jaw,  and  limbs 
do  not  drop  when  the  child  is  raised.  There  is  general  venous  congestion  ; 
the  skin  is  warm,  and  of  a  dusky  or  livid  red  colour,  up  to  deep  cyanosis  ; 
the  mucous  membranes  are  somewhat  dusky.  The  pupils  are  normal ; 
the  tongue,  lips,  and  face  may  be  swollen  ;  the  heart  beats  slowly  ;  the 
pulse  is  full,  and  the  umbilical  vessels  are  full  of  blood.  Reflex  excitability 
is  retained,  and  the  temperature  is  normal.  Breathing  may  be  absent, 
shallow  and  infrequent,  or  spasmodic  ;  sometimes  there  are  rales  and 
hiccough.  Generally  the  respiratory  movements  become  more  vigorous, 
and  respiration  is  established.  After  being  apparently  normal  it  may 
slowly  fail.  The  heart  then  becomes  slower  and  weaker  ;  the  skin  and 
mucous  membranes  of  a  livid  pallor  ;  and  the  condition  passes  into  the 
second  variety,  and  ends  fatally. 

Asphyxia  Pallida  is  a  further  and  more  serious  stage  of  asphyxia  livida. 
There  is  marked  loss  of  muscular  tonicity  ;  the  head,  lower  jaw,  and  limbs 
drop  when  raised  ;  and  the  whole  of  the  body  seems  limp  and  relaxed. 
Anaemia  is  general  and  severe  ;  the  skin  is  pale  or  white  and  cold  ;  the  face 
of  a  livid  pallor,  and  the  lips  blue.     The  eyes  are  glassy,  and  the  pupils 


116  Chapter    VIII. 

more  or  less  dilated  ;  cutaneous  sensibility  is  slight  or  absent ;  the  reflexes 
are  absent ;  the  sphincters  are  relaxed ;  the  temperature  subnormal ; 
the  heart  impulse  and  sounds  are  weak,  usually  slow,  and  the  umbilical 
vessels  nearly  empty.  A  few  ineffective  convulsive  attempts  at  respiration 
may  be  made,  but  soon  cease.  Under  energetic  treatment  breathing  may  be 
partially  established,  but  it  quickly  fails  ;  the  temperature  falls  and  the 
end  comes  in  a  few  hours  or  days.  The  air  passages  are  often  filled  with 
mucus  and  amniotic  fluid.  Favourable  cases  pass  through  the  stages  of 
asphyxia  livida  before  recovery. 

Cases  of  mild  or  even  severe  asphyxia  livida  often  recover  under  suitable 
treatment.  The  frequent  association  with  intracranial  haemorrhage 
( Apoplexy  Neonatorum),  into  the  ventricles  from  the  choroidal  vessels 
or  meningeal,  makes  the  diagnosis  and  prognosis  difficult.  Haemorrhage  is 
generally  recognised  by  the  history  of  prolonged  labour  or  the  use  of 
forceps,  the  presence  of  increasing  coma  or  paralysis,  and  irregularity  of 
respiration  and  failing  pulse,  in  spite  of  treatment.  It  produces  more  or 
less  mental  impairment  and  spastic  paraplegia.  The  outlook  is  still  worse 
in  asphyxia  pallida.  The  unfavourable  signs  are  dilated  pupils,  failing 
heart,  and  a  fall  of  3-4°  F.  It  may  be  simulated  by  severe  anaemia,  due  to 
profuse  haemorrhage  from  the  cord.  It  is  probable  that  mere  asphyxia 
never  leaves  any  permanent  mental  defect.  If  the  lungs  are  not  expanded 
death  may  ensue  from  atelectasis  and  secondary  pneumonia. 

Treatment  must  be  directed  to  establishing  or  improving  respiration 
and  circulation,  and  maintaining  the  body  temperature.  The  mouth  and 
fauces  are  cleared  of  any  mucus  or  secretion  by  swabs  ;  by  a  mucus  evacua- 
tor,  an  india-rubber  ball  attached  to  a  glass  tube  curved  at  one  end ;  by 
suction  through  a  catheter  ;  or  suspending  the  child  by  the  heels.  Eespira- 
tion  is  stimulated  by  reflex  irritation  of  the  nose  and  fauces  with  a  feather, 
or  ammonia  to  the  nostrils ;  by  dipping  the  child  alternately  in  hot  and  cold 
water  for  a  few  moments,  or  douching  with  cold  water  after  a  hot  plunge, 
finishing  with  heat ;  by  swinging  the  child  in  the  air,  or  spanking  the  nates  ; 
or  by  rhythmical  traction  of  the  tongue  (Laborde)  8-12  times  per  minute  ; 
or  by  artificial  respiration.  Schultze's  swinging  method  consists  of  6-8 
successive  swings,  and  then  immersion  in  hot  water  100°  F.,  with  friction 
and  rapid  rhythmical  compression  of  the  heart.  Reflex  irritation  is  value- 
less in  asphyxia  pallida.  For  this  the  cord  is  tied  ;  mucus  removed  from 
the  air  passages,  while  suspended  head  downwards  ;  and  the  child  put  in  a 
hot  bath,  110°  F.  and  4  ins.  deep,  in  a  supine  position  with  a  rolled  towel  under 
the  head  and  shoulders,  and  a  pair  of  clip  forceps  on  the  tongue  and 
hanging  out  of  the  side  of  the  mouth.  Artificial  respiration  is  adopted  ; 
2  oz.  of  hot  saline  injected  into  the  rectum,  and  strych.  gr.  xu^  sub- 
cutaneously,  and  repeated  in  15  minutes.  At  intervals  the  child  is  sus- 
pended by  the  legs  for  15  sees,  at  a  time,  and  the  spine  rubbed  with  whisky 
or  liniment.     On  the  whole  simple  rhythmical  compression  of  the  chest. 


Asphyxia   Neonatorum  and  Atelectasis.  117 

10  times  a  minute,  is  better  than  any  other  method  of  artificial  respiration. 
It  should  be  continued  for  a  long  time,  until  the  heart  stops,  and  as  much 
as  possible  in  a  hot  bath,  avoiding  undue  roughness.  Tn  favourable  cases 
the  treatment  must  be  continued  until  the  lungs  expand  equally,  otherwise 
secondary  atelectasis  results.  Hot  bottles,  brandy,  and  oxygen  are  of 
assistance.  Gasping  inspiration  can  be  assisted  by  elevation  of  the  arms  ; 
and  expiration  in  crying  by  compression  of  the  chest.  The  signs  of 
improvement  are  that  the  pupils  begin  to  contract,  the  heart  is  stronger 
and  more  regular,  the  body  less  limp  and  flabby,  the  colour  slowly  darkens, 
and  the  reflexes  return.  Sometimes  it  is  useful  to  inflate  the  lungs  by  mouth 
or  catheter,  with  the  nostrils  closed.  As  the  catheter  is  inserted  into  the 
larynx,  not  much  force  must  be  used.  Most  of  the  air  returns  by  the  side 
of  the  tube.  In  the  mouth  to  mouth  inflation  the  epiglottis  may  be  forced 
over  the  glottis,  fluids  may  be  driven  into  the  lungs,  or  air  forced  into  the 
stomach.  Skilled  observation  is  necessary  for  2  days  as  relapses  are  by  no 
means  uncommon,  though  breathing  may  have  been  going  on  satisfactorily 
for  several  hours. 

Atelectasis. — Atelectasis,  or  imperfect  expansion,  is  the  name  given  to 
non-expansion  of  the  lung,  a  persistence  of  the  foetal  state,  found  in  the 
newborn  and  sometimes  in  older  infants.  The  congenital  variety  is  strictly 
the  persistence  of  the  fcetal  state,  while  the  post-natal  is  really  an  acquired 
atelectasis  or  pulmonary  collapse,  due  to  mucus,  etc.,  getting  into  the 
bronchial  tubes  during  labour.  Congenital  atelectasis  is  most  frequent 
in  the  weak  and  premature,  and  is  the  chief  cause  of  asphyxia  neonatorum. 
A  few  cases  are  due  to  the  pressure  of  diaphragmatic  hernia ;  others  have  been 
ascribed  to  administration  of  ergot  in  prolonged  labour,  malformations  and 
intra-uterine  disease  of  the  respiratory  and  circulatory  organs  ;  or  to  cerebral 
disease  and  hemorrhagic  pressure  on  the  respiratory  centre.  The  anato- 
mical appearances  are  those  of  collapse  with  compensatory  emphysema. 
It  is  more  or  less  symmetrical,  affecting  the  lower  lobes  and  the  posterior 
portions  of  the  upper  lobes,  varying  from  a  mere  patch  up  to  two-thirds 
of  the  whole  lung.  In  a  child,  aged  31  days,  both  upper  lobes  were  affected. 
The  anterior  edges,  and  often  the  superficial  portions  of  the  unexpanded 
areas,  are  emphysematous.  The  non-expanded  lung  is  darkish  red,  solid, 
sinks  in  water,  non-crepitant,  vascular,  and  shows  foetal  lobulation.  If 
the  child  has  only  lived  a  few  days,  the  areas  can  be  readily  inflated.  In 
prolonged  cases  secondary  broncho-pneumonia  and  hypostatic  congestion 
are  often  present.  Hence  arise  difficulty  in  forcible  expansion,  and  the 
need  of  microscopic  examination  for  diagnosis.  The  right  side  of  the 
heart  is  engorged  and  distended,  leading  to  backward  pressure,  with 
hepatic  and  splenic  congestion  and  enlargement.  Often  the  foramen 
ovale  is  open,  and  the  ductus  arteriosus  imperfectly  closed. 

At  birth  the  child  may  be  merely  feeble  or  show  temporary  blueness, 
sometimes  permanent.      There  is  a   history  of  difficult  resuscitation  or 


118  Chapter    VIII. 

asphyxia  at  birth,  a  feeble  cry  during  the  first  few  days,  somnolence,  and 
often  a  subnormal  temperature.  Physical  signs  are  doubtful  or  absent. 
Cyanosis  is  out  of  proportion  to  the  other  symptoms,  and  is  generally 
present  in  the  cases  which  have  not  been  completely  resuscitated  from 
the  asphyxia.  They  gradually  get  worse,  and  die  in  a  few  days  from 
asphyxia,  asthenia,  or  convulsions.  In  others  there  is  no  cyanosis,  yet  the 
lungs  are  not  completely  expanded. 

The  infant  remains  feeble,  sucks  badly,  cries  feebly  or  not  at  all, 
progresses  slowly  or  actually  wastes,  and  has  cold  extremities  and  a  low 
temperature.  Cough  and  catarrhal  sounds  in  the  chest,  paroxysms  of 
dyspnoea,  twitching,  and  lividity,  general  convulsions,  and  sudden  cyanosis 
are  sometimes  present,  or  induced  by  slight  causes,  and  last  for  3  or  4  minutes. 
The  prognosis  must  be  guarded,  for  these  attacks  may  be  slight  and  easily 
recovered  from,  or  at  any  moment  severe  and  fatal  from  collapse  or  con- 
vulsions. Fatal  syncope  may  occur  quite  suddenly.  The  duration  and 
prospect  of  recovery  vary  with  the  extent  of  the  mischief. 

The  diagnosis  depends  more  on  the  history  of  asphyxia  at  birth,  feeble- 
ness of  the  child  and  its  circulation,  the  presence  of  cyanosis  or  temporary 
attacks  of  blueness,  and  malnutrition,  than  on  physical  signs.  The  latter 
are  often  slight  or  absent.  If  symmetrical  and  of  a  medium  extent,  it  is 
impossible  to  be  certain  that  the  note  is  impaired,  but  a  limited  affection  of 
one  lung  may  give  rise  to  differences  in  the  physical  signs  on  the  two  sides. 
As  a  rule  the  non-expanded  areas  are  surrounded  by  over-expanded  ones, 
and  there  is  very  little  or  no  alteration  in  percussion.  In  prolonged  cases 
dulness  is  found,  perhaps  limited  to  one  base  or  apex,  and  the  breath  sounds 
are  weak,  and  only  occasionally  somewhat  bronchial.  Attacks  of  cyanosis 
in  newborns  generally  indicate  atelectasis  or  congenital  morbus  cordis,  and 
are  often  induced  by  over-distension  of  the  stomach,  by  food  or  wind. 

Secondary  pneumonia  gives  rise  to  crepitations  and  fever. 

Treatment. — Encourage  crying  in  the  newborn  and  in  delicate  infants  ; 
make  them  cry  vigorously,  at  least  twice  a  day  for  10  minutes  at  a  time, 
to  induce  lung  expansion.  Stimulating  liniments  to  the  chest,  and  a  hot 
or  mustard  bath,  twice  a  day  for  5  minutes,  are  useful.  Do  not  allow  the 
child  to  lie  much  on  its  back  ;  feed  it  on  the  breast  or  breast-milk  by 
spoon  ;  keep  it  in  a  temperature  of  70-80°  F.,  in  an  incubator  if  necessary. 
Sal  volatile,  brandy,  and  oxygen  are  necessary  during  the  attacks  of 
asphyxia. 


Chapter  IX. 

THE  UMBILICUS  AND  SEPTIC  AFFECTIONS  OF  THE 
NEWBORN. 

The  Cord  at  Birth —  Abnormalities  and  Diseases  of  the  Cord  and  Navel — 
Pycemia  Neonatorum — BuhVs  Disease — WinckeVs  Disease  —  Ery- 
sipelas—  Hcemorrhagic  Disease — Suprarenal  Apoplexy — Trismus  or 
Tetanus. 

The  Cord  at  Birth. — A  few  minutes  after  birth  the  cord  is  tied  with 
sterilised  tape  i^-i  in.  wide,  kept  in  saturated  solution  of  boric  acid,  or 
with  several  strands  of  strong  thread  or  silk,  at  a  distance  of  2  ins.  from 
the  navel  and  again  a  little  beyond  this.  It  must  be  tied  sufficiently  tightly 
to  cut  through  Wharton's  jelly.  If  not,  the  ligature  may  come  loose  as  the 
jelly  shrinks.  The  cord  should  be  gently  squeezed  towards  the  navel 
before  tying,  to  avoid  the  possible  inclusion  of  a  hernial  protrusion,  or 
Meckel's  diverticulum,  and  strangulation.  It  is  then  cut  between  the  two 
ligatures. 

After  the  bath  the  cord  is  thoroughly  dusted  with  boric  acid  or  salicylic 
acid,  5  per  cent,  in  starch  powder,  wrapped  up  in  dry  antiseptic  gauze  or 
wool,  and  fixed  with  strapping  to  the  abdomen,  the  free  end  being  directed 
upwards.  Sometimes  it  is  first  disinfected  with  perchloride  of  mercury 
0*1  per  cent.,  carbolic  acid  5  per  cent.,  rectified  spirit,  or  alcohol.  It  should 
be  left  alone  and  kept  dry,  until  it  undergoes  desiccation  or  mummification 
in  the  next  3  days,  and  separation  in  4-9  days,  leaving  a  healed  surface. 
The  epidermis  spreads  from  the  periphery  over  the  small  raw  surface, 
covered  with  secretion  or  crust,  which  may  not  heal  until  2  or  3  weeks 
after  birth.  After  separation  of  the  cord  an  antiseptic  dusting  powder,  and 
a  pad  of  gauze  are  applied,  and  a  broad  piece  of  strapping  or  an  abdominal 
belt  is  kept  on  for  about  a  month  to  prevent  umbilical  protrusion. 

Abnormalities  of  the  Cord. — In  the  sixth  to  the  tenth  week  of  foetal 
life  the  cord  contains  loops  of  intestine,  which  are  later  withdrawn  into  the 
abdomen.  The  persistence  of  this  condition  is  known  as  Congenital  Umbili- 
cal Hernia  (Hernia  into  the  Umbilical  Cord),  or  Exomphalos.  This  may 
rupture  during  labour,  and  the  child  be  born  with  extruded  viscera.  It 
may  be  associated  with  other  congenital  defects,  notably  spina  bifida. 
In  two  cases  under  my  observation  a  large  portion  of  the  intestines  pro- 
truded, covered  by  smooth  transparent  membrane,  and  forming  a  bluish 


120  Chapter  IX. 

tumour.  Other  cases  have  contained  both  intestine  and  liver,  ileum  and 
Meckel's  diverticulum,  or  the  diverticulum  alone.  The  tumour  has  a 
broad  base  or  pedicle,  and  is  fusiform  or  globular,  the  shape  of  half  an  egg 
or  pear,  as  big  as  an  apple,  with  the  cord  attached  at  the  apex  or  lower 
portion.  The  covering  membrane  is  sharply  defined  from  the  skin,  and  is 
composed  of  amnion  and  parietal  peritoneum,  which  is  transparent,  or 
may  be  partially  or  entirely  thickened.  It  dries  up  with  the  cord  and 
separates.  If  small,  the  hernia  may  be  withdrawn,  and  the  umbilical  area 
healed  by  granulation,  or  the  exposed  gut  becomes  covered  by  granulations, 
and  the  epidermis  spreads  over  it.  More  usually  it  ends  in  general  peri- 
tonitis, due  to  infection,  and  death.  Of  32  cases  operated  on  at  birth 
6  died;  of  7  treated  expectantly  4  died  (Meyer  1905).  Kindt's  statistics  ; 
50  out  of  65  cured  by  operation. 

Amniotic  Navel. — The  skin  is  deficient  round  the  base  of  the  cord 
and  in  the  adjacent  area,  so  that  the  amnion  extends  over  this  defective 
area  and  the  cord.  It  dries,  separates,  and  leaves  a  raw  surface  which 
heals  by  granulation. 

Skin  Navel. — The  navel  projects  as  a  somewhat  dome-shaped  structure, 
due  to  the  failure  of  the  normal  infolding  of  the  skin  at  the  edges  when  the 
cord  separates.  It  gradually  becomes  normal  as  the  child  gets  older.  There 
may  be  hernial  protrusion. 

Umbilical  Hernia. — The  common  hernia  is  a  protrusion  through  a 
sharply-defined  umbilical  ring  in  the  first  months  of  life  of  a  small  piece 
of  gut  or  omentum,  occasionally  a  Meckel's  diverticulum,  from  yielding  of 
the  umbilical  cicatrix.  It  is  associated  with  distension  of  the  abdominal 
wall,  and  more  or  less  separation  (diastasis)  of  the  recti.  The  peritoneal 
diverticulum,  corresponding  with  the  passage  for  the  umbilical  vein,  pre- 
disposes. The  exciting  cause  is  straining  set  up  by  crying,  vomiting, 
constipation,  or  cough.  It  is  most  common  in  girls  and  thin  babies.  The 
protrusion  is  button-like  or  resembles  the  short  thick  finger  of  a  glove  ; 
the  skin  is  normal  or  thinned  by  stretching  ;  the  navel  scar  is  found  at  or 
below  the  apex.  It  may  gurgle  on  reduction.  During  growth  the  pro- 
trusion is  gradually  retracted  within  tbe  abdomen,  and  practically  all  get 
well  before  puberty,  leaving  no  extra  liability  to  hernia  in  later  life.  Treat- 
ment consists  of  careful  diet,  and  an  umbilical  pad.  A  penny  or  similar 
disc  is  wrapped  in  lint  and  strapped  on  with  wide,  long  strapping,  applied 
so  as  to  approximate  the  recti,  and  changed  once  a  week ;  or  an  india- 
rubber  umbilical  belt  can  be  worn.  The  pad  should  be  large  enough  to 
well  overlap  the  edges  of  the  orifice,  and  worn  for  3-12  months,  or  for 
3  months  after  birth  as  a  preventive.  Operation  is  rarely  required.  If  it  is, 
the  sutures  should  extend  well  above  and  below  the  navel,  to  approximate 
the  recti.     Occasionally  strangulation  occurs. 

Umbilical  Fistula. — The  urachus,  a  remnant  of  the  allantois,  normally 
obliterated  in  the  second  month  of  fcetal  life,  may  be  patent  throughout 


The  Umbilicus  and  Septic  Affections  of  the  Newborn.  121 

and  discharge  urine,  giving  rise  to  a  congenital  umbilical  fistula.  Neuge- 
bauer,  of  Warsaw,  in  1890,  collected  over  40  cases.  It  is  more  common  in 
boys  than  in  girls,  and  due  to  urethral  obstruction.  It  may  form  by  eversion 
of  the  mucosa  a  small  red  tender  tumour.  It  is  treated  by  cauterisation  or 
siiture.  Occasionally  a  cyst  is  formed  in  the  median  line,  through  closure 
of  the  duct  at  each  end.  Calculi  have  been  found  in  a  patent  urachus. 
Another  variety  of  fistula  is  due  to  patency  of  a  Meckel's  diverticulum,  and 
is  lined  with  columnar  epithelium. 

Non-congenital  fistulae  may  be  umbilical  or  hypogastric.  The  former 
are  usually  due  to  abscess,  communicating  with  the  bowel  and  forming  a 
fsecal  fistula ;  the  latter  to  wounds,  abscess,  or  caries  of  the  os  pubis.  The 
diagnosis  depends  on  the  character  of  the  discharge. 

Umbilical  Polypus. — The  simplest  form  is  a  Granuloma.  This  consists 
of  exuberant  granulations,  forming  a  flat  and  sessile  fleshy  papillomatous, 
sometimes  pedunculated,  red  tumour  which  bleeds  readily,  and  discharges 
serum  or  sero-pus.  It  is  found  in  the  second  or  third  week,  perhaps  hidden 
in  the  folds,  and  is  due  to  the  navel  wound  not  healing.  Untreated  ones 
last  for  weeks  but  finally  shrink.  It  s  easily  cured  by  nitrate  of  silver, 
powdered  alum,  or  tannic  acid.  Ligature  and  cut  off  a  pedunculated 
tumour. 

The  Diverticulum  Tumour  or  polypus  is  covered  by  mucous  membrane, 
like  that  of  the  small  intestine,  and  is  due  to  prolapse  of  a  persistent 
Meckel's  diverticulum. 

In  foetal  life  the  intestine  communicates  with  the  navel  by  the  vitelline 
or  omphalo-mesenteric  duct,  leading  to  the  yolk  sac  during  the  first 
2  months  of  life.  Normally  this  becomes  obliterated  towards  the  end  of  the 
seventh  week  of  foetal  life,  leaving  no  trace.  Super-involution  may  cause 
stenosis  or  atresia  of  the  small  intestine,  e.g.,  imperforate  ileum  with 
umbilical  fistula.  The  duct  may  persist  as  a  ligamentous  cord  stretching 
from  the  navel  to  the  gut ;  or  a  finger-like  pouch  communicating  freely 
with  the  gut  and  attached  by  a  cord  to  the  navel,  gut,  mesentery,  etc., 
or  the  cord  free  in  the  abdominal  cavity.  Bands  of  this  nature  are  a 
common  cause  of  intestinal  obstruction  under  the  age  of  20.  It  frequently 
persists  as  a  simple  blind  pouch  a  few  inches  long.  This  may  become  con- 
stricted and  not  communicate  with  the  gut ;  it  may  then  dilate  into  a  cyst 
which  discharges  mucus,  if  the  rest  of  the  duct  is  pervious  and  opens  at  the 
navel.  Sometimes  it  persists  as  a  pervious  duct  throughout,  discharging  fasces 
at  the  navel.  A  faecal  fistula  is  occasionally  due  to  the  projection  of  a  per- 
sistent diverticulum  into  the  umbilical  cord,  and  inclusion  in  the  ligature 
applied  at  birth.  A  pervious  duct  gives  rise  to  a  simple  umbilical  fistula, 
or,  by  eversion  of  the  mucosa,  to  a  red  raspberry-like  polypus,  from  a  pea 
to  a  cherry  in  size  and  sometimes  much  larger,  through  the  centre  of  which 
a  probe  can  be  passed  into  the  duct.  If  the  prolapse  is  extreme  two  lateral 
fistulse  are  produced.     There  is  a  history  of  navel  discharge,  intestinal  in 


122  Chapter  IX. 

character.  If  there  is  no  polypus,  the  duct  may  be  closed  spontaneously, 
by  applying  a  ligature,  or  on  cauterisation.  Usually  it  is  necessary  to 
excise  the  diverticulum  in  order  to  cure  the  fistula  and  prevent  possible 
intestinal  strangulation. 

Meckel's  diverticulum  is  present  in  1-2  per  cent,  of  all  people.  It  is 
situated  between  the  duodenum  and  caecum,  usually  at  right  angles  to  the 
duct,  at  a  distance  of  from  10-80  cm.  above  the  ileo-ceecal  valve,  the 
distance  increasing  with  the  age  of  the  patient.  It  may  have  a  definite 
mesentery.  It  is  a  cause  of  umbilical  fistula  and  polypus,  enterocysts, 
intussusception  from  inversion,  intestinal  obstruction,  torsion,  volvulus, 
and  strangulation.  It  may  undergo  inflammation,  ulceration,  and  per- 
foration, and  simulate  appendicitis.  Indiawing  of  the  umbilicus  or  excess 
of  umbilical  scarring  indicates  adhesion  to  the  abdominal  wall  or  past 
fistula. 

Umbilical  Eczema,  acute  or  chronic,  is  due  to  sebum  and  dirt  collecting 
in  the  sulci.  It  extends  to  the  summit  of  the  folds  and  adjacent  skin,  and 
gives  rise  to  oedema,  exudation,  itching,  crusts,  and  bleeding.  Apply  a 
powder  of  calomel,  zinc  oxide,  and  starch. 

Umbilical  Hemorrhage. — Bleeding  from  the  cord  or  navel  results  from 
accident  or  disease.  Accidental  Hemorrhage  takes  place  from  the  larger 
vessels,  and  is  due  to  inefficient  ligation  of  the  cord,  the  ligature  too  narrow 
and  too  tight,  too  loose,  or  tied  too  near  the  navel.  The  arteries  ought  to 
contract,  without  ligation,  sufficiently  to  prevent  bleeding.  Failure  to  do 
so  depends  on  prematurity,  asphyxia,  morbus  cordis,  and  other  causes 
of  high  blood  pressure.  Then,  on  shrinking  of  the  cord,  the  ligature  becomes 
loose  and  bleeding  occurs.  A  second  ligature  must  be  applied.  If  the  cord 
is  too  short  or  has  dropped  off,  pass  a  hare-lip  pin  for  about  1  in.  through  the 
abdominal  wall  at  the  lower  level  of  the  umbilicus,  and  apply  a  figure  of 
eight  loop.  Two  pins  at  right  angles  to  each  other  may  be  needed.  If 
this  fails  to  stop  the  bleeding,  do  an  abdominal  section,  and  ligature  the 
cord  before  exit.  If  the  bleeding  takes  place  from  the  navel,  it  may  be  due 
to  forcible  avulsion  of  the  cord,  ruptures  or  tears,  or  excessive  granulations. 
Spontaneous  Hemorrhage  from  cord  or  navel  is  due  to  sepsis,  haemophilia, 
or  congenital  syphilis  ;  it  usually  takes  the  form  of  capillary  oozing. 
Sometimes  it  is  sudden  and  profuse.  It  begins  after  separation  of  the 
cord  and  occasionally  takes  place  into  the  cord,  before  it  has  dropped  off, 
within  24-48  hours  of  birth.  It  may  occur  alone  or  with  other  haemorrhages. 
For  treatment  vide  Hemorrhagic  Disease. 

Sepsis  or  Pyaemia  Neonatorum. — Infective  organisms  reach  the  foetus 
in  utero  through  the  maternal  blood.  During  birth  infected  liquor  amnii 
or  secretions  may  be  swallowed  or  aspirated  into  the  air  passages.  After 
birth  the  infecting  agent  is  conveyed  by  dirty  hands,  ligatures,  powders, 
dressings,  bath  water,  flannels  or  sponges,  instruments,  clothes,  utensils, 
etc.    The  site  of  infection  is  commonly  the  umbilical  cord  or  navel,  via  the 


The  Umbilicus  and  Septic  Affections  of  the  Nexoborn.  123 

blood  vessels  or  lymphatics.  Less  often  the  infection  enters  through  an 
abrasion  of  the  skin  ;  mucous  membrane  of  mouth,  fauces,  naso-pharynx, 
or  conjunctiva  ;  respiratory  or  alimentary  tract ;  or  the  genitals.  Some- 
times the  source  of  infection  cannot  be  found  or  is  overlooked.  Thus,  the 
pyaemic  origin  of  severe  broncho-pneumonia  may  not  be  recognised  unless 
the  cord,  navel,  etc.,  are  examined.  In  one  baby  the  infection  was  secondary 
to  a  general  mild  pustular  dermatitis ;  in  another,  to  a  patch  of  gangrene  in 
front  of  the  ear,  due  to  the  pressure  of  forceps  during  delivery.  Four-fifths 
of  the  cases  are  umbilical  in  origin.  Bottle-fed  infants  are  more  susceptible 
than  the  breast-fed  for  they  lack  the  protective  antigens  of  the  colostrum. 
The  common  infective  organisms  are  streptococci  and  staphylococci. 
Premature,  young,  and  weak  infants  are  very  prone  to  septic  infection 
because  of  their  low  resisting  power,  undeveloped  glandular  system,  and  late 
closure  of  the  umbilical  vessels. 

Infections  of  the  Cord. — Mild  forms  of  infection  lead  to  putrefaction  and 
delay  in  separation  of  the  cord.  Earely  the  cord  undergoes  a  kind  of 
organisation,  and  forms  a  tumour  which  requires  removal.  More  severe 
infection  causes  moist  gangrene  or  sloughing,  with  softening,  offensive  odour 
and  discharge.  Anomalies  in  separation  of  the  cord,  and  in  healing  of  the 
navel  after  separation,  and  umbilical  infections  are  most  liable  to  occur  in 
weak  and  premature  infants.  Separation  of  the  cord  must  never  be  hurried 
by  mechanical  means,  or  a  raw  surface  and  liability  to  hernia  are  produced. 
For  infective  conditions  powder  with  iodoform  after  cleaning  with  1  in  5000 
perchloride  lotion. 

The  navel  heals  quickly  under  normal  conditions,  but  is  a  frequent 
source  of  infective  disease.  Among  the  chief  affections  may  be  mentioned 
omphalitis,  gangrenous  lymphangitis,  umbilical  ulcer  and  gangrene, 
subnavel  abscess,  arteritis  and  phlebitis,  and  general  infective  conditions, 
including  enteritis,  pyaemia  and  general  sepsis,  hsemorrhagic  disease, 
Winckel's  disease,  Buhl's  disease,  erysipelas,  and  tetanus. 

Omphalitis  is  an  inflammation  of  the  skin  and  cellular  tissues  of  the 
navel,  with  redness,  swelling  and  sero-purulent  or  purulent,  sometimes 
hsemorrhagic  discharge,  and  the  formation  of  granulations.  These  may 
be  profuse  and  polypoid  (v.  polypus)  in  appearance.  A  milder  type  may  be 
due  to  chemical  and  mechanical  irritants.  In  the  infective  form  the  dusky 
inflamed  ring  at  the  navel  spreads  peripherally  and  may  reach  the  pubes. 
The  abdominal  wall  becomes  brawny  and  cedematous.  Its  onset  is  in 
the  second  week  before  the  navel  has  healed.  It  gives  rise  to  fever,  anorexia, 
whining,  abdominal  distension,  and  general  malaise.  The  course  varies 
with  the  severity  of  the  infection  ;  it  may  become  superficially  very 
extensive.  It  may  undergo  resolution,  terminate  in  one  or  more  abscesses, 
ulceration,  gangrene  of  cord  or  navel,  or  sloughing  and  secondary  peritonitis. 

Gangrenous  Lymphangitis  is  commonly  the  result  of  umbilical  infec- 
tion and  affects  the  umbilicus,  scrotum,  thighs  and  crural  arch.    It  begins 


124  Chapter  IX. 

with,  the  red  striae  of  lymphangitis,  oedema,  and  slight  general  redness. 
The  public  region,  scrotum,  and  penis  may  become  suddenly  red  and 
swollen.  The  scrotum  gets  hard  and  tender,  dark  red,  with  purplish  patches 
and  occasionally  bullse  on  the  surface.  It  may  become  necrosed,  exposing 
the  testes.  During  healing  these  bodies  may  be  included  in  scar  tissue  and 
subsequently  atrophy.  It  simulates  erysipelas,  gives  rise  to  signs  of 
general  infection,  and  is  treated  by  free  incision  with  the  thermocautery. 

Umbilical  Ulcer  and  Gangrene. — An  ulcer  is  situated  at  the  bottom  of 
the  navel  and  often  hidden  by  folds.  It  is  usually  from  J-^  in,  in  diameter, 
but  may  extend  to  the  skin  and  become  large.  The  stump  of  the  umbilical 
artery  may  be  visible.  In  gangrene  a  dirty  scab  forms  at  the  umbilicus,  and 
is  surrounded  by  a  ring  of  dusky  infiltration  which  spreads  outwards  and 
inwards.  Bullse  sometimes  form.  It  occurs  in  feeble  and  ill-nourished 
babies,  usually  secondary  to  omphalitis.  It  causes  destruction  of  the 
muscles,  peritonitis,  perhaps  extrusion  of  viscera,  faecal  fistula,  or  severe 
haemorrhage.    It  generally  ends  fatally,  in  collapse  or  coma. 

Subnavel  abscess  occurs  in  the  course  of  the  vessels,  or  is  secondary  to 
and  beneath  a  localised  omphalitis.  Redness  is  commonly  absent,  but 
there  may  be  some  local  tenderness,  just  under  the  navel.  Sometimes 
there  are  no  local  symptoms,  and  it  is  only  found  after  death.  It  may 
discharge  through  the  navel,  spread  by  the  lymph  channels  to  the  peri- 
toneum or  general  system,  and  very  occasionally  rupture  into  the  peritoneal 
cavity.     All  these  conditions  are  treated  on  ordinary  surgical  principles. 

Arteritis  and  Phlebitis. — Arteritis  is  much  more  common  than  phlebitis, 
and  is  due  to  extension  from  the  connective  tissues  of  the  cord,  or  secondary 
to  local  ulceration  or  omphalitis.  Usually  it  is  a  peri-arteritis,  not  an 
arteritis.  It  may  be  limited  to  the  cord  or  extend  as  far  as  the  bladder. 
The  vessels  contain  septic  thrombi  and  pus  which  can  sometimes  be 
squeezed  out  from  the  end  of  the  cord.  It  may  lead  to  thickening  of  the 
arteries,  palpable  under  the  abdominal  wall,  and  to  abscesses  between 
the  peritoneum  and  the  abdominal  wall.  If  the  cord  has  separated,  there 
may  be  no  visible  changes  at  the  navel,  though  the  mischief  is  great  and 
toxaemia  profound.  Occasionally  it  gives  rise  to  general  pyaemia,  involving 
the  viscera,  joints,  and  bones,  but  not  producing  jaundice.  It  lasts  from 
days  to  weeks,  and  is  fatal  from  sepsis,  peritonitis,  pneumonia,  or  mal- 
nutrition. 

Phlebitis  on  the  other  hand  rarely  gives  rise  to  local  signs,  unless  it  is 
associated  with  arteritis.  It  affects  the  umbilical  vein,  and  causes  throm- 
bosis, pus  formation,  and  secondary  hepatitis,  with  jaundice  which  increases 
daily  and  becomes  intense.  Pus  can  rarely  be  squeezed  out  of  the  vein. 
Abscess  may  be  found  just  beneath  the  navel,  anywhere  in  the  course  of  the 
vein,  or  under  the  liver.  General  pyaemia  ensues.  The  liver  shows  acute 
interstitial  and  parenchymatous  inflammation,  and  often  multiple  abscesses. 
Portal  thrombosis,  peritonitis,  and  pneumonic  affections  of  the  lung  are  not 


The  Umbilicus  and  Septic  Affections  of  the  Newborn.  125 

infrequent  complications  ;  umbilical  gangrene  may  occur,  and  occasionally 
endocarditis.  The  spleen  is  enlarged  and  soft ;  fatty  changes  are  found  in 
the  liver,  spleen,  and  kidneys,  and  embolic  foci  in  the  kidneys.  Phlebitis 
is  practically  always  fatal.  Comparatively,  the  prognosis  of  arteritis  is 
favourable,  though  very  bad,  for  it  may  be  quite  local. 

Pycemia. — From  the  above  description  there  are  clearly  two  types 
of  pycemia  in  the  newborn.  One  corresponds  in  character  with  pysemic 
infection  generally,  the  other  is  distinguished  by  its  effects  on  the  liver 
and  jaundice.  Both  may  result  from  infection  through  the  cord  or  navel, 
and  the  disease  may  be  local  or  general.  If  due  to  infection  through  the 
cord  it  begins  2-5  days  after  birth.  If  due  to  umbilical  infection  it  may 
occur  at  any  date  before  the  navel  has  healed.  The  onset  is  characterised 
by  fever,  gastro-intestinal  derangement,  loss  of  weight,  and  erythematous 
rashes,  and  by  early  jaundice  if  due  to  phlebitis. 

Various  types  may  be  described.  It  may  give  rise  to  no  symptoms 
except  sudden  collapse,  rapid  fall  of  temperature,  and  death ;  this  type  is 
most  common  in  the  premature.  Often  it  simulates  acute  gastro- 
enteritis, with  vomiting,  diarrhoea,  and  high  fever.  Occasionally  there 
are  severe  cerebral  or  meningeal  symptoms.  Thus,  a  child  developed  a 
pustular  rash  on  the  fifth  day  of  life  and  twitching  on  the  seventh  day  ; 
next  day  the  temperature  rose  to  105°  F.,  fever  persisted  for  3  weeks  with 
almost  constant  attacks  of  general  tonic  and  clonic  spasms,  in  which  the 
child  sometimes  became  livid.  The  spasms  ceased  entirely  2  weeks  after 
the  fever  subsided,  and  apparently  left  no  permanent  affection  of  the  brain. 
They  were  probably  due  to  toxaemia.  Or  the  infection  assumes  a  pneumonic 
type  ;  or  is  indicated  by  fever,  greyish  pallor,  and  haemorrhages,  e.g.,  many 
cases  of  melaena. 

General  Symptoms. — Fever  usual  at  the  onset,  variable  in  its  course, 
and  subnormal  temperature  at  the  end  ;  it  may  be  very  high,  even  up  to 
109°  F.  Restlessness,  crying,  and  disturbed  sleep,  tremors,  twitchings, 
tetanic  spasms  of  the  muscles,  a  torpid  or  comatose  condition,  and  rarely 
convulsions.  Jaundice,  cyanosis,  oedema  of  the  feet,  and  sclerema,  especially 
in  the  premature.  Erythematous  rashes,  petechial  haemorrhages,  purpura 
and  bullae  ;  epistaxis,  haematuria,  haemorrhages  from  mucous  membrane, 
retinal  haemorrhages.  Furunculosis,  skin  abscesses,  and  bed  sores.  Rhinitis, 
stomatitis  and  otitis.  Dyspnoea,  bronchitis,  pleurisy,  broncho-pneumonia, 
empyema,  and  infarction  of  the  lung.  Gastro-enteritis.  Vomiting  is  not 
common.  The  stools  are  green,  undigested,  often  offensive,  and  may 
contain  blood.  Diarrhoea  is  common.  Encephalitis,  septic  meningitis, 
purulent  pericarditis,  purulent  bronchitis,  minute  abscesses  in  the  lungs, 
purulent  arthritis  of  one  or  several  joints,  and  subcutaneous  abscesses  are 
occasional  complications. 

The  blood  is  deficient  in  red  cells,  in  coagulability,  and  may  contain 
an  excess  of   polymorphs.      The  red  cells  undergo  destruction,  and  iron 


126  Chapter  IX. 

pigment  is  deposited  in  the  tissues.  Sepsis  produces  acute  cellular  degenera- 
tion or  undue  fibrosis  of  the  liver,  functional  disorders,  often  jaundice  ; 
changes  in  the  vessel  walls  and  congestion  of  organs,  inducing  haemorrhage. 
Post  mortem  appearances  include  parenchymatous  degeneration  of  the 
heart,  liver  and  kidneys  ;  haemorrhages  into  the  skin,  under  the  pleura, 
on  the  surface  of  the  brain,  and  in  one  or  more  of  the  other  organs.  Encepha- 
litis and  meningitis  are  occasionally  found. 

The  diagnosis  is  usually  comparatively  simple.  Fever  and  jaundice, 
apart  from  local  evidence,  are  very  suggestive  in  those  conditions  in  which 
infection  is  liable  to  occur.  Peritonitis  is  a  common  complication  ;  indicated 
by  tympanites,  tenderness,  effusion,  vomiting,  flexion  of  the  thighs,  and 
protrusion  of  the  umbilicus.  It  may  be  localised  about  the  umbilicus  or 
liver,  but  is  more  often  of  the  general  septic  type  seen  in  older  patients. 
Diarrhoea  and  broncho-pneumonia  may  be  the  only  signs  ;  the  latter  gives 
rise  to  rapid  breathing,  cyanosis,  and  recession,  but  the  physical  signs 
may  be  of  little  assistance.  Cases  have  to  be  diagnosed  from  acute  gastro- 
enteritis, pneumonia,  atelectasis,  and  meningeal  haemorrhage.  Bacterio- 
logical examination  of  the  blood  is  inefficient  for  there  are  few  organisms 
present,  and  it  is  difficult  to  obtain  enough  blood  for  thorough  examination. 

The  prognosis  is  worst  in  the  weak  and  premature,  and  depends  on  the 
extent  and  severity  of  the  infection,  and  the  nature  of  the  infective  organism. 
Erysipelas  and  tetanus  are  almost  always  fatal.  Cases  in  which  the  liver, 
peritoneum,  lungs,  or  pleura  are  involved  nearly  always  die.  Pyaemia  is 
often  fatal  in  2-5  days.  Its  course  is  very  variable,  and  symptoms  may  be 
slight  or  absent.  Loss  of  weight  is  rapid,  and  may  be  the  only  symptom. 
A  sudden  increase  shortly  before  death  may  be  due  to  oedema  or  ascites. 
Haemorrhages  are  common  and  may  be  fatal.  Death  is  sometimes  quite 
sudden. 

Buhl's  Disease  begins  on  the  fifth  or  sixth  day  of  life,  and  has  been 
ascribed  to  asphyxia  at  birth.  The  child  may  be  cyanotic  from  birth,  or 
the  lividity  may  subside,  but  breathing  remain  weak.  It  gradually  becomes 
feeble,  develops  swelling  of  the  subcutaneous  tissues,  pitting  of  the  skin, 
severe  anaemia,  jaundice,  multiple  haemorrhages,  and  dies  from  collapse 
in  the  course  of  2  weeks.  Acute  fatty  degeneration  and  parenchymatous 
inflammation  are  found  in  the  heart,  liver  and  kidneys,  the  cells  of  the 
pulmonary  alveoli,  and  muscles  ;  much  as  in  acute  yellow  atrophy  and 
phosphorus  poisoning.    Probably  it  is  a  variety  of  sepsis. 

Winckel's  Disease  is  characterised  by  jaundice,  cyanosis,  and  haemo- 
globinuria.  It  is  sometimes  called  epidemic  hsemoglobinuria,  icteric 
cyanosis,  maladie  bronzee,  or  haematuric  bronzed  disease.  It  is  very  rare. 
Charrin  (1873)  reported  14  cases.  Bigelow  observed  it  in  epidemic  form  in 
1875  ;  and  Winckel,  in  1879,  fully  described  23  cases  in  a  Dresden  Hospital. 
It  has  generally  occurred  epidemically  in  institutions,  and  is  probably 
due  to  some  infection.    The  red  blood  cells  undergo  rapid  disintegration. 


The  Umbilicus  and  Septic  Affections  of  the  Newborn.  127 

It  begins  during  the  first  week  of  life,  generally  on  the  second  day,  and 
proves  fatal  in  a  day  or  two  from  rapid  asthenia,  convulsions,  or  coma. 
The  symptoms  are  restlessness,  whining,  anorexia,  vomiting  or  bilious 
diarrhoea,  frequent  pulse  and  respiration,  cyanosis,  jaundice,  and  some- 
times slight  convulsions.  The  bronze  colour  of  the  skin,  which  may  become 
as  dark  as  that  of  a  mulatto,  is  due  to  the  combination  of  jaundice  and 
cyanosis.  Fever  is  slight  or  absent,  and  prostration  profound.  The  urine 
is  passed  often,  in  small  quantities,  with  pain  and  straining.  It  is  brown 
or  smoky,  contains  haemoglobin,  and  sometimes  renal  epithelium,  granular 
casts  and  blood  cells,  and  occasionally  albumin. 

After  death  there  are  found  fatty  degeneration  of  the  organs  ;  many 
haemorrhages,  especially  in  mucous  and  serous  membranes ;  a  large  spleen 
filled  with  masses  of  granular  blood  pigment ;  enlarged  liver  ;  large  kidneys 
containing  haemorrhages,  and  altered  urine  in  the  bladder.  The  umbilical 
vessels  are  usually  normal.  Possibly  there  is  a  haematuria,  not  a  haemo- 
globinuria. 

Erysipelas  is  generally  umbilical  in  origin,  coming  on  at  the  end  of 
the  first  or  beginning  of  the  second  week.  If  due  to  infection  of  the  cord 
it  begins  earlier.  It  may  cause  a  mild  local  induration,  or  a  general  infection 
with  severe  local  and  general  symptoms.  The  local  redness  and  oedema 
have  a  well  defined  border,  and  spread  rapidly  downwards  over  the  lower 
abdomen  and  limbs,  rarely  upwards,  occasionally  over  the  whole  body. 
Sometimes  bullae  form,  and  often  superficial  areas  of  necrosis.  It  may  cause 
sloughing  of  skin  and  exposure  of  muscles.  Fever  may  be  absent  or  high. 
Vomiting,  diarrhoea,  drowsiness,  and  fits  occur.  It  spreads  rapidly,  and 
death  results  from  asthenia  or  peritonitis.  Bouchet  regards  it  as  invariably 
fatal  in  the  newborn.  Of  30  cases  under  one  year  of  age  16  died  (Billard). 
After  the  first  fortnight  of  life  it  may  be  due  to  infection  through  micro- 
scopic abrasions  or  cutaneous  inflammations,  e.g.,  in  napkin  area.  A  few 
cases  are  secondary  to  vaccination.  Treat  on  general  principles  ;  maintain 
the  strength  as  far  as  possible  ;  and  apply  locally  peroxide  of  hydrogen, 
iodoform,  or  ichthyol,  10  per  cent,  in  lanoline. 

General  Treatment  of  Sepsis  Neonatorum. — Prophylaxis  is  of  the  ut- 
most importance,  for  in  quite  three-fourths  of  the  cases  infection  is  umbilical 
and  preventable.  The  disease  is  the  fault  of  some  one  or  other  of  the 
attendants.  The  local  condition  is  treated  on  ordinary  surgical  principles. 
Nervous  symptoms  are  relieved  by  6  hourly  baths  at  90-95°  F.  for  5-10 
minutes,  and  4  hourly  small  doses  of  phenazone  or  phenacetin.  Spasmodic 
conditions  are  best  relieved  by  chloral,  with  or  without  bromide,  by  mouth 
or  rectum.  Caffein,  digitalis  nux  vomica,  brandy,  sal  volatile,  and  saline 
injections  are  valuable  in  collapse  and  debilitated  conditions.  Keep  the 
child  warm,  and  be  sure  that  the  diet  is  simple  and  easily  digested. 

The  Haemorrhagic  Disease  of  the  Newborn. — Haemorrhage  in  the  new- 
born may  be    Accidental  (p.   122)  ;     Traumatic  from  injury  during  labour 


]28  Chapter  IX. 

(p.  108);  or  Pyogenic.  The  last  variety  is  sometimes  called  H  cematemesis 
or  Melcena  Neonatorum,  but  these  terms  include  also  rare  cases  not  due  to 
sepsis.  In  true  Hemorrhagic  Disease  there  is  a  spontaneous  capillary 
oozing,  which  begins  at  a  variable  period  after  birth,  and  may  prove  rapidly 
fatal,  or  last  for  a  few  days  to  a  few  weeks,  and  yet  end  in  recovery.  It 
occurs  in  the  well  nourished  as  well  as  in  the  weakly  ;  is  more  frequent  in 
males  than  females  ;  and  may  be  epidemic  in  institutions.  The  bleeding 
takes  place  from  the  umbilicus  ;  from  the  mucous  membrane  of  the  nose, 
mouth,  stomach,  or  intestines  ;  from  the  genito-urinary  organs  ;  from 
any  abrasion  of  the  skin  or  subcutaneously  ;  into  the  thymus,  lungs,  and 
various  abdominal  viscera  ;  into  the  serous  cavities  ;  intracranially  ;  and 
even  through  the  skin  of  the  palms  and  soles. 

Predisposing  factors  include  prematurity,  congenital  debility,  and  bad 
hygiene.  The  circulatory  disturbances,  due  to  ligature  of  the  cord  at  birth 
or  compression  of  the  cord  during  labour,  may  cause  hyperemia  of  the 
mucous  membranes  and  throughout  the  body,  hemorrhagic  oozing,  and 
extravasation.  Similar  congestion  can  be  produced  by  backward  pressure 
from  congenital  heart  lesions,  the  respiratory  obstruction  in  asphyxia 
and  atelectasis,  and  hepatic  cirrhosis.  G astro-intestinal  hemorrhage  may 
thus  be  a  kind  of  epistaxis  from  the  congested  membrane  in  consequence 
of  its  sudden  functional  activity,  possibly  associated  with  deficient  coagu- 
ability  of  the  blood.  Or  the  congestion  and  hemorrhage  may  be  set  up  by 
purgatives  and  ingesta.  Sometimes  the  bleeding  comes  from  a  duodenal 
or  gastric  ulcer,  still  more  rarely  an  oesophageal  one.  Care  must  be  taken 
to  exclude  hematemesis  and  melena  due  to  blood  swallowed  during  par- 
turition or  suckling  from  a  fissured  nipple,  epistaxis,  wounds,  ulcers,  and 
sores  of  mouth  and  gums.  Congenital  syphilis  is  regarded  as  an  important 
predisposing  factor.  Abt,  of  Chicago  (1903),  found  it  present  in  2  out  of  12 
cases,  but  Machell,  of  Toronto,  obtained  no  evidence  of  it  in  either  child  or 
parent,  in  14  cases.  Undoubtedly  hemorrhage  can  occur  in  congenital 
syphilis.  Endarteritis  of  small  vessels,  possibly  syphilitic,  has  been  found  in 
some  fatal  cases.  The  worst  cases  which  have  come  under  my  notice  have 
not  been  associated  with  any  trace  of  this  disease.  The  affection  is  not  due 
to  hemophilia,  for  hemophiliacs  rarely  bleed  before  the  end  of  the  first  year, 
and  infants  who  recover  from  hemorrhagic  disease  do  not  subsequently 
prove  bleeders. 

The  important  attacks  are  those  due  to  pyogenic  infection  by  various 
organisms,  present  in  many  cases  and  giving  rise  to  pyemia  or  toxemia. 
Possibly  toxins  reach  the  foetus  in  utero,  traversing  the  placenta  ;  or  the 
infection  is  a  sepsis  neonatorum.  On  the  other  hand  sepsis  and  hemorrhage 
often  occur  independently  of  each  other.  Some  change  is  produced  in  the 
blood  or  blood  vessels,  permitting  extravasation.  The  effects  depend  on 
the  amount  of  blood  lost  and  the  causation. 

Gastro-intestinal  bleeding  may  be  taken  as  the  type  of  this  disease.    As 


The  Umbilicus  and  Septic  Affections  of  the  Newborn.  129 

a  rule  haematernesis  starts  from  12-36  hours  after  birth.  It  may  begin  at  the 
sixth  hour,  be  delayed  until  the  sixth  day,  or  even  as  late  as  the  sixth  week  ; 
varying  with  its  site  and  causation.  Few  cases  begin  after  the  first  week. 
Bleeding  is  the  first  sign.  In  one  instance  fever  was  present  from  birth, 
melaena  began  12  hours  and  haeinatemesis  18  hours  after  birth,  lasting  for 
12  hours  more  and  ending  in  recovery.  Another  apparently  healthy  child 
passed  bright  red  blood  on  the  seventh  day,  got  rapidly  worse  with  more 
severe  bleeding,  and  died  on  the  tenth  day  ;  there  was  no  jaundice  or  fever. 
A  third  case  was  that  of  a  premature  baby,  under  4  lbs.  in  weight,  with  a 
little  jaundice,  but  no  fever  ;  melaena  began  on  the  seventh  day,  and  ended 
fatally  on  the  tenth  day,  no  cause  being  found  post  mortem.  In  other 
instances  the  cases  were  of  the  type  described  as  sepsis  in  the  newborn, 
coming  on  with  fever  a  few  days  after  birth,  the  haemorrhage  being  a 
subsidiary  symptom.  The  blood  may  be  dark  in  colour  at  first  and  contain 
clots,  if  it  comes  from  the  stomach  or  high  up  in  the  intestine.  In  profuse 
haematemesis  or  bleeding  from  the  colon  it  is  bright  red,  thin,  and  watery. 
Bleeding  may  begin  before  food  has  been  taken,  or  follow  vomiting  or  the 
passage  of  mucus.  Meconium  is  evacuated  first,  next  dark  or  very  tarry 
blood  mixed  with  fasces,  and  perhaps  finally  profuse  bright  red  watery 
blood.  Bleeding  may  take  place  also  from  the  nose  and  navel,  from  any 
single  site,  or  from  several  places  and  into  various  organs  more  or  less 
simultaneously.  Melaena  and  haematemesis  occur  in  one-fourth  of  all 
hemorrhagic  cases,  of  which  50-60  per  cent,  are  melaena  only  ;  15-20  per 
cent,  haematemesis  without  melaena.  Both  are  often  associated  with  bleed- 
ing from  other  sources,  jaundice,  and  fever. 

Diagnosis. — The  diagnosis  is  important  in  view  of  the  serious  nature 
of  the  true  hcernorrhagic  disease.  Care  must  be  taken  to  exclude  haemat- 
emesis due  to  swallowed  blood.  Gastro-intestinal  haemorrhage  may  be 
concealed  until  melaena  is  noted,  or  even  prove  fatal  before  blood  appears 
in  the  stools.  Haematuria  may  be  due  to  uric  acid  infarcts  ;  vaginal 
haemorrhage  to  local  congestion,  injury,  or  polypus  ;  haemorrhage  from  the 
ears,  due  to  fracture  of  the  base  of  the  skull  at  birth  ;  bleeding  from  the 
eyes  or  into  the  retina,  due  to  injury.  Generally  the  diagnosis  is  based  on  the 
multiplicity  of  the  haemorrhages,  the  date  of  onset,  and  the  presence  of 
fever.  Fever  may  be  absent.  In  mild  cases  the  bleeding  is  slight,  and  ceases 
in  a  few  hours  or  a  day  or  two.  Some  are  more  prolonged  and  serious,  with 
loss  of  weight,  anaemia,  and  prostration.  The  greater  and  more  sudden  the 
bleeding,  the  worse  is  the  prognosis.  Umbilical  and  vaginal  haemorrhage  are 
the  least  serious.  Gastro-intestinal  haemorrhage,  with  little  or  no  fever,  is 
not  grave  unless  the  bleeding  is  profuse,  bright  red,  and  watery.  One  or 
two  attacks  of  severe  haematemesis  may  be  recovered  from.  A  purpuric 
rash  is  a  very  bad  sign.  If  only  the  septic  cases  are  regarded  as  the  true 
haemorrhagic  disease  the  prognosis  is  very  bad.  It  is  bad  if  the  blood  is 
bright  red  and  continuously  oozing  from  a  mucous  membrane  ;    if  high 

K 


130  Chapter  IX. 

fever  and  jaundice  are  present,  indicating  sepsis  ;  if  there  is  an  enlarged 
spleen  or  history  of  syphilis  ;  or  if  there  is  diarrhoea,  common  in  septic  cases. 

Mortality  statistics  vary  from  35-78  per  cent.,  according  to  the  type  of 
cases  included.  In  fatal  cases  death  results  from  profound  anaemia,  collapse, 
asthenia  or  convulsions.  Death  or  recovery  ensues  in  3  or  4  days.  Usually 
nothing  abnormal  is  found  post  mortem  ;  sometimes  acute  fatty  degenera- 
tion, umbilical  and  portal  phlebitis,  enlargement  of  spleen  and  liver,  or 
syphilis. 

For  local  bleeding  apply  calcium  salts,  adrenalin,  or  sterile  gauze 
soaked  in  gelatine  solution,  10  per  cent.  Accidental  bleeding  is  treated  by 
astringent  powders,  alum  and  tannic  acid,  or  cauterisation.  In  all  forms  of 
the  hsemorrhagic  disease  give  gelatine,  with  water  or  whey,  by  the  mouth  ; 
a  2-5  per  cent,  solution  by  the  rectum  ;  or  in  very  severe  cases  a  2  per  cent, 
solution  in  normal  saline  in  doses  of  10-15  c.c,  every  3-6  hours  subcutan- 
eously.  The  fluid  must  be  boiled  for  6  hours  first,  as  it  may  contain  tetanus 
organisms.  Sometimes  it  gives  rise  to  toxic  symptoms.  In  addition,  give 
hazeline,  hamamelis,  calcium  lactate,  and  bismuth  by  the  mouth  for  bleeding 
from  the  alimentary  tract.    Avoid  irritating  food  and  keep  the  child  warm. 

Suprarenal  Haemorrhage  or  Apoplexy  may  be  traumatic,  the  result  of 
injury  during  labour.  Usually  the  child  is  stillborn,  death  occurring  before 
or  during  labour.  Undoubtedly  the  delicate,  fragile  character  of  the 
circulation  in  these  glands  is  a  predisposing  factor.  The  vessels  may  give 
way  in  consequence  of  asphyxial  conditions  or  compression  of  the  cord.  In 
some  instances  congenital  syphilis  or  haemophilia  may  be  to  blame.  Rare 
causes  include  convulsions,  vaso-motor  disturbance,  and  thrombosis  of  the 
inferior  vena  cava  or  renal  vein.  Probably  the  most  constant  cause  is  some 
form  of  septic  infection.  The  amount  of  haemorrhage  varies  from  severe 
congestion  to  the  production  of  a  large  bloody  tumour,  the  size  of  an 
orange.  It  is  often  bilateral.  In  the  newborn  it  is  frequently  associated 
with  other  haemorrhages  ;  and  in  older  children  with  purpuric  rashes  and 
high  fever,  sometimes  due  to  cerebro-spinal  fever.  The  onset  is  sudden, 
perhaps  with  screaming,  acute  abdominal  pain,  vomiting  and  convulsions. 
The  child  soon  becomes  seriously  ill,  the  temperature  rises,  diarrhoea  is 
present,  and  purpura  is  not  uncommon.  Death  may  take  place  in  a  few 
hours,  or  in  a  few  days,  from  collapse,  or  with  symptoms  like  peritonitis. 
Riviere  (1902)  collected  6  cases  of  this  type,  and  added  4  more.  In  his 
patients  the  Peyer's  patches  and  mesenteric  glands  were  enlarged.  Bacterio- 
logical examinations  proved  negative.  He  suggested  intestinal  toxaemia 
as  a  possible  explanation.  In  a  child,  aged  3  months,  with  somewhat 
similar  symptoms,  viz.,  anorexia,  convulsive  movements,  drowsiness,  and 
death  from  collapse,  53  hours  after  the  onset,  I  found  (1908)  an  extensive 
bilateral  renal  apoplexy  of  uncertain  causation. 

Trismus  or  Tetanus. — Trismus  or  Tetanus  of  the  newborn,  sometimes 
known  as  the  "  Eight  Days  Sickness  of  St.  Kilda,"  is  due  to  the  tetanus 


The   Umbilicus  and  Septic  Affections  of  the  Newborn.  131 

bacillus  infecting  the  umbilical  wound,  or  rarely,  via  the  skin  or  genitals. 
It  is  common  in  the  tropics,  especially  the  West  Indies,  Cuba,  and  America ; 
and  comparatively  rare  in  Europe.  In  1782  one  out  of  every  six  babies  born 
in  the  Rotunda  Hospital,  Dublin,  died  from  it.  At  St.  Kilda,  in  1880,  14 
couples  had  had  125  children,  of  whom  84  died  from  trismus  during  the  first 
14  days  of  life.  The  organism  is  widely  distributed  in  the  dust  of  streets 
and  houses,  and  is  conveyed  by  the  hands  of  the  attendant  or  the  bandages, 
pads,  charred  brown  paper,  Fuller's  Earth,  or  ointment  applied  after 
birth. 

Trismus  commonly  begins  on  the  fourth  day,  and  rarely  later  than  the 
tenth  day  after  birth  unless  the  navel  is  unhealed.  The  first  sign  is  difficulty 
in  suckling,  and  apparent  anorexia  because  of  the  trismus  or  spasm  of  the 
masseters  on  suckling.  There  are  marked  restlessness  ;  frequent  sharp 
cries  ;  general  corrugation  of  the  forehead,  facial  muscles,  and  lips  ;  the 
"  risus  sardonicus  "  ;  retraction  of  the  head  and  opisthotonos.  The  limbs 
are  rigid,  the  upper  ones  acutely  flexed,  and  the  lower  ones  usually  extended. 
The  pulse  and  breathing  are  increased  in  frequency.  The  temperature  rises 
to  104-106°  F.  or  more,  and  often  there  is  a  further  rise  after  death.  Some- 
times there  is  no  fever.  Gradually  sucking  and  swallowing  becomes 
impossible,  the  spasms  or  fits  are  more  and  more  frequent,  or  longer  in 
•duration,  induced  by  the  slightest  external  stimulus,  and  ending  in  cyanosis. 
The  breathing  becomes  shallow  and  irregular,  and  death  ensues  from 
asthenia,  spasm  of  the  larynx  or  spasm  of  the  diaphragm.  The  navel  may 
appear  normal,  or  discharge  pus.  Although  the  organism  can  grow  in  pus, 
pure  cultures  are  rapidly  destroyed  at  the  seat  of  inoculation  by  the  toxin 
produced.  Early  diagnosis  is  important.  The  spasms  and  rigidity  must 
be  distinguished  from  those  due  to  developmental  errors  of  the  cerebrum, 
■encephalitis,  meningitis,  and  cerebral  toxaemia. 

Some  cases  are  quite  mild,  and  even  limited  to  trismus.  A  few  continue 
many  weeks  and  recover.  These  chronic  cases  generally  come  on  a  few  days 
later  in  life  with  twitching,  jaundice,  and  a  peculiar  pallor.  Of  the  acute 
cases  many  die  within  48  hours  of  the  onset.  Finlay,  of  Havana,  states 
that  131  out  of  141  died  in  the  first  week  and  10  in  the  second  week  of  life. 

Tetanus  in  older  children  is  common  m  Australia,  and  in  the  United 
States  of  America  about  Independence  Day,  July  4th,  due  to  wounds  by  the 
blank  cartridge  of  toy  pistols.  The  earliest  symptoms  are  temporary  local 
contractions  at  the  site  of  the  wound,  sighing  and  yawning,  or  other  signs 
of  dyspnoea  up  to  cyanosis  and  glottic  spasm.  Stiffness  of  the  neck,  jaw, 
back,  and  abdomen  develop  1-7  days  later  ;  constipation  is  very  common. 
Its  course  is  similar  to  that  in  adults.  In  both  babies  and  children  the 
prognosis  depends  upon  the  duration  of  incubation,  the  nature  of  the 
wound,  the  height  of  the  temperature,  and  th.e  duration  of  the  symptoms. 
The  incubation  period  averages  11  days  ;  less  in  the  newborn.  If  only  10 
•days,  4  per  cent,  recover;    if  11-15  days,  27  per  cent,  recover  (Rose). 


132  Chapter  IX. 

After  a  duration  of  5  or  6  days  recovery  is  probable.  The  outlook  is  less 
serious  in  the  so-called  idiopathic  cases,  and  worse  in  those  secondary  to 
abrasions  and  jagged  irregular  wounds.  It  is  favourable  if  the  temperature 
is  under  101°  F.,  and  very  serious  if  over  103°  F. 

Local  treatment  consists  in  the  use  of  antiseptics  ;  cauterisation  ; 
incision  and  curetting,  swabbing  with  pure  carbolic,  and  packing  with 
iodoform  gauze  ;  excision  or  amputation.  Babies  should  be  fed  on  the 
breast-milk,  given  by  gavage  if  unable  to  swallow.  Protect  them  from 
external  irritants,  cold,  draught,  noise,  etc.,  and  give  a  dose  of  calomel 
or  an  enema,  and  a  warm  bath  every  3  hours.  Give  chloral  in  doses  of 
grs.  1-5,  every  2-4  hours,  combined  with  double  the  quantity  of  potassium 
bromide.  Continue  this  from  24-48  hours,  and  then  in  smaller  doses. 
Atropin  gr.  inho-stho,  curare  gr.  /o,  physostigniin  gr.  itb,  and  phenol 
have  been  given  3  times  a  day  subcutaneously.  For  high  temperature 
the  coal  tar  products  are  better  than  hydrotherapeutic  measures. 
Chloroform  inhalations  relieve  the  spasms  temporarily.  Anti-tetanic 
serum  can  be  tried,  but  has  not  proved  of  much  value.  It  neutralises  toxin 
formed  at  the  seat  of  inoculation  and  circulating  in  the  blood,  but  does  not 
affect  it  when  it  has  combined  with  the  nerve  cells.  It  may  cause  rash  and 
painful  synovitis.  It  may  be  injected  in  the  neighbourhood  of  the  wound, 
intramuscularly  into  the  buttock,  intravenously,  or  by  lumbar  puncture. 
Behring's  and  Tizzoni's  serums  are  the  best.  Meltzer  found  that  magnesium 
salts  inhibited  the  functional  activity  of  the  nervous  tissues,  and  caused 
surgical  anaesthesia  in  monkeys  on  lumbar  injection.  It  may  be  injected 
in  doses  of  1  c.c.  of  a  25  per  cent,  solution  to  every  25  lbs.  of  body  weight 
every  36  hours  for  4  doses,  and  sometimes  controls  the  rigidity  and  con- 
vulsions. It  is  very  difficult  to  estimate  the  value  of  remedies,  because  of  the 
impossibility  of  judging  accurately  the  course  of  the  disease,  if  untreated. 
On  the  whole  it  is  best  to  rely  upon  chloral,  careful  feeding,  nursing,  and 
warm  baths.    Morphia  prevents  elimination  and  may  do  harm. 


Chapter  X. 

JAUNDICE. 

Icterus  Embryonum — Icterus  Neonatorum  —  Biliary  Concretions — Pycemic 
Jaundice — Congenital  Defects  of  the  Bile  Ducts. 

In  rare  instances  the  infants  of  women  suffering  with  prolonged 
jaundice  have  been  born  similarly  affected.  Still  more  rarely  the  mother  is 
apparently  healthy.  This  is  known  as  Icterus  Embryonum.  These  babies 
may  be  premature,  stillborn  at  full  time,  or  may  live.  Jaundice  at  birth  is 
occasionally  seen  as  the  result  of  syphilitic  hepatitis,  malformations  of  the 
bile  ducts,  or  in'the  rare  cases  of  family  acholuric  jaundice. 

Icterus  Neonatorum  is  a  common  form  of  jaundice  in  newborns,  varying 
from  a  pale  to  an  intense  yellowness.  It  appears  usually  on  the  third  to  the 
fifth  day  of  life,  rarely  on  the  first,  and  not  often  after  the  fifth;  and  is 
found  in  from  30-85  per  cent,  of  all  babies,  more  especially  in  the  premature, 
the  small,  and  the  firstborn.  It  is  first  noticed  in  the  nose  and  cheeks,  and 
may  be  limited  to  the  face.  Next  it  affects  the  thorax,  abdomen,  conjunc- 
tivae, and  extremities.  The  sclerotic  is  not  always  involved.  By  pressure 
of  the  finger  on  the  skin  a  yellowish  print  is  produced.  In  the  early  red  or 
pre-icteric  stage  the  yellowness  is  partly  concealed  by  the  hyperemia  of  the 
skin.  The  yellowness  increases  in  depth  for  two  or  three  days,  and  then 
slowly  disappears.  In  mild  cases  the  urine  is  unaffected,  but  in  more 
severe  ones  it  may  contain  bile  salts,  and  pigment.  Golden  yellow,  shining, 
insoluble  masses  of  pigment  have  been  found  in  the  urine.  They  are  soluble 
in  alcohol,  soluble  in  strong  H2S04  with  red  colouration,  and  insoluble  in 
ether.  These  are  masses  of  bilirubin  (Cruse).  Bilirubin  is  feebly  soluble  in 
the  urine  of  the  newborn,  because  of  the  scanty  amount  of  alkaline  phos- 
phates. The  colour  of  the  stools  is  unaffected,  except  in  very  bad  cases, 
and  nutrition  rarely  suffers.  It  lasts  for  a  week  or  two,  and  occasionally 
for  many  months,  without  making  the  child  ill,  and  ending  in  complete 
recovery.  In  prolonged  cases  the  occasional  presence  of  bile  in  the  stools 
is  a  favourable  sign.  A  fatal  issue  may  ensue  on  some  coincident  affection, 
and  post  mortem  every  organ  in  the  body  is  more  or  less  bile-stained,  except 
the  liver,  which  is  rarely  discoloured,  or  only  in  patches.  Bilirubin  crystals, 
the  "  hsematoidin  infarcts  "  of  Virchow,  have  been  found  in  the  apices  of 
the  renal  papilla?,  and  are  peculiar. 


134  Chapter  X. 

Its  pathology  is  uncertain.  At  birth  the  abrupt  cessation  of  the 
foetal  circulation  induces  more  or  less  congestion  of  the  liver  and  venous 
stasis.  The  dilated  veins  press  on  the  bile  capillaries  and  ducts,  and  cause 
retention  of  bile  in  the  liver.  This  condition  has  been  demonstrated  in  fatal 
cases,  and  is  favoured  by  anything  which  interferes  with  the  expansion  of 
the  lungs,  and  the  action  of  the  heart ;  hence  jaundice  is  more  common  in 
feeble  infants  and  in  those  born  asphyxiated. 

It  has  been  ascribed  to  the  rapid  destruction  of  the  red  cells  in  the  first 
few  days  of  life,  and  solution  of  the  colouring  matter  in  the  serum  which 
reaches  the  tissues,  where  it  is  reduced  to  some  kind  of  yellow  pigment. 
It  is  no  longer  generally  accepted  that  any  such  disintegration  of  red  cells 
takes  place  after  birth.  Estimations  based  on  the  number  per  c.nim.  are 
unreliable  for  the  percentage  varies  with  the  quantity  of  plasma.  Moreover, 
the  occasional  presence  of  bile  acids  in  the  urine  indicates  that  the  affection 
is  not  hsematogenous. 

In  all  probability  an  increased  formation  of  bile  takes  place  at  birth, 
due  to  the  stimulus  of  a  rich  blood  supply  (Knopfelmacher),  and  the 
capillaries  become  overdistended  with  viscid  tenacious  secretion  at  a  low 
pressure,  in  consequence  of  which  some  of  it  passes  into  the  blood.  It  may 
therefore  be  regarded  as  a  physiological  manifestation.  It  is  unlikely  that 
it  can  be  due  to  any  more  serious  cause. 

No  special  treatment  is  needed,  but  small  doses  of  calomel  or  grey 
powder,  and  bicarbonate  of  soda  may  be  given.  In  making  a  diagnosis 
we  have  to  exclude  those  cases  of  jaundice  due  to  septic  infections,  Buhl's 
disease,  and  Winckel's  disease,  syphilitic  hepatitis,  malformations  of  the 
bile  ducts,  and  the  rare  cases  of  family  acholuric  jaundice.  A  tendency  to 
the  secretion  of  viscid  bile  may  be  a  family  peculiarity  in  those  cases  where 
many  successive  infants  have  died  from  jaundice  in  the  first  month  of  life. 
It  is  important  to  remember  that  simple  jaundice  in  the  newborn  may  be 
very  prolonged,  and  yet  not  necessarily  due  to  malformation  of  the  bile 
ducts,  sepsis,  or  liver  disease.  Nevertheless,  if  the  discolouration  increases 
in  intensity  in  the  second  week,  it  is  in  favour  of  a  more  serious  diagnosis. 
Severe  jaundice  from  any  cause  may  lead  to  multiple  haemorrhages. 

Biliary  Concretions  are  more  common  in  the  liver  of  infants  than  at 
any  other  period  of  childhood,  and  even  occur  in  the  foetus.  This  is  a  further 
proof  of  the  tendency  to  stagnation  of  bile  at  this  age.  Intense  jaundice 
at  birth  or  shortly  after  results,  and  calculi  are  found  in  the  ducts  in  fatal 
cases.  Stone  in  the  gall  bladder  is  extremely  rare  before  puberty,  and  gives 
rise  to  the  usual  symptoms  of  colic  and  jaundice,  and  the  passage  of  a  stone. 
In  a  boy  of  4,  who  had  attacks  of  colic  for  2  years,  the  gall  bladder  was 
dilated,  and  the  cystic  duct  contained  a  stone  (Friedlander,  1907). 

The  Gall  Bladder  is  very  rarely  absent.  It  may  be  transposed,  bifid 
or  duplicated,  or  show  hour-glass  constriction.  Dilatation  is  generally  due 
to  obstruction,  but  may  occur  without  any  evidence  thereof. 


Jaundice.  135 

Malformations  of  the  Bile  Ducts  are  rare.  The  common  duct  may  be 
absent,  represented  by  a  fibrous  cord,  or  obliterated  at  its  entrance  into  the 
duodenum.  The  cystic  and  hepatic  ducts,  alone  or  associated  with  some 
defect  of  the  common  duct,  may  be  impervious.  Developmental  errors  and 
obstruction  are  ascribed  to  adhesions  from  foetal  peritonitis,  foetal  cholan- 
gitis, and  congenital  syphilis.  If  the  cystic  duct  is  alone  affected  there 
may  be  no  symptoms.  With  other  malformations  jaundice  is  a  marked  sign. 
It  is  present  in  about  one-fourth  of  the  cases  at  birth,  and  in  the  rest  comes 
on  in  2  or  3  days,  possibly  not  for  a  fortnight.  It  steadily  increases,  and 
becomes  very  intense.  The  liver  is  enormously  enlarged,  and  may  reach 
the  anterior  superior  spine  of  the  ilium.  The  spleen  is  large.  The  urine 
becomes  greenish  brown,  and  the  stools  pale  and  offensive.  Bleeding 
may  occur  subcutaneously,  from  mucous  membranes,  and  from  the  umbilicus 
due  to  backward  pressure  through  the  ductus  venosus  and  the  left  portal 
vein.  The  child  suffers  from  flatulent  distension,  wasting,  ascites,  and 
oedema  ;  and  dies  in  about  6-8  weeks  from  asthenia  or  convulsions  ; 
occasionally  life  has  been  prolonged  for  8  or  9  months.  John  Thomson  (1892) 
tabulated  49  cases  of  Congenital  Obliteration  of  the  Bile  Ducts,  and  ascribed 
it  to  a  primary  malformation.  H.  D.  Eolleston  (1903)  added  12  more,  and 
held  that  it  was  due  to  a  descending  cholangitis,  causing  primary  cirrhosis 
and  secondary  obliteration  ;  the  cirrhosis  being  of  a  mixed  monolobular 
and  multilobular  type.  Morse  (1907)  stated  that  there  are  about  80  cases 
on  record.  Emanuel  (1907)  reported  a  case  which  supports  Rolleston's 
view.  In  addition  to  absent  ducts,  rudimentary  gall  bladder,  and  biliary 
cirrhosis,  both  the  spleen  and  the  pancreas  were  fibrosed.  Possibly  the 
condition  is  due  to  some  toxin,  which  is  active  during  early  foetal  life,  and 
sets  up  cholangitis  and  arrest  of  development.  The  affection  may  be 
present  in  many  children  of  the  same  family.  No  doubt  the  name  is  used 
for  many  conditions,  some  primary  and  others  secondary,  in  which  absence 
or  obliteration  of  the  bile  ducts  is  present  at  or  shortly  after  birth.  The 
common  duct  is  the  most  frequently  affected.  At  one  end  of  the  scale  is 
obliteration  of  the  common  duct  at  the  duodenal  end  ;  and  at  the  other, 
complete  absence  of  the  gall  bladder  and  all  the  ducts  ;  with  many  inter- 
mediate varieties.  Life  has  been  prolonged  for  months  or  only  for  a  few 
days.  The  liver  is  deep  olive  green  or  bronze  in  colour,  rough,  hard,  and 
very  cirrhotic  in  prolonged  cases,  and  contains  an  excessive  number  of 
dilated  bile  ducts.  The  gall  bladder  is  distended,  small,  rudimentary,  or 
even  absent.  Congenital  Hepatic  Cirrhosis  with  Obliteration  of  the  Bile 
Ducts  is  another  name  for  this  variety  of  cirrhosis.  It  has  been  found 
associated  with  retention  and  inspissation  of  bile,  dilated  bile  capillaries, 
and  obstruction,  but  no  obliteration.  Cystic  Dilatation  of  the  Common 
Bile  Duct  simulates  a  dilated  gall  bladder.  It  is  due  to  obliteration  of  the 
ends  of  the  duct,  and  probably  of  congenital  origin.  It  is  progressive  from 
birth.  Five  such  cases  died  between  the  ages  of  13  and  23  years.  In 
Oxley's  patient  the  cyst  held  36  oz. 


136  Chapter  X. 

Family  Acholuric  Jaundice  has  been  described  under  the  names  of 
simple  acholuric  jaundice;  congenital  family  cholaemia;  chronic  acholuric, 
persistent,  family  or  congenital  jaundice  with  splenomegaly;  chronic  infec- 
tious splenomegalic  jaundice ;  and  the  congenital  acholuric  icterus  of 
Minskowski,  who  reported  eight  cases  in  three  generations.  One  of  these 
was  fatal  and  showed  splenic  hy  perplasia,  but  no  cirrhosis  or  angiocholitis. 
More  than  one  of  a  family  in  successive  generations  may  be  affected.  The 
symptoms  are  jaundice  of  almost  indefinite  duration,  of  a  lemon  yellow 
colour,  starting  in  early  life  and  possibly  at  birth ;  the  presence  of  bile  pigment 
in  the  serum  and  stools  ;  and  no  bile  in  the  urine.  Usually  there  is  more  or 
less  anaemia  and  leucopenia,  splenomegaly,  and  to  a  less  extent  enlargement 
of  the  liver.  The  spleen  is  not  invariably  enlarged.  The  affection  is  com- 
patible with  long  life  and  good  health,  and  does  not  affect  growth  or  mental 
capacity.  Sometimes  there  are  attacks  of  malaise,  slight  fever,  diarrhoea, 
increased  jaundice,  pain  over  the  liver  and  spleen,  and  nervous  distress. 
Hayem  found  specific  chorio-retinitis  in  some  cases.  It  is  possible  that 
Family  Jaundice  may  be  due  to  simple  cholaemia,  splenomegalic  jaundice, 
or  biliary  cirrhosis  ;  or  that  these  are  different  stages  of  the  same  affection, 
the  result  of  a  congenital  defect  in  the  blood-forming  organs,  operative 
through  haemolysis  of  red  cells. 

Syphilitic  Jaundice. — The  treatment  of  severe  jaundice  in  the  newborn, 
when  not  due  to  pyaemic  infection,  is  by  anti-syphilitic  remedies,  on  the 
assumption  that  syphilitic  hepatitis  or  peri-hepatitis  may  be  the  cause. 
Gubler  (1882)  described  this  variety,  but  few  cases  are  on  record.  The 
jaundice  is  usually  present  at  birth  or  comes  on  in  a  few  days,  perhaps  not 
for  two  or  three  weeks.  It  is  by  no  means  an  invariable  symptom,  but, 
when  present,  it  becomes  intense  and  is  persistent.  Occasionally  it  sub- 
sides and  recurs  after  an  interval.  Ascites  may  be  a  prominent  symptom. 
Haemorrhages  take  place  under  the  skin  and  from  the  mucous  membranes, 
and  the  child  dies  in  a  few  weeks.  Recovery  may  take  place.  Congenital 
syphilis  may  be  an  indirect  cause  of  Pycemic  Jaundice  by  setting  up 
epiphysitis,  which  in  its  turn  may  become  suppurative  from  secondary 
infection  and  produce  pyaemia.  More  commonly  pyaemic  jaundice  is  due 
to  umbilical  infection  and  phlebitis,  and  inflammatory  pressure  on  the 
bile  ducts.  It  is  almost  invariably  fatal  from  the  pyaemia,  the  jaundice 
being  a  minor  complication.  The  diagnosis  is  based  on  the  fever  and  the 
symptoms  of  septic  infection,  viz.,  anorexia,  convulsions,  and  coma ; 
foul  smelling  pus  exuding  from  the  umbilicus,  and  sometimes  fatal  haemor- 
rhage when  the  cord  drops  off.  Other  hemorrhages  are  liable  to  occur,  and 
the  abdomen  is  generally  swollen  and  tender.  The  pyaemic  condition  is  more 
fully  described  under  the  head  of  pyaemia  (p.  125). 


Chapter  XI. 

OPHTHALMIA    NEONATORUM. 

Syn.  :  Purulent  conjunctivitis — Purulent   Ophthalmia. 

This  disease  accounts  for  about  10-30  per  cent,  of  all  cases  of  blindness — 
36  per  cent,  in  the  London  Blind  Schools  (Bishop  Harraan)  ;  and  4-2  per 
cent,  in  Sheffield  (Snell).  Because  of  popular  prejudices  it  is  more  common 
here  than  abroad,  yet  it  is  easily  preventable. 

The  gonococcus  is  the  infecting  organism  in  from  ^-f  of  the  cases. 
Others  are  due  to  staphylococci,  streptococci,  bacillus  coli,  micrococcus 
luteus,  pneumococcus,  meningococcus,  Klebs-Lcefner  bacillus,  Koch-Week's 
bacillus,  and  the  diplobacillus  of  Morax  and  Axenfeld.  In  many  instances 
no  organism  is  found. 

The  incubation  period  of  the  gonococcal  cases  has  been  shown,  as  a 
result  of  treating  inveterate  trachomatous  pannus  by  inoculation  with 
gonorrhoeal  matter,  to  be  60  hours.  In  the  newborn  it  is  probably  less. 
A  maternal  leucorrhoea  is  present  in  two-thirds.  Although  the  infant's 
eyelids  are  separated  at  the  fifth  month  of  pregnancy,  they  are  closed 
during  delivery,  and  can  only  become  infected  if  the  lids  are  separated  by 
the  fingers  or  instruments.  At  birth  they  are  tightly  closed,  the  skin 
wrinkled,  and  covered  with  fatty  substance.  Infection  is  due  to  vaginal 
secretion,  sticking  to  the  margins  of  the  lids  and  the  eyelashes,  passing  into 
the  conjunctival  sac  when  the  eyes  are  open,  and  hence  is  generally  due  to 
insufficient  care  in  washing  and  wiping  the  eyes.  Congenital  or  ante-partum 
cases  are  due  to  premature  rupture  of  the  membranes  or  the  infective 
organisms  passing  into  the  amniotic  fluid.  If  the  ophthalmia  is  not  present 
at  birth,  it  develops  within  a  few  hours — less  than  24.  Stephenson  (1907) 
collected  19  such  cases,  more  than  half  gonococcal.  Commonly  the  eyes  are 
infected  immediately  after  birth  ;  sometimes  during  labour  ;  or  from  one 
to  several  days  subsequently.    A  few  cases  may  be  of  nasal  origin. 

In  three-fourths  of  the  cases  it  is  bilateral;  it  is  more  frequent  in  boys, 
because  labour  is  longer,  and  more  frequent  in  the  left  eye.  It  begins  on  the 
second  or  third  day,  almost  invariably  before  the  fifth.  Gonorrhoeal 
infection  may  set  up  a  simple  catarrh.  Generally  it  begins  with  slight 
irritation  which  progresses  into  excessive  inflammatory  oedema  and 
tenseness  of  the  eyelids  ;   chemosis,  i.e.,  swelling,  tenseness  and  oedema  of 


138  Chapter   XI. 

the  ocular  conjunctiva  ;  and  copious  purulent  secretion.  Ihe  upper  lid  is 
red,  glossy,  and  overhangs  the  lower  one.  The  lids  are  gummed  together 
and  separated  with  difficulty.  The  palpebral  conjunctiva  is  villous  and 
scarlet,  and  false  membrane  forms  in  5  per  cent.  A  papillary  form, 
resembling  follicular  hypertrophy,  is  not  uncommon.  Gradually  the 
discharge  becomes  muco-purulent  and  finally  serous,  the  swelling  and 
redness  subside,  the  granular  conjunctiva  becomes  smooth,  and  the  con- 
dition clears  up.  Even  with  prompt  treatment  the  attack  lasts  from  2-f> 
weeks. 

Complications  are  rare  in  early  stages.  The  cornea  is  very  susceptible 
in  the  newborn,  for  there  are  no  tears  to  wash  away  the  discharge.  It  is 
affected  in  4-14  days.  Central  ulcer  is  more  common  in  infants  than  in 
adults,  for  the  epithelium  is  thin  and  becomes  devitalised  from  stasis  in  the 
circumcorneal  vessels,  and  then  gets  infected.  Marginal  ulcers,  due  to  pent 
up  discharge,  are  more  common  in  later  life,  and  may  become  confluent. 
The  cornea  is  not  primarily  involved,  and  generally  escapes,  except  in 
gonococcal  infection.  Ulceration  begins  as  a  circumscribed  yellow  spot. 
It  increases  the  gravity  of  the  prognosis,  as  it  may  lead  to  perforation  and 
its  sequels.  Perforating  abscess  of  the  cornea  may  occur  as  late  as  the 
fifth  week.  Relapses  are  common,  and  the  gonococcus  may  be  found  in  the 
sac  for  weeks  after  the  discharge  has  ceased.  Arthritis  of  one  or 
more  joints  has  been  recorded,  and  even  gonorrhceal  stomatitis. 
Arthritis  may  be  very  acute,  or  milder,  with  much  effusion  and  pain  on 
movement.  Suppuration  may  occur  as  the  result  of  infection  by  other 
organisms. 

The  diagnosis  has  an  important  bearing  on  the  prognosis.  In  non- 
gonococcal cases  the  discharge  is  more  often  thick  mucus,  or  muco-pus, 
than  pure  pus,  and  the  hard  tense  swelling  of  the  lids  is  uncommon.  The 
gonococcus  is  readily  stained  by  pyronine  methylene  green.  Like  the 
meningococcus  and  the  micrococcus  catarrhalis  it  is  Gram-negative.  In 
glucose  and  galactose  media  it  forms  acid.  The  other  organisms  do  not ; 
except  the  meningococcus  in  glucose  media  (Mayou,  1904). 

The  prognosis  is  good  in  all  cases,  provided  proper  treatment  is  begun 
early,  before  the  cornea  is  invaded.  If  it  is  clear,  a  favourable  issue  may  be 
predicted.  Under  efficient  treatment  it  should  remain  unaffected.  There 
is  more  risk  in  feeble  infants,  because  the  treatment  cannot  be  carried  out 
as  thoroughly.  Permanent  blindness  may  ensue,  or  patches  of  opaque 
cicatricial  tissue  in  the  cornea  which  may  in  time  be  replaced  by  clear 
corneal  connective  tissue.  Two-thirds  of  the  patients  recover  with  un- 
impaired sight.  Rarely  cases  are  so  serious  that  no  treatment  is  successful. 
Streptococcal  cases  are  rare,  severe  and  dangerous,  for  the  cornea  may 
become  necrotic  in  12  hours. 

Prophylaxis  consists  in  cleanliness  and  the  adoption  of  Crede's  method 


Ophthalmia   Neonatorum.  139 

in  all  newborns.  Wipe  the  eyes  clean  from  maternal  secretions  with  a 
damp  swab,  while  the  lids  are  still  protected  by  the  vernix  caseosa,  as  soon 
as  the  head  is  born.  Keep  the  water  of  the  bath  from  contact  with  the  eyes, 
and  afterwards  again  wash  the  eyes  with  boiled  water,  normal  saline,  or 
weak  Condy.  If  the  mother  suffers  from  a  leucorrhoea,  even  though  not 
known  to  be  gonococcal,  antiseptic  vaginal  douches  should  be  given  before 
delivery,  and  subsequently  2-3  drops  of  1-2  per  cent,  solution  of  nitrate  of 
silver  should  be  instilled  into  each  conjunctival  sac.  Crede  recommended  a 
2  per  cent,  solution,  but  1  per  cent,  is  said  to  be  efficacious,  and  not  cause 
catarrh.  It  reduces  the  incidence  of  the  disease  from  nearly  10  to  under 
0-1  per  cent.  (Treacher  Collins).  It  must  not  be  adopted  for  ante-partum 
ophthalmia,  or  when  the  inflammation  has  already  started  ;  nor  should 
midwives  or  nurses  be  allowed  to  assume  the  responsibility  involved  in  its 
use.  The  solution  must  be  fresh,  and  kept  in  a  dark  bottle  away  from  light. 
The  great  objections  to  its  use  are  that  it  is  painful,  sets  up  a  mild  con- 
junctivitis, and  medical  men  are  loathe  to  adopt  a  system  of  treatment 
which  enables  parents  to  say  that  the  doctor  always  does  something  to 
inflame  the  baby's  eyes.  It  is  not  an  absolute  security,  and  is  unnecessary 
in  90  per  cent,  of  newborns.  There  is  no  stigma  involved  in  its  use,  for 
one-third  of  the  cases  are  not  gonococcal.  The  chief  substitutes  are  the 
colloidal  salts  of  silver,  protargol  and  argyrol,  10-20  per  cent,  strength,  and 
perchloride  of  mercury  1  in  2000.  The  instillation  of  one  drop  of  1  per 
cent,  solution  of  perchloride  alone  of  all  antiseptics  approaches  Crede's 
method  in  safety,  and  is  quite  as  irritating. 

Active  treatment  must  be  adopted  at  the  very  earliest  commencement 
of  the  disease,  and  the  reddening  eye  not  assumed  to  be  "  only  a  cold." 
All  discharge  must  be  washed  away  by  free  irrigation  with  a  non-irritating 
antiseptic  solution,  and  a  strong  antiseptic  and  astringent  applied  to  the 
inflamed  conjunctiva. 

The  baby  is  placed  on  its  back  in  the  nurse's  lap  with  the  head  towards 
the  operator,  who  must  sit  down  and  hold  it  firmly  between  his  knees. 
Separate  the  lids,  using  a  retractor  at  the  first  examination,  for  pressure  on 
the  globe  might  cause  rupture  of  a  necrotic  cornea.  A  bent  hair-pin  will  do,. 
if  a  proper  retractor  is  not  available.  The  cornea  usually  comes  into 
view  as  soon  as  the  eye  is  moved,  if  the  tips  of  the  thumbs  are  pressed  on 
the  extreme  borders  of  the  eye-lids  and  eye-ball.  Dip  sterilised  cotton 
tampons  in  warm  antiseptic  fluid,  and  squeeze  them  so  that  the  fluid  drops 
gently  into  the  eye  without  splashing,  or  use  a  douche  with  a  sterile  glass 
nozzle,  but  never  a  syringe  for  fear  of  injuring  the  cornea.  Gently  open 
and  close  the  lids  to  expel  retained  pus.  Wash  until  all  pus  is  removed, 
and  then  sponge  lightly  with  the  tampon  to  remove  coagulated  masses  of 
false  membrane.  Repeat  the  douching  with  plenty  of  fluid  every  1-3  hours 
day  and  night.    Use  for  the  douche  normal  saline,  boric  acid  3  percent.,  or 


140  Chapter  XI. 

permanganate  of  potash  1  per  cent.  ;  the  last  is  not  irritating  or  painful, 
does  not  injure  the  cornea.  The  discolouration  can  be  removed  by  bi- 
sulphide of  soda,  10-20  per  cent,  solution.  As  the  case  improves  the 
strength  can  be  reduced  to  0*5  and  0-25  per  cent.  Other  lotions  are  per- 
chloride  1  in  5000,  formol  1  in  2000,  chlorine  water,  quinine  1-25  per  cent., 
and  zinc  chloride  0-5  per  cent.,  if  used  at  the  onset. 

Once  a  day,  after  thorough  irrigation,  the  lids  should  be  everted  and 
painted  with  a  2  per  cent,  solution  of  silver  nitrate  (grs.  10  to  the  ounce), 
avoiding  the  cornea.  A  thin  film  of  slough  is  formed  and  soon  thrown  off 
in  the  discharge  with  many  organisms.  If  there  is  very  great  oedema  and 
profuse  suppuration,  the  solid  or  mitigated  stick  of  nitrate  of  silver  may 
be  used.  It  dissolves  slowly,  and  does  not  reach  the  cul-de-sac,  so  a  few 
drops  of  a  1  per  cent,  solution  must  also  be  instilled.  Then  wash  with  a 
salt  solution  to  neutralise  any  excess  of  nitrate.  Mild  cases  can  be  treated 
by  the  instillation  twice  a  day  of  a  few  drops  of  a  1  per  cent,  solution  ;  or 
instil  1  drop,  hourly  during  the  day  and  2  hourly  at  night,  of  a  0-25  per 
cent,  solution,  first  washing  away  the  discharge  with  a  mild  antiseptic 
lotion. 

Another  method  of  treatment  is  to  irrigate  the  sac  every  half  hour, 
and  apply  hot  fomentations  every  half  hour  of  borax  (2  drachms  to  1  pint)  ; 
instilling  protargol,  10  per  cent,  hourly,  and  20  per  cent,  daily.  Examine 
the  cornea  twice  a  day,  and  instil  atropin,  grs.  2  to  the  ounce,  in  addition, 
if  it  becomes  hazy.  Argyrol  is  preferred  by  some,  collargol  by  others  ; 
none  of  these  silver  compounds  is  as  reliable  as  the  nitrate,  and  they  have 
to  be  used  much  more  frequently.  The  amount  of  silver  in  an  organic 
compound  is  no  criterion  of  its  bactericidal  powers.  They  are  useful  in  the 
early  stages  and  in  mild  cases,  for  they  are  neither  painful  nor  irritating, 
and  can  be  entrusted  to  the  nurse.  Protargol  is  the  best.  It  must  be 
prepared  with  cold  water,  kept  in  the  dark  in  a  coloured  bottle,  and  not 
used  too  long,  as  it  stains  the  conjunctiva. 

The  nitrate  can  be  painted  on  daily,  or  every  other  day,  until  suppura- 
tion has  ceased,  and  the  case  passes  into  the  stage  of  "  ocular  gleet  "  ;  then 
use  a  lotion  of  zinc  sulphate.  The  margins  of  the  lids  should  be  anointed 
with  vaseline,  yellow  oxide  of  mercury,  or  aristol,  boric  acid  or  iodoform 
ointment.  Ice  compresses  are  sometimes  used  in  early  stages,  but  I  regard 
them  as  liable  to  lower  the  nutrition  of  the  cornea.  Warm  compresses  are 
much  better,  and  render  the  use  of  greasy  ointments  for  the  lids  unnecessary. 

General  Warnings. — Strong  nitrate  of  silver  treatment  must  only  be 
applied  by  the  doctor,  not  in  early  stages,  and  not  more  than  once  a  day. 
Irrigation  is  the  most  important  factor  in  the  treatment.  Do  not  bandage 
up  the  eye.  If  only  one  is  affected,  the  infected  eye  may  be  covered  with  a 
circular  watch  glass,  fixed  above  and  at  the  sides  by  plaster,  but  open 
below  to  allow  air  to  enter,  and  1  drop  of  nitrate  of  silver  solution,  1  per 


Ophthalmia   Neonatorum.  141 

cent.,  instilled  daily  into  the  healthy  conjunctival  sac.  Examine  the 
cornea  twice  daily,  and  in  everting  the  lids  be  careful  not  to  scrape  the 
corneal  epithelium ;  do  not  use  a  speculum,  elevators,  or  retractors.  Instil 
a  few  drops  of  cocaine,  2-5  per  cent,  solution,  before  examination  and 
treatment  of  the  eye.  Never  leave  pus  in  the  conjunctival  sac  or  in  contact 
with  the  cornea.  If  the  cornea  becomes  hazy  instil  atropin,  grs.  2-5  to  the 
ounce,  t.d.s.    For  marginal  ulcers  instil  eserin  1  per  cent. 


Chapter  XII. 

SKIN  AFFECTIONS  OF  THE  NEWBORN. 

Exfoliative    Dermatitis — Pemphigus — Epidermolysis — Foetal    Ichthyosis — 
Xerodermia — Sclerema — (Edema — Pigmentation. 

Exfoliative  Dermatitis  was  described  by  Eitter  in  1870.  It  usually 
begins  in  the  second  week.  Following  normal  desquamation,  which  com- 
mences in  a  few  days,  and  is  completed  in  about  two  weeks,  a  superficial 
redness  appears  on  the  lower  part  of  the  face,  and  is  followed  by  a  dry  scaly 
condition.  It  spreads  rapidly,  and  the  whole  surface  becomes  of  a  pale  red 
up  to  an  intense  purple  colour.  The  skin  is  thickened  and  undergoes  exfolia- 
tion in  large  flakes.  Characteristic  fissures  form  at  the  angles  of  the  mouth. 
Sometimes  small  vesicles,  due  to  exudation  beneath  the  stratum  corneum, 
precede  exfoliation.  The  epidermis  is  soon  regenerated,  but  the  skin  remains 
irritable  for  some  time.  The  buccal  mucosa  and,  occasionally,  the  corneal 
epithelium  are  involved.  There  is  no  fever.  About  half  the  cases  die  of 
a  secondary  infection,  enteritis,  pneumonia,  or  asthenia.  It  is  either  an 
exaggerated  form  of  normal  desquamation  in  the  badly  nourished  or  a 
severe  type  of  pemphigus  neonatorum.  It  may  occur  in  epidemics,  and  has 
given  rise  to  pemphigus  by  contagion  (Leiner  and  Knopf elmacher,  1908). 
It  is  treated  by  calamine  lotion,  zinc  pastes,  or  boracic  acid  ointment ; 
baths  of  bran,  oak  bark,  or  tannic  acid  5  per  cent,  strength  ;  and  aseptic 
powders. 

Pemphigus  Neonatorum  is  an  acute  bullous  eruption  due  to  infection, 
occurring  sometimes  in  epidemics,  and  conveyed  by  midwives.  Its  dis- 
tribution is  irregular,  but  the  palms  and  soles  are  generally  free.  According 
to  Pernet  it  is  a  bullous  form  of  impetigo  contagiosa.  Both  are  highly 
contagious.  Impetigo  in  the  adult  sets  up  pemphigus  in  the  child,  and 
pemphigus  in  the  child  causes  impetigo  in  the  adult.  It  is  commonly  a 
staphylococcal  infection.  Streptococci  have  been  found  in  some  cases,  and 
Chuprina  states  that  the  majority  are  gonococcal.  The  infection  enters 
through  the  umbilicus  or  the  skin,  and  may  produce  acute  toxaemia.  The 
onset  is  generally  on  the  fourth  to  the  sixth  day,  and  the  mortality  frequently 
high.    It  must  be  diagnosed  from  syphilitic  pemphigus  (q.v.). 

Congenital  Pemphigus  or  Epidermolysis  Bullosa  is  a  rare  peculiar 
tendency  of  the  skin,  very  early  in  life,  and  even  at  or  before  birth,  to  form 


Skin  Affections  of  the  Newborn.  143 

large  bullae  as  the  result  of  trifling  injury,  friction,  or  pressure.  It  is  often 
hereditary,  and  may  be  limited  to  one  sex.  The  bullae  are  very  superficial, 
like  those  due  to  slight  burns,  scalds,  and  irritants  ;  with  flaccid  walls  and 
serous  contents,  which  may  be  haemorrhagic  or  become  purulent,  unless 
emptied  when  full.  The  parts  liable  to  injury  are  most  affected,  especially 
the  feet,  calves,  and  hands.  Occasionally  the  whole  skin  is  involved,  and 
becomes  thin  and  like  tissue-paper  in  appearance.  The  nails  are  badly 
formed  and  often  lost ;  the  tongue  sometimes  affected,  and  the  teeth 
frequently  irregular.  Mental  development  is  backward  because  of  the 
physical  disabilitj- ;  the  general  health  is  unaffected.  The  symptoms  are 
limited  to  burning,  itching,  and  pain.  It  is  worst  in  warm  moist  weather, 
in  summer  ;  and  is  probably  vaso-motor  in  origin.  German-bred  children 
seem  particularly  liable.  It  may  be  followed  by  atrophy,  pigmentation,  or 
scarring  of  the  skin.  Groups  of  milium-like  subepidermic  cysts  develop 
round  the  bullae  or  scars.  Possibly  there  is  a  dystrophic  type  of  case  as 
well  as  one  of  vaso-motor  origin.  It  continues  to  evolve  throughout  life, 
is  comparatively  benign,  and  resists  all  treatment.  The  health  may  suffer 
because  of  the  mouth  affection  and  deficient  teeth.  Cleanliness  and  pro- 
tection from  injury,  with  attention  to  the  general  health,  cod-liver  oil, 
arsenic,  ergot,  and  tonics,  are  the  chief  measures  of  treatment. 

Xerodermia  is  of  three  varieties  : — (1)  exaggerated  dryness  and 
roughness  of  the  skin,  with  liability  to  squamous  or  fissured  eczema,  as  in 
Keratosis  palmaris  or  eczema  'palmare  ;  (2)  Keratosis  or  Lichen  pilaris, 
a  permanent  exaggerated  goose-flesh,  in  which  acuminate  horny  projections 
from  the  follicles  make  the  skin  somewhat  like  a  nutmeg  grater.  It 
especially  affects  the  extensor  surface  of  the  upper  arm  and  thigh,  and  is 
more  common  in  girls,  and  in  the  later  half  of  childhood  ;  (3)  Ichthyosis. 
This  is  a  hyperkeratosis  ;  excessive  epidermal  proliferation  and  retention 
of  the  horny  layer,  abeyance  of  exfoliation,  and  atrophy  of  the  deeper 
layers  of  the  corium.  It  is  congenital,  hereditary,  or  acquired.  Byrom 
Bramwell  reported  six  cases  in  one  family  of  four  generations,  only  one  male, 
and  the  disease  being  chiefly  limited  to  the  palms  and  soles,  parts  which 
are  usually  spared  or  little  affected.  C.  J.  Bond  (1905)  found  in  another 
family  that  males  only  were  affected,  and  females  transmitted  it.  Oes- 
tereicher  recorded  the  case  of  a  woman  who  had  three  normal  children 
by  the  first  husband,  and  three  ichthyotic  by  the  second,  both  parents 
being  free.  The  hereditary  cases  are  usually  in  abeyance  until  some 
months  after  birth. 

Foetal  Ichthyosis  was  first  recorded  by  Bichter  in  1792.  Lebert 
(1864)  collected  nine  cases,  and  described  a  similar  condition  in  a  calf. 
In  1908  sixty  had  been  recorded.  It  begins  about  the  fourth  month  of 
fcetal  life.  Most  grave  cases  are  born  prematurely.  The  disease  may  be 
incompatible  with  life,  or  the  child  live  for  a  few  days  or  months,  or  it 
may  develop  at  or  shortly  after  birth.    In  the  foetus  the  skin  looks  too  small, 


144  Chapter   XII. 

and  is  cracked  and  fissured.  It  forms  irregular  polygonal  plates,  1-3  mm., 
thick,  dirty  white  or  yellow  in  colour,  and  separated  by  red  or  purplish 
furrows.  They  are  largest  over  the  back,  and  especially  thick  over  the  scalp 
and  forehead,  producing  ectropion  of  the  upper  lid.  The  skin  somewhat 
resembles  irregularly  cracked  and  fissured  parchment,  and  forms  a  stiff 
covering,  rather  like  the  shell  of  a  tortoise.  The  orifices  are  deepened 
by  contraction  of  the  skin  or  plugged  by  epidermal  scales.  The  mouth  is 
open,  the  angles  fissured,  and  the  tongue  projects.  The  nose  is  represented 
by  round  holes  level  with  the  face.  The  scalp  is  seborrhceic,  hair  harsh 
and  dry,  and  nails  badly  developed.  The  temperature  is  low  and  sweating 
absent.  The  palms  and  soles  are  unaffected  ;  or  thickened,  coarse,  dry, 
yellow,  and  cracked.  The  disease  is  due  to  increased  activity  of  the 
rete  Malpighii  or  faulty  desquamation.  Dumesnil  and  Bowen  suggested 
that  it  was  due  to  the  persistence  of  an  epitrichial  layer,  a  membrane 
found  by  Welcker,  covering  the  hair  in  embryos  of  lower  animals,  and 
normally  disappearing  about  the  sixth  month.  Against  this  it  must  be 
pointed  out  that  complete  exfoliation  may  take  place  after  measles,  or 
indeed  every  few  months,  and  the  condition  re-appear.  The  underlying 
skin  is  moist  and  red,  but  soon  becomes  dry,  hard,  and  cracked.  Moreover, 
the  acquired  cases  only  differ  in  degree.  The  thyroid  gland  has  been 
found  atrophied,  absent,  or  normal.  The  severity  of  the  affection,  the 
development  of  the  child,  and  the  duration  of  life  are  variable.  The  develop- 
ment of  the  nose,  ears,  fingers,  and  toes  is  interfered  with  mechanically. 
Many  remain  small  and  delicate,  some  die  early  from  a  kind  of  toxaemia, 
a  few  show  infantilism,  while  others  develop  normally  though  the  disease 
is  well  marked.  As  a  rule  the  prognosis  varies  directly  as  the  extent 
of  the  disease.  They  should  be  treated  by  persistent  massage  with  oil 
and  weak  mercurial  ointment.  Systematic  exfoliation  must  be  encouraged 
by  resorcin  dr.  £-1,  glycerin  or  almond  oil  oz.  -|,  and  glycerin  of  starch  or 
lanolin  oz.  1|-,  applied  once  or  twice  a  day,  and  daily  washing  with  a 
superfatted  soap.    Thyroid  extract  and  pilocarpin  are  useless. 

Ichthyosis  Herpetiformis  (Biett's  Bands)  is  a  variety  of  Ichthyosis 
in  which  the  patches  are  in  streaks  and  the  unaffected  parts  of  the  skin 
remain  healthy.  It  is  limited  to  one  child  in  a  family,  rare  on  the  scalp, 
uncommon  on  the  neck  and  face,  of  no  special  nerve  distribution,  and 
usually  unilateral.  These  congenital  streaks  or  bands  of  thick  rugose  skin 
may  resemble  moles,  or,  more  often,  patches  of  rough  unwashed  skin,  for 
the  dry  papillary  outgrowths  become  almost  black  with  dirt.  They  can  be 
destroyed  by  cautery  when  the  child  has  grown  up. 

General  Treatment  of  Ichthyosis  :  Polish  down  rough  and  scaly  pro- 
jections, and  stimulate  the  secretion  of  sweat  and  sebum.  Give  a  warm 
alkaline  bath,  dry,  and  rub  in  diluted  glycerine  of  starch,  salicylic  acid 
ointment,  gr.  5-10  ad  oz.  1.  For  bad  cases  use  a  stronger  ointment  of 
salicylic  acid  and  resorcin.    Internally  try  thyroid  extract  and  cod-liver  oil. 


Shin  Affections  of  the  Neiobom.  145 

Sclerema  Neonatorum. — This  rare  affection,  known  in  the  time  of 
Galen,  was  first  described  by  Uzemberius  (1718).     It  is  more  common  in 
France  and  Italy  than  elsewhere.    It  is  also  described  under  the  names  of 
Sclerema   (Edematosum  and  Scleroedema  ;    and  it  must  be  distinguished 
from  Sclerema  Adiposum  or  Symptomatic  Sclerema,  also  sometimes  called 
Scleroedema  or  (Edema  Neonatorum.    It  occurs  at  birth  or  shortly  after, 
not  later  than  six  months.     It  is  most  frequent  in  illegitimate   children, 
foundlings,  the  weak  and  premature,  and  in  those  of  women  who  have 
suffered  privation  during  pregnancy.     It  is  not  seen  in  children  of  the 
better  classes,  is  not  due  to  syphilis,  and  apparently  is  a  result  of  intra- 
uterine malnutrition,  or  the  solidification  of  subcutaneous  fat  on  account 
of  feebleness  and  rapid  loss  of  heat.     No"  less  than  three  cases  have  been 
reported  in  twins  during  the  last  few  years.    A  mild  type  is  not  very  rare 
in  Great  Britain.     It  is  confined  to  the  skin  and  subjacent  tissues,  may 
affect  normal  full-time  infants,  and  ends  in  recovery  at  about  6  months. 
The  severe  variety  is  more  prevalent  on  the  Continent,  in  the  weakly 
and    the    premature,    and    produces    serious    constitutional    symptoms, 
especially  in  the  alimentary,  respiratory   and  renal  organs.     It  is  charac- 
terised by  an  induration,  a  progressive  thickening  and  hardening  of  the 
skin  and  subcutaneous  tissues,  which  may  or  may  not  pit  on  pressure 
according  to  the  degree  of  infiltration.    The  parts  are  doughy  or  hard,  and 
may  be  painful  on  pressure  or  handling.    There  are  no  definite  histological 
changes.     The  induration  is  progressive,  but  does  not  involve  the  joints. 
It  may  be  limited  or  general,  in  patches  which  coalesce,  and  cause  general 
rigidity.     It  especially  affects    the    gluteal  regions,  legs  and  calves,  the 
deltoid  and  pectoral  regions,  the  back  and  back  of  the  neck,  the  cheeks, 
and  may  spread  on  to  the  abdomen.     The  chest  is  affected  late  or  not  at 
all ;    the  face  may  escape,  thus  enabling  the  babe  to  continue  suckling  ; 
the  penis,  scrotum,  palms  and  soles  are  unaffected.    The  child  is  generally 
badly  nourished,  weak  and  somnolent,  with  a  subnormal    temperature, 
even  down  to  85°  F.,  superficial  and  weak  breathing,  and  almost  inaudible 
cry  ;    and  dies  from  asthenia  or  coma,  occasionally  from  broncho-pneu- 
monia or  convulsions.    The  skin  feels  cold  and  is  adherent,  and  cannot  be 
raised  from  the  subjacent  tissues,  nor  these  from  those  below.    It  is  usually 
board-like,   smooth,   and  regular,   but  may  be  roughly  nodular,   with  a 
waxen,  yellowish,  red,  or  bluish  discolouration.     On  pressure  the  colour 
fades   to   white,   and  slowly  returns,   and  there  is  rarely  pitting.      The 
condition  has  been  aptly  compared  to  that  of  a  half  frozen  corpse  or  a 
flitch  of  bacon.    The  limbs  become  rigid  and  motionless,  and  the  face  mask- 
like.   Kespiration  and  circulation  are  feeble,  and  the  lips  blue.    There  is  no 
albuminuria.     Obstinate  constipation  has  been  ascribed  to  serous  infiltra- 
tion of  the  intestinal  mucosa.     The  prognosis  depends  upon  the    extent, 
the  general  condition  of  the  child,  and  the  temperature.    It  is  worst  if  the 
temperature  is  low  and  the  thorax  or  face  involved.     Atelectasis  is  often 


146  Chapter  XII. 

present.  Many  die  in  3  or  4  days,  but  a  few  have  recovered  (70  per  cent. 
Clementowsky).  In  mild  cases  extensions  may  take  place,  and  clear  np 
irregularly  and  continuously.  The  treatment  consists  in  the  use  of  an 
incubator,  systematic  hot  baths,  and  massage  with  olive  oil  or  a  weak 
mercurial  ointment. 

(Edema  Neonatorum  presents  the  ordinary  signs  of  cedema,  pits  on 
pressure,  and  affects  the  penis  and  scrotum.  It  is  due  to  debility,  cold,  and 
venous  congestion.  The  most  common  sites  are  the  dorsum  of  the  feet  and 
hands,  and  the  eyelids. 

Sclerema  Adiposum  or  Symptomatic  Sclerema  is  characterised  by  a 
stiffness  of  the  skin.  It  is  due  to  loss  of  fluid  from  the  body  in  prolonged 
illness,  acute  diarrhoea,  and  some  forms  of  pneumonia. 

H  Congenital  Pigmentation  of  the  Skin. — For  over  150  years  Japanese 
physicians  have  noted  that  the  infants  of  their  race  present,  at  or  soon  after 
birth,  one  or  more  bluish  pigment  patches,  darker  in  the  centre,  in  the 
sacro-gluteai  region  and  over  the  back.  They  vary  in  size,  and  may  be 
found  on  the  extensor  surfaces  of  the  extremities.  These  patches  disappear 
in  a  few  years,  and  rarely  persist  up  to  puberty  or  throughout  life.  They  are 
found  in  negroes,  and  in  many  Asiatic  races  of  mixed  descent,  and  have 
been  regarded  as  evidence  of  negroid  ancestry.  Similar  spots  were 
demonstrated  in  a  white  baby  by  A.  Edmunds  (1906),  and  have  been 
discovered  in  pure  German  infants.  Probably  they  represent  an  earlier 
stage  of  evolution,  or  an  atavistic  tendency.  They  are  more  marked  in 
males  than  females. 


Chapter  XIIL 

DISORDERS    OF    METABOLISM. 

Acholia — Lithcemia — Acidosis —  Delayed    Anaesthetic   Poisoning — 
Recurrent    Vomiting —  Diabetes — Scurvy. 

Acholia. — Under  the  name  of  "Coeliac  Disease"  or  Belly  Affection, 
Gee  (1888)  described  a  condition  in  infants  in  which  the  stools  contain 
little  or  no  bile.  Cheadle  (1903)  named  it  "  Acholia."  According  to  the 
degree  of  deficiency  in  bile,  the  stools  vary  from  pale  straw  colour,  clay 
colour,  dirty  grey  like  putty  or  porridge,  to  the  whiteness  of  white  paint  or 
pipe-clay.  They  are  much  the  same  as  those  seen  in  obstructive  jaundice, 
but  there  is  no  yellowness  of  the  skin  or  bilinuria.  They  are  acid  or  slightly 
alkaline  ;  glistening,  greasy  and  fatty  ;  often  frothy  ;  very  offensive  and 
larger  than  normal ;  and  slightly  loose,  or  like  a  mass  of  dirty  grey  or  white 
paint. 

The  size  of  the  stools  is  due  to  defective  absorption  ;  the  offensive 
odour  to  the  decomposition  of  excessive  fat ;  and  the  absence  of  bile  to 
deficient  secretion  of  bile,  or  to  lack  of  conversion  of  bilirubin  into  the 
hydrobilirubin  of  the  faeces,  from  occlusion  of  the  pancreatic  duct.  Most 
probably  it  is  due  to  deficiency  of  bile,  for  in  the  most  marked  cases  there 
are  no  bile  acids  in  the  stools.  Both  a  decrease  and  an  increase  of  the 
urea  and  leucin  have  been  found  in  the  urine.  No  definite  changes  are  seen 
after  death.  The  liver  is  normal  in  appearance  and  the  spleen  may  be 
enlarged. 

These  cases  occur  under  5  years  of  age,  usually  under  2.  Sometimes 
the  attacks  are  preceded  by  coldness  of  the  extremities,  and  can  be  warded 
off  by  keeping  them  warm.  There  may  be  a  little  fever  at  the  onset.  The 
child  is  irritable,  fretful,  languid,  flabby  and  pale.  The  appetite  fails, 
vomiting  is  not  uncommon,  and  the  stools  are  as  above  described.  The 
abdomen  is  full,  flaccid,  and  distended  by  gas.  Progressive  wasting  and 
a  subnormal  temperature  are  constantly  present.  The  course  is  chronic. 
It  is  liable  to  relapse  but  rarely  proves  fatal. 

The  causation  is  doubtful.  From  the  fact  that  it  is  apt  to  arise  during 
the  period  of  dentition,  it  has  been  ascribed  to  difficult  and  painful  teething, 
which  is  supposed  in  some  way  to  cause  reflex  irritation  of  the  liver. 
More  probably  it  is  due  to  chill  and  overfeeding. 


148  Chapter   XIII. 

The  chief  difficulty  in  diagnosis  is  its  similarity  to  abdominal  tuber- 
culosis. Some  undernourished  infants,  overfed  on  cow's  milk,  pass  almost 
white  stools.  These  are  not  acholic,  but  are  due  to  a  perversion  of  liver 
function.  Bilirubin  is  converted  into  a  colourless  urobilinogen  instead 
of  into  urobilin.  Urobilinogen  is  derived  from  hydrobilirubin  and  forms 
a  colourless  compound  in  an  alkaline  solution.  Possibly  this  is  the 
true  explanation  of  the  colour  of  the  stools  in  the  cases  described 
as  acholia. 

In  treating  these  cases  it  is  essential  to  reduce  the  work  of  the  liver 
and  digestion.  Fats  and  starches  must  be  given  in  small  quantities  only, 
and  predigested.  Milk  may  have  to  be  stopped.  Malted  foods  are  useful. 
For  looseness  of  the  bowels  give  bismuth  and  soda  ;  salol  and  sulphocar- 
bolates  for  offensive  smell ;  chloral  and  bromide  to  allay  nervous  irritation. 
As  hepatic  stimulants  give  brandy,  tincture  of  podophyllin,  sodium  sali- 
cylate, and  ammonium  chloride.  Glycocholate  of  sodium  may  be  tried 
as  bile  salts  stimulate  bile  secretion.  Small  doses  of  grey  powder  are  also 
useful;  and  iron  and  arsenic  during,  convalescence.  Cod-liver  oil  is 
generally  injurious,  and  the  seaside  rarely  beneficial. 

Lithaemia. — Lithseniia  is  a  common  functional  disorder  which 
probably  depends  on  disturbance  of  the  normal  activities  of  the  liver. 
No  one  name  is  absolutely  appropriate,  for  the  symptoms  are  due  to 
different  kinds  of  toxic  products,  resulting  from  the  defective  metabolism 
of  protein  in  several  organs  and  the  non-excretion  of  various  retrograde 
products.  It  is  called  Lithuria,  because  of  the  excessive  elimination  of 
urates  in  the  form  of  pink  amorphous  urates,  or  of  uric  acid  crystals  as  a 
brick-dust  deposit.  The  mere  precipitation  of  uric  acid  crystals  must 
not  by  itself  be  regarded  as  proof  of  excess  of  uric  acid,  for  it  is  often 
due  to  mere  concentration  of  the  urine.  This  is  indicated  by  high  specific 
gravity.  Lithuria  is  not  a  specific  disease,  nor  limited  to  disturbance  of 
liver  functions.  It  arises  from  a  variety  of  conditions  associated  with 
disturbance  of  nutrition.  Temporary  attacks  are  common,  and  may  be 
due  to  excessive  production  rather  than  abnormal  elimination. 

Lithaemia  is  common  in  children,  especially  those  of  a  gouty  or  neurotic 
constitution.  The  attacks  come  on  suddenly  after  errors  in  diet,  excess  of 
nitrogenous  food,  or  exposure  to  cold  winds.  Many  can  be  traced  to 
injudicious  feeding  on  rich  dishes  and  sweets ;  or  to  over-stimulation  of  the 
nervous  tissue  by  brain  fatigue,  amusements  and  late  hours.  Regular 
periodical  attacks  occur  in  some  children,  and  perhaps  explain  sick 
headache  and  migraine. 

The  child  is  fretful,  irritable,  and  complains  of  headache  and  languor. 
The  complexion  is  pale  and  sallow,  with  a  slightly  yellowish  tinge  and 
dark  rings  under  the  eyes.  The  tongue  is  furred  and  the  breath  offensive  ; 
the  appetite  variable,  capricious,  and  perhaps  excessive ;  the  bowels 
confined,  and  the  stools  deficient  in  bile. 


Disorders  of  Metabolism.  149 

The  treatment  consists  in  an  immediate  dose  of  calomel  or  grey 
powder,  followed  by  a  saline  purge  if  needful,  and  limitation  of  the  diet 
to  plain  easily  digested  food,  allowing  no  excess  of  sweets,  meat  or 
extractives.  Tea  and  coffee  must  be  forbidden,  and  alkaline  or  aerated 
waters  given  freely.  Occasional  small  doses  of  calomel  should  be  given 
for  2-4  weeks  ;  and  a  mixture  of  tincture  of  nux  vomica  with  bicarbonate 
of  soda  or  with  dilute  nitrohydrochloric  acid,  to  assist  digestion. 

Acidosis. —  Syn. :  Acidcemia  —  Acetonemia  —  Aciduria  —  Acetonuria 
—  Acid  Intoxication. — Acidosis  may  be  defined  as  an  abnormal  meta- 
bolism of  carbon  leading  to  the  appearance  of  organic  acids  in 
the  blood  and  urine,  and  the  formation  of  ammonia  to  neutralize 
these  acids.  The  normal  chemical  reaction  of  the  tissue  fluids  is 
faintly  alkaline,  because  the  basic  ions  slightly  exceed  the  acid  ones. 
In  acidosis  the  tissue  fluids  become  less  alkaline.  The  organic 
acids,  or  acetone  bodies,  are  diacetic  and  B-oxybutyric  acids,  and  are 
derived  from  fat  imperfectly  metabolised  in  the  liver  and  tissues. 
They  are  rapidly  neutralized  by  sodium  in  the  tissue  fluids,  potassium  in 
the  cells,  and  by  alkaline  earths  chiefly  derived  from  bones.  If  this  is  not 
enough,  the  excess  is  neutralized  by  ammonia,  derived  from  protein,  which 
would  normally  have  been  metabolised  into  urea.  Should  more  acid  be 
produced  than  can  be  thus  neutralized,  the  reaction  of  the  tissue  fluids 
may  be  altered  and  cause  symptoms  of  acid  intoxication.  It  is,  therefore, 
evident  that  acidosis  may  be  very  common,  though  acid  intoxication  is 
rare.  It  can  exist  long  before  the  tissue  fluids  are  rendered  less  alkaline, 
and  before  toxic  symptoms  arise.  One  passes  gradually  into  the  other. 
But  acetone  bodies  are  not  poisonous,  so  some  further  factor  must  be 
sought  for  to  account  for  acid  intoxication. 

The  diagnosis  of  acidosis. — An  excess  of  organic  acids,  not  normally 
present  in  the  urine,  is  excreted.  If  more  are  produced  than  can  be  neu- 
tralized, the  urine  is  hyperacid.  The  breath  and  urine  have  the  peculiar 
smell  of  acetone,  and  acetone  bodies  are  found  in  the  urine.  Acetone, 
diacetic  acid,  and  B-oxybutyric  acid  appear  consecutively  in  the  urine,  in 
accordance  with  the  increasing  failure  in  the  oxidation  powers  of  the 
tissues.  When  acetone  is  heated  to  100°  C,  it  is  split  up  into  diacetic  acid 
and  carbonic  acid.  Hence,  no  satisfactory  means  have  been  devised  for 
estimating  the  two  bodies  separately  in  the  urine.  Small  amounts  of  acetone 
in  the  urine  are  unimportant,  and  may  be  found  in  the  healthy.  Large 
amounts  and  the  presence  of  the  other  bodies  are  pathological. 

Tests  for  Acetonuria. — Add  10  drops  of  caustic  soda  solution  to  the  urine,  and 
20  drops  of  fresh  solution  of  sodium  nitroprusside.  A  bright  red  colour  is  produced. 
If  this  is  due  to  creatinin  it  is  discharged  by  adding  glacial  acetic  acid.  If  acetone 
is  present  the  colour  turns  dark  claret  or  purplish.  In  the  absence  of  creatinin, 
acetone  causes  a  carmine-like  colour,  becoming  purplish  on  adding  acetic  acid. 
With  ammonia,  instead  of  caustic  soda,  the  colour  varies  from  magenta  to 
deep  violet.  If  the  urine  is  boiled  first  the  acetone  and  diacetic  acid  are  volatilised 
and  driven  off,  so  the  colour  reactions  fail. 


150  Chapter   XIII. 

The  usual  test  for  diacetic  acid  is  the  addition  of  solution  of  perchloride  of 
iron,  which  changes  the  colour  of  the  urine  to  red  or  reddish  purple.  Salicyluric 
acid  causes  a  similar  colour  reaction,  but  it  is  not  prevented  by  boiling  the  urine. 

If  2  drachms  of  bicarbonate  of  soda  are  taken  by  a  normal  individual  the 
urine  becomes  alkaline  for  24  hours  or  so.  In  acidosis,  the  sodium  is  seized  on  by 
the  acid  radicles  and  passed  out  as  neutral  salts,  and  the  urine  remains  acid. 

Normally,  too,  the  ammonia-]Sr  in  the  urine  is  inconsiderable,  but  in  acidosis 
the  ammonia  excretion  is  much  increased. 

As  a  final  test,  the  reduction  in  the  alkalinity  of  the  blood  must  be  mentioned. 

Acetonuria  is  undoubted  evidence  of  acidosis.  It  does  not  occur 
until  the  acidosis  is  of  such  a  degree  that  the  acid  products  of  metabolism 
are  no  longer  fully  neutralized  before  excretion.  The  absence  of  acetonuria 
does  not  disprove  the  presence  of  acidosis,  but  it  is  unlikely  that  serious 
symptoms  of  acid  intoxication  can  occur  without  such  evidence.  Another 
point  of  some  importance  is  the  occurrence  of  variations  in  the  total 
acidosis  without  a  corresponding  change  in  the  colour  reactions  in  the  urine. 
The  Conditions  under  which  Acidosis  occurs. — It  is  more  common 
and  more  easily  produced  in  children  than  in  adults,  and  in  women  than 
in  men.  Acetone  may  appear  in  the  urine  in  the  apparently  healthy. 
It  is  regarded  as  a  constant  and  unimportant  constituent  in  children 
by  Baginsky.  Metabolism  is  less  stable,  and  the  reserve  of  carbohydrate 
in  the  liver  is  smaller. 

It  is  found  in  starvation  and  cachexia  ;  on  the  omission  of  carbo- 
hydrates from  the  diet ;  as  the  result  of  the  excessive  ingestion  of  fat ; 
in  pyrexial  states,  such  as  scarlatina,  pneumonia  and  broncho-pneumonia  ; 
in  severe  vomiting  and  diarrhoea,  gastro-intestinal  disorders,  epidemic 
diarrhoea,  appendicitis,  acute  peritonitis,  and  intestinal  obstruction ; 
in  eclampsia,  tuberculous  meningitis,  and  nervous  disturbance  due  to 
fright ;  in  poisoning  by  morphine,  salicylates,  phosphorus,  and  phloridzin  ; 
after  anaesthesia  ;  in  hepatic  inadequacy,  acute  yellow  atrophy,  recurrent 
vomiting,  and  diabetes.  Acetonuria  must  be  regarded  as  a  sign  of  faulty 
metabolism.    It  may  be  acute  or  chronic. 

In  considering  the  above  causes  it  is  obvious  that  one  or  more  factors 
in  the  production  of  acidosis  may  be  present  in  the  particular  case.  The 
deficient  oxidation  in  pneumonia,  the  auto-intoxication  of  intestinal 
disorders,  the  toxaemia  of  scarlatina,  sepsis  and  appendicitis,  and  the 
delayed  oxidation  and  fatty  changes  the  result  of  poisons  may  all  be 
invoked  as  explanations  of  the  acidosis.  On  the  whole  our  present  know- 
ledge indicates  that  it  is  due  to  : — 

(1)  An  excess  of  fat  in  the  diet,  or  a  superfatted  liver  with  hepatic 

inadequacy  in  the  metabolism  of  fat  and  carbohydrates.  A 
fatty  liver  may  be  due  to  excess  of  carbohydrate  food,  or  to 
infiltration  with  unsaturated  fats  which  are  fully  oxidised  in  the 
muscles  and  tissues. 

(2)  A  deficiency  of,  or  inability  to  make  use  of,   carbohydrates  in 

the  diet. 


Disorders  of  Metabolism.  151 

(3)  The  effect  of  toxins  or  other  poisons  on  the  metabolism  of  the 
liver,  which  may  or  may  not  be  overloaded  with  fat.  This  is 
the  most  general  explanation. 

Acetonuria  may  occur  without  symptoms.  Acid  intoxication  is 
commonly  a  complication  of  other  diseases,  and  occasionally  occurs 
independently,  as  in  delayed  anaesthetic  poisoning  and  recurrent  vomiting. 

The  Pathogenesis  of  Acidosis. — Acetonuria  is  increased  by  the 
addition  of  lower  fatty  acids,  and  fat  to  a  less  extent,  to  the  diet.  It  is 
decreased  by  adding  protein  and  abolished  by  adding  carbohydrates, 
for  they  act  as  fat-sparers,  reduce  the  amount  of  fat  used,  and  aid  its 
complete  metabolism.  Acetone  is  due  to  the  incomplete  combustion 
of  fat  into  carbonic  acid  and  water.  Diacetic  acid  is  a  combination  of 
acetone  and  carbonic  acid,  and  on  deoxygenation  forms  B-oxybutyric 
acid.  Acetone  can  be  formed  from  gelatin,  leucin,  and  albumin  in  vitro. 
Possibly  it  can  be  formed  in  the  body  to  a  limited  extent  from  protein,  but 
the  amount  cannot  be  much  for  the  nitrogen  and  sulphur  are  not  increased 
in  the  urine  to  the  extent  which  would  be  the  case  if  this  were  the  source. 

Carbon  leaves  the  body  as  carbonic  acid,  neutral  salts,  or  combined 
with  nitrogen  in  the  urine.  Abnormally  it  may  appear  in  the  urine  un- 
combined  with  nitrogen,  as  sugar  ;  that  is,  unkatabolised.  Or  it  is  abnor- 
mally katabolised,  and  appears  as  acetone. 

The  complete  combustion  of  fat  appears  to  be  dependent  on  an 
adequate  simultaneous  consumption  of  carbohydrate  to  supply  the 
necessary  oxygen.  A  deficiency  of  carbohydrate  alone  may  be  sufficient 
to  cause  defective  oxidation  and  metabolism  of  fat,  and  acidosis.  This 
may  account  for  the  acidosis  in  all  states  of  starvation ;  and  in  diabetes, 
in  which  must  be  considered  in  addition  the  effects  of  an  excess  of  fat 
in  the  diet,  possibly  some  deficiency  in  the  oxidising  power  of  the  body 
cells,  and  perhaps  some  breaking  down  of  protein  as  well. 

Alkaline  soaps  are  formed  in  the  intestines  from  fat  in  the  food. 
If  an  excess  of  fat  is  ingested,  alkalies,  which  would  otherwise  reach  the 
tissues,  are  used  up  in  the  intestine,  and  are  consequently  not  available 
for  the  neutralization  of  the  inorganic  acid  end-products  of  metabolism. 
Under  such  circumstances  the  alkalies  in  the  cells,  tissue  fluids  and  bones 
are  utilised  as  far  as  possible.  Finally,  ammonia  is  formed  to  neutralize 
these  end-products,  and  appears  in  excess  in  the  urine.  Thus,  an  excess 
of  fat  in  the  diet  does  not  lead  to  an  abnormal  production  of  organic  acids 
in  the  body,  but  does  cause  an  excessive  loss  of  alkaline  bases  by  the 
intestinal  tract  in  the  form  of  soaps,  sometimes  in  such  excess  as  to  reduce 
the  alkali  balance  of  the  body. 

The  normal  ammonia  excretion  in  the  urine  is  about  5  per  cent.,  but 
in  sick  children  it  may  reach  30-50  per  cent,  of  the  total  N-excretion. 
It  can  be  increased  by  adding  fat  to  the  diet.  Such  an  increase  can  be 
reduced  to  nil  by  the  reduction  of  fat  ingested,  and  the  administration  of 


152  Chapter  XIII. 

sodium  bicarbonate,  and  other  alkaline  bases.  Folin  found  it  increased 
on  a  diet  of  starch  and  cream,  an  excess  of  inorganic  acids  being  ingested. 
The  ammonia  excretion  is  also  increased  if  the  patient  has  to  live  on  the 
protein  and  fat  in  the  tissues,  as  in  severe  vomiting  and  diarrhoea,  the 
toxaemic  vomiting  of  pregnancy,  starvation  of  various  kinds,  and  lack 
of  carbohydrate  food.  The  increased  excretion  is  due  to  the  fact  that  the 
body  has  to  manufacture  ammonia  to  neutralize  the  acid  end-products  of 
metabolism,  which  are  normally  neutralized  by  alkaline  bases.  If  there 
is  sufficient  alkali  available  the  ammonia  is  converted  into  urea.  Most 
of  these  acid  end-products  are  organic  acids.  Some  are  formed  by  the 
oxidation  of  phosphorus  or  sulphur  from  broken  down  protein. 

Excess  of  fat  in  the  diet  causes  Fat  Diarrhoea,  a  relative  increase  in 
the  amount  of  neutral  fat  in  the  faeces.  It  gives  rise  to  increased  soap 
formation,  and  the  withdrawal  of  alkalies  and  earthy  salts.  Lime  salts 
and  alkalies  are  also  found  in  excess  in  the  faeces  during  fever.  In  acid 
dyspepsia  an  excess  of  free  fatty  acid  is  found  in  the  faeces.  And,  finally, 
it  increases  the  ammonia  in  the  urine,  an  increase  which  disappears  on  the 
exclusion  of  fat  from  the  diet. 

We  are  justified  in  concluding  that  a  relative  acidosis  may  be  simply 
the  result  of  an  excess  of  fat  in  the  diet,  in  consequence  of  an  excessive 
loss  of  alkaline  bases  by  the  alimentary  canal,  without  an  abnormal  pro- 
duction of  organic  acids  in  the  body.  The  extent  of  the  ammonia  excretion 
is  a  measure  of  the  degree  of  acidosis.  A  high  ammonia  excretion  may  be 
due  to  an  insufficient  intake  of  fixed  bases,  and  is  then  cured  by  giving 
bicarbonate  of  soda. 

The  Liver  and  Acidosis. — The  appearance  of  ammonia  in  the  urine 
is  not  due  to  any  diminution  of  the  urea-forming  function  of  the  liver. 
Even  very  sick  children  can  convert  ammonia  salts  into  urea.  In  some 
cases  degeneration  of  the  liver  is  present.  Richardson  and  Howland  have 
brought  forward  evidence  that  in  recurrent  vomiting  there  is  a  deficiency 
in  the  oxidising  power  of  the  liver  and  body  cells.  In  post-anaesthetic  cases, 
and  those  of  recurrent  vomiting,  the  most  striking  anatomical  feature  is 
the  superfatted  liver.  The  heart  and  kidneys  are  also  fatty.  A  liver  may 
be  intensely  fatty  without  evidence  of  disturbed  function  ;  but  acidosis 
and  acid  intoxication  may  occur.  The  metabolism  of  fat  is  an  important 
function  of  the  liver. 

A  superfatted  liver  results  from  various  causes  : — 

(1)  An  actual  excess  of  fatty  food  ;    or  a  relative  excess  and  defect 

in  the  capacity  to  metabolise  fat. 

(2)  An  excess  of  carbohydrates  ;   or  a  relative  excess  and  defect  in  the 

capacity  to  metabolise  carbohydrates,  e.g.,  recurrent  vomiting. 

(3)  Deprivation  of  carbohydrates,  as  in  starvation.    The  fat  is  carried 

from  the  other  tissues  to  the  liver  in  order  to  be  elaborated  for 
oxidation  and  utilization  in  the  system  generally. 


Disorders  of  Metabolism.  153 

(4)  Sepsis,   specific  organisms  and  toxins,   poisons  and  anesthetics. 
These  lead  to  further  overloading  of  the  liver  and  check  oxidation. 

The  storage  of  fat  may  be  absolute  or  relative  to  the  metabolic  powers 
of  the  tissues,  or  due  to  the  mobilisation  of  fat  in  the  liver  as  the  result  of 
starvation  or  auto-intoxication.  It  probably  precedes  acidosis  and  acid 
intoxication.  The  characteristic  liver  is  found  in  post-anaesthetic  cases 
and  in  recurrent  vomiting.  Possibly  it  is  the  effect,  and  not  the  cause,  for  a 
great  accumulation  of  fat  in  the  liver  can  appear  and  disappear  with 
remarkable  rapidity,  in  a  few  days  or  hours,  certainly  within  24  hours. 
But  it  is  difficult  to  believe  that  such  a  profound  change  could  be  produced 
by  half  a  drachm  of  chloroform,  as  seen  in  some  anaesthetic  cases. 

Probably  the  fatty  liver  is  only  dangerous  as  a  predisposing  cause, 
in  that  it  implies  defective  metabolism  and  oxidation.  Then  a  further 
perversion  causes  imperfect  oxidation  and  toxaemia  due  to  the  breaking 
down  of  all  the  hepatic  functions,  proteolytic,  glycogenic,  and  antitoxic. 
On  the  other  hand,  a  very  small  portion  of  normal  liver  seems  to  be  sufficient 
to  carry  on  its  functions.  In  the  post-anaesthetic  cases  the  drug  must  be 
regarded  as  the  last  straw.  It  has  been  shown  experimentally  that  chloro- 
form, and  ether  to  a  less  extent,  increase  the  fat  in  the  liver  of  dogs,  and 
that  the  heart  and  kidneys  are  also  affected  through  autolysis. 

Acetone  bodies  are  found  in  the  urine  and  stomach  for  some  hours 
after  prolonged  anaesthesia.  The  severe  vomiting  is  probably  due  to  acidosis, 
and  may  be  relieved  by  bicarbonate  of  soda  by  mouth  or  lavage  of  the 
stomach  therewith.  Such  vomiting  exaggerates  the  symptoms,  for  severe 
vomiting  aggravates  acidosis,  causes  serious  loss  of  fluid,  and  disposes  to 
acute  degeneration  of  the  liver.  Thus,  acute  yellow  atrophy  and  severe 
vomiting,  with  increased  ammonia  excretion,  may  occur  in  pregnancy. 
In  anaesthesia  oxidation  is  checked  by  the  preliminary  starvation,  enforced 
rest,  mental  disturbance,  narcosis,  and  the  anaesthetic.  It  may,  therefore, 
be  argued  that  the  post-anaesthetic  cases  are  true  cases  of  anaesthetic 
poisoning,  or  that  they  are  due  to  acid  intoxication  in  a  predisposed  child, 
the  anaesthetic  acting  as  the  final  straw. 

Thus,  there  are  two  definitely  associated  factors,  viz.,  a  morbid  state 
of  the  liver,  a  fatty  infiltration  with  sometimes  areas  of  necrosis,  and 
manifestations  of  acid  intoxication.  Both  the  fatty  liver  and  acidosis  may 
occur  independently  of  toxic  symptoms,  and  the  state  of  the  liver  may 
precede  or  be  secondary  to  the  acidosis. 

Acid  Intoxication. — Acetone  bodies  are  not  poisonous,  so  we  must 
seek  for  some  additional  factor  as  the  cause  of  the  symptoms  of  poisoning. 
Probably  fatty  acid  intoxication  alone  cannot  cause  death. 

It  is  not  due  to  an  insufficient  supply  of  alkaline  bases  to  neutralize 
the  acids  formed,  for  the  alkalinity  of  the  blood  may  be  even  lower  than 
in  diabetic  coma  without  any  of  the  symptoms  of  intoxication  (Benedikt). 
It  must  not  be  ascribed  to  personal  idiosyncrasy,  for  in  anaesthetic  cases 


154  Chapter  XIII. 

a  similar  anaesthetic  may  have  been  taken  previously  without  ill  effect. 
There  is  no  evidence  of  poisoning  by  carbonic  acid.  Diabetic  coma  can  be 
produced  by  the  abrupt  omission  of  carbohydrates  from  the  diet  and 
stayed  by  administering  them,  but  the  clinical  evidence  in  post-ansesthetic 
cases  does  not  support  the  theory  of  carbohydrate  starvation. 

Eustace  Smith  has  described  as  "  food  fever "  cases  of  recurrent 
pyrexia,  vomiting  and  gastro-intestinal  disturbance.  He  regards  chill  as 
an  exciting  cause,  and  ascribes  them  to  an  excess  of  carbohydrate  food, 
fermentation,  gastro-intestinal  catarrh,  and  intestinal  auto-intoxication. 
In  some  respects  they  are  analogous  to  cyclical  vomiting.  Many  children 
with  this  latter  affection  crave  for  and  eat  much  carbohydrate  food  ; 
possibly  because  of  their  inability  to  make  use  of  it.  An  excessive  fattening 
diet,  cod-liver  oil  and  such  like,  produces  an  intensely  fatty  liver,  something 
like  foie  gras.  The  defect  may  be  a  hepatic  inadequacy  to  deal  with  more 
than  a  small  amount  of  carbohydrate  or  fat.  Some  cases  are  cured  by  a 
simple  mixed  diet. 

In  the  ansesthetic  cases  it  is  possible  that  the  culminating  effect  is  due 
to  the  destruction  of  oxidising  enzymes  in  the  liver.  Possibly  the  additional 
factor  is  a  toxsemia  of  intestinal  origin  or  due  to  the  autolysis  of  liver 
cells.  In  cyclical  vomiting  Howland  and  Richards  found  excessive 
indicanuria,  increased  excretion  of  uric  acid,  especially  at  the  onset ; 
decrease  in  the  excretion  of  sulphuric  acid,  and  increase  in  that  of  unoxidised 
sulphur  ;  and  acidosis.  The  excess  of  uric  acid  could  not  be  due  to  excess 
of  exogenous  purins,  and  must  consequently  be  due  to  deficient  oxidation 
of  endogenous  ones,  which  are  normally  oxidised  to  the  extent  of  50  per  cent, 
in  the  body.  It,  therefore,  showed  increased  tissue  destruction.  The 
excess  of  unoxidised  sulphur  is  further  evidence  of  deficient  oxidation. 
Lactic  acid  was  also  found  in  the  one  instance  in  which  it  was  sought 
for.  It  is  an  intermediate  product  in  the  combustion  of  dextrose,  and 
its  presence  was  additional  evidence  of  deficient  oxidation. 

The  excess  of  indican  showed  increased  intestinal  putrefaction.  Indol 
is  oxidised  into  indoxyl,  and  this  combines  with  sulphuric  acid  to  form 
indoxyl-sulphate  or  indican.  Skatol  is  a  methyl-indol  formed  in  an 
analogous  manner.  Phenol  combines  directly  with  the  sulphuric  acid.  By 
experiments  on  animals  these  observers  obtained  some  interesting  results. 
Decreasing  the  ability  of  the  cells  to  utilise  oxygen,  by  inhalation  of 
chloroform  or  injection  of  potassium  cyanide,  and  giving  measured  doses 
of  indol  and  phenol,  they  found  that  the  non-toxic  indol  and  phenol  became 
toxic,  or  if  toxic  were  much  increased  in  virulence.  Marked  gastro- 
intestinal congestion  and  necrosis,  and  degeneration  of  the  liver  were 
produced  in  dogs.  Hence  under  conditions  of  imperfect  oxidation,  indol, 
and  probably  skatol  and  cresols,  become  toxic.  Constipation  is  a  factor 
in  so  far  as  it  increases  absorption.  It  must  be  mentioned  that  hydro- 
cyanic acid  interferes  with  ferment  action,  and  might  be  the  cause  of  some 
of  the  results. 


Disorders  of  Metabolism.  155 

Symptoms. — Although  involving  a  certain  amount  of  repetition,  for 
the  symptoms  ascribed  to  acid  intoxication  occur  in  several  affections 
described  subsequently,  it  is  advisable  to  give  a  concise  summary.  Vomiting 
is  incessant,  sometimes  haemorrhagic  or  coffee-ground  in  character.  It  may 
occur  without  nausea,  or  there  may  be  nausea  and  excessive  retching. 
Intense  thirst,  constipation  or  diarrhoea,  and  some  degree  of  epigastric 
pain  and  tenderness  are  present.  Sometimes  there  is  slight  jaundice, 
usually  towards  the  end.  Air-hunger,  restlessness  and  sleeplessness  are 
noticeable.  Irritability  alternates  with  dulness  and  apathy.  Prostration 
is  great  and  emaciation  rapid.  Delirium  and  convulsions,  or  drowsiness 
and  coma  end  the  scene.    Or  attacks  of  collapse,  perhaps  fatal,  ensue. 

The  eyes  are  bright  and  sunken,  the  face  pinched  and  drawn,  and  pale 
or  flushed  in  early  stages.  The  breath  smells  of  acetone.  The  tongue  is 
often  clean  at  first,  and  later  becomes  dry  and  furred  ;  the  mouth  being 
dry  and  covered  with  viscid  mucus.  The  skin  is  dry  and  inelastic.  Occasion- 
ally measliform,  urticarial,  or  purpuric  rashes  develop.  The  abdomen, 
and  sometimes  the  head,  is  retracted.  The  pulse  is  rapid,  weak,  and  apt 
to  be  intermittent  or  irregular.  The  temperature  may  be  normal,  but 
more  usually  is  raised,  seldom  above  102°  F.  Occasionally  there  is 
hyperpyrexia.  Acetonuria  is  not  invariable,  for  the  acetone  bodies  may  not 
be  eliminated  by  the  kidneys  in  some  of  the  anaesthetic  cases  and  early 
stages  of  recurrent  vomiting.  In  diabetes  they  may  decrease  before  the 
onset  of  coma.  Urea  excretion  is  variable,  usually  decreased,  while  the 
ammonia-N  is  increased.  It  is  noteworthy  that  the  symptoms  of  post- 
anaesthetic  cases  resemble  those  of  acute  yellow  atrophy,  and  that  acute 
yellow  atrophy  is  an  occasional  cause  of  death  after  operation.  Generally 
the  liver  shows  extensive  fatty  infiltration. 

Treatment. — Encourage  excretion  by  diuretics,  diaphoretics  and 
purgatives,  if  they  can  be  retained.  Wash  out  the  stomach  and  put  in  sugar 
solution.  Saline  injections  are  useful.  Give  fluids  freely.  Omit  fat  from 
the  diet.  Try  rectal  feeding.  Caffein,  ammonia  and  strychnia  are  the 
best  stimulants.  Alkalies  are  given  freely,  up  to  180  grs.  of  bicarbonate 
of  soda  daily,  in  order  to  relieve  the  strain  on  the  ammonia  compensation 
for  acidosis.  If  they  are  not  retained  by  mouth  give  them  with  salt  by 
rectum.  Experience  has  shown  that  they  are  not  of  much  value,  unless 
the  supply  of  base  to  neutralize  the  acids  has  failed.  If  the  cause  is  toxic, 
an  autolysis  of  liver  cells  leading  to  defective  protein  metabolism,  alkalies 
are  unlikely  to  do  good.  The  cells  can  utilise  carbohydrates  well,  but 
oxidise  protein  badly  and  fat  even  less.  On  the  assumption  that  the 
carbohydrates  have  been  used  up  and  a  state  of  starvation  is  produced, 
it  is  worth  while  to  give  dextrose  freely. 

Delayed  Anaesthetic  Poisoning. — Syn.  ;  Delayed  Chloroform  Poison- 
ing—  Fatty  Liver  and  Death  after  Anaesthesia. — It  is  to  Guthrie 
that  the  credit  is  due  of  establishing  the  connection  between 
anaesthetics,    fatty   infiltration   of    the    liver,    acidosis,    and    the    severe 


156  Chapter   XIII. 

or  fatal  illness  which  sometimes  ensues  on  the  administration  of 
anaesthetics  to  apparently  healthy  children.  His  first  paper  was  published 
in  the  Lancet  in  1894.  As  long  ago  as  1850  Caspar  suggested  it  as  a  cause 
of  death,  and  Langenbeck  found  a  fatty  liver  in  a  fatal  case.  Three  cases 
were  reported  by  Bastianelli,  and  one  by  Thiem  and  Fischer,  in  1890. 
Fraenkel  investigated  five  in  1892.  Now  there  are  quite  a  hundred  on 
record. 

Most  of  the  cases  have  followed  the  administration  of  chloroform.  A 
few  have  been  due  to  ether,  ethyl  chloride,  and  nitrous  oxide.  The 
halogen  group  is  present  in  both  chloroform  and  ethyl  chloride.  The 
amount  of  the  anaesthetic  and  the  duration  of  the  operation  seem  to  have 
little  bearing  on  the  production  of  the  affection  or  the  degree  of  acetonuria. 
Patients  have  developed  it  after  less  than  two  drachms  of  chloroform  in 
an  operation  lasting  seven  minutes,  and  after  ethyl  chloride  and  the 
removal  of  adenoids  in  about  a  minute. 

The  patient  may  seem  to  have  quite  recovered  from  the  anaesthetic. 
Then  in  about  12  hours,  or  at  any  rate  within  36  hours,  the  child  becomes 
restless,  tosses  about,  struggles,  grinds  its  teeth  and  utters  piercing  shrieks. 
It  is  pale  or  flushed,  looks  anxious  or  terrified  and  has  bright  red  lips, 
which  may  become  cyanotic  later.  The  pupils  are  often  dilated,  some- 
times unequal,  sometimes  small.  The  pulse  is  frequent  and  breathing 
accelerated.  The  breath  smells  of  acetone.  Vomiting  is  almost  invariable, 
frequent,  copious  and  continuous.  The  vomitus  sooner  or  later  resembles 
coffee  grounds  or  the  dregs  of  beef  tea,  or  may  be  quite  black.  Thirst  is 
sometimes  intense. 

Or  the  onset  may  be  characterised  by  drowsiness  and  apathy.  In 
some  instances  vomiting  and  restlessness  are  the  only  symptoms  throughout. 
The  cerebral  symptoms  may  take  the  form  of  maniacal  delirium,  much 
like  that  of  acute  yellow  atrophy  of  the  liver.  They  may  be  suggestive 
of  acute  meningitis  or  diabetic  coma.  Apathy  and  delirium  may  alternate. 
Consciousness  is  generally  lost  early  and  remains  absent.  Occasionally 
it  returns  in  intervals  of  apathy  and  dulness. 

Incontinence  or  retention  and  partial  anuria  occur,  with  acetonuria, 
albumin  and  casts.  The  chance  of  recovery  is  less  in  the  absence  of 
acetonuria.  Headache  and  pain  are  absent ;  or  there  may  be  slight  epi- 
gastric tenderness  due  to  the  vomiting.  The  temperature  varies  from 
normal  to  hyperpyrexia,  and  is  usually  irregular.  Air-hunger  and  cyanosis 
are  frequent.    Jaundice  and  haemorrhage  into  the  lungs  have  been  reported. 

The  pulse  becomes  frequent,  running  and  uncountable.  Vomiting 
becomes  less  frequent  and  often  ceases.  Unconsciousness  passes  into 
coma.  The  circulation  and  breathing  gradually. fail.  Death  ensues  from 
asthenia,  and  sudden  or  gradual  cardiac  or  respiratory  failure,  perhaps 
during  an  attack  of  black  vomiting.  Consciousness  may  persist  until  the 
end. 


Disorders  of  Metabolism.  157 

Death  commonly  takes  place  in  24-48  hours  after  operation  ;  in  one 
case  not  until  after  8  days.  Even  severe  attacks,  with  much  haemorrhagic 
vomiting,  may  be  recovered  from. 

Morbid  Anatomy. — The  liver  is  generally,  but  not  necessarily,  enlarged. 
Its  colour  is  a  pale  uniform  fawn,  buff  or  canary  yellow,  studded  with 
purplish  spots  due  to  the  intralobular  veins.  The  capsule  is  not  thickened. 
Its  substance  is  firm  and  brittle,  and  much  oil  can  be  scraped  from  the 
surface  on  section.  The  whole  organ  is  affected,  and  shows,  microscopically, 
an  extensive  fatty  degeneration  and  infiltration.  The  colour  is  due  to 
the  excess  of  fat  and  not  to  bile  staining  of  necrotic  liver  tissue,  such  as  is 
seen  in  acute  yellow  atrophy  and  after  phosphorus  poisoning,  in  which 
the  amount  of  fat  is  diminished.  Cloudy  or  fatty  degeneration  is  also 
found  in  the  kidneys,  heart,  muscles  and  gastric  mucosa.  The  fatty 
degeneration  may  be  more  marked  in  the  kidneys  than  the  liver.  Most 
of  these  changes  have  been  found  after  chloroform  anaesthesia,  but  they 
may  be  due  to  other  anaesthetics. 

Pathogenesis. — It  has  been  stated  that  acidosis  is  common  in  children  ; 
that  it  is  frequently  present  after  anaesthesia  and  may  account  for  the 
after-vomiting  ;  and  that  it  is  often  associated  with  a  fatty  liver.  A  similar 
fatty  change  can  be  produced  experimentally  in  animals  by  chloroform, 
and  to  a  less  extent  by  ether.  Even  admitting  that  a  fatty  liver  can  be 
thus  produced,  the  fatal  cases,  after  the  short  period  of  anaesthesia  induced 
by  ethyl  chloride  and  nitrous  oxide  gas,  suggest  that  the  fatty  change  is 
not  due  to  the  drug.  Sepsis  is  a  cause  of  extremely  fatty  liver,  and  many 
of  the  cases  have  occurred  after  operations  for  septic  conditions. 

Probably  there  is  a  pre-existent  fatty  liver,  functionally  inadequate 
or  on  the  verge  of  inadequacy,  and  the  action  of  the  anaesthetic,  combined 
with  the  effects  of  preparation  for  the  operation  and  the  shock  thereof, 
proves  the  last  straw.  The  excretory  power  of  the  liver  and  kidneys  is 
decreased  by  the  anaesthetic  ;  more  by  chloroform  than  by  ether.  Though 
there  may  be  acid  intoxication,  it  is  probable  that  the  fatal  factor  is  a 
toxaemia  dependent  on  disturbance  of  the  proteolytic  and  antitoxic  functions 
of  the  liver,  for  the  symptoms  are  more  suggestive  of  acute  yellow  atrophy 
than  of  diabetic  coma. 

The  excretion  of  acetone  depends  on  idiosyncrasy,  its  previous  existence 
in  the  urine,  and  the  nature  of  the  anaesthetic.  Sepsis,  constipation  and 
nephritis  delay  excretion.  In  chronic  acetonuria  the  excretory  organs 
are  trained  in  its  elimination.  Acute  acetonuria,  such  as  is  developed  in 
acute  infective  conditions,  e.g.,  appendicitis,  is  much  more  dangerous. 
Chloroform  hinders  its  excretion  more  than  ether.  Both  drugs  induce  an 
acute  temporary  acetonuria,  which  may  be  fatal  if  the  excretion  is  deficient. 
Yet,  up  to  the  present,  it  is  not  certain  that  the  acid  intoxication  is  the 
cause  of  the  symptoms.  The  signs  thereof  in  the  urine  may  have  to  be 
regarded  merely  as  indicative  of  inadequacy  of  the  liver,  and  that  autolysis 


158  Chapter  XIII. 

of  the  liver  is  actively  proceeding.  On  the  other  hand,  it  is  not  absolutely 
proved  that  the  fatty  changes  in  the  liver  are  the  primary  cause.  Such 
changes  are  more  common  in  chronic  suppurations  and  tuberculosis  than 
in  acute  suppurations,  and  one  would  expect  delayed  anaesthetic  poisoning 
to  be  more  common  in  these  cases  if  the  fatty  liver  is  to  blame.  Experience 
does  not  confirm  this  expectation.  It  is  quite  possible  that  the  fatty 
change  can  be  accounted  for  by  the  action  of  an  anaesthetic,  even  in  small 
doses  though  sufficient  to  produce  anaesthesia,  on  tissues  predisposed  to 
acute  fatty  degeneration  by  some  form  of  toxaemia. 

In  the  diagnosis  it  is  important  to  exclude  fat  embolism,  acute  yellow 
atrophy,  acute  septic  intoxication  and  poisoning  by  antiseptics,  notably 
carbolic  acid  and  iodoform,  causes  to  which  the  affection  has  been  ascribed 
in  the  past. 

Treatment  is  essentially  prophylactic.  Highly  neurotic  and  fat 
children  are  most  liable.  So,  too,  those  who  are  subject  to  bilious  attacks 
or  acute  gastric  catarrh.  Examine  the  child  for  fatty  liver  and  acetonuria, 
and  do  not  give  chloroform  if  either  of  these  conditions  is  present.  No 
anaesthetic  should  be  permitted  during  acute  acetonuria  ;  ether  should  be 
used  by  preference  in  acute  infective  states.  In  preparing  a  child  for 
operation  reduce  or  omit  the  fat  in  the  diet,  and  protect  from  fright  and 
mental  anxiety. 

Once  the  symptoms  have  arisen  the  treatment  is  that  of  acid 
intoxication. 

Recurrent  Vomiting. — Syn.  :  Fitful,  Cyclical,  or  Periodic  Vomiting — 
Lithasmic  or  Bilious  Vomiting — Vomiting  with  Acetonemia  (Marfan) — 
Migrainous  Gastric  Neurosis  (Rachford). — Occasionally  cases  of  recurrent 
vomiting  are  seen.  They  are  not  due  to  mechanical  causes,  nor 
associated  with  dietetic  errors,  nor  with  abdominal  pain  beyond  what  is 
due  to  the  strain  of  the  vomiting.  Often  these  children  are  fed  with  an 
excess  of  caution. 

Lombard  described  the  affection  in  1861.  Gee  reported  some  cases  in 
1882  under  the  title  of  "  Fitful  and  Kecurrent  Vomiting."  Leyden  in  the 
same  year  described  it  as  periodic  vomiting. 

Etiology. — It  is  most  common  among  nervous,  highly-strung,  precocious 
children  of  the  upper  classes,  with  a  hereditary  history  of  neuroses,  gout 
or  migraine.  Occasionally  it  affects  several  children  in  the  family.  It  is 
rather  more  common  in  girls  than  boys,  and  in  the  winter  months.  The 
most  common  age  is  the  sixth  to  the  eighth  year,  but  it  may  have  begun 
much  earlier.  Eachford  states  that  in  one  instance  it  began  in  the  third 
month  of  life.  Certainly  it  may  occur  in  the  first  year,  and  persist  up  to 
puberty.  As  a  rule  it  does  not  begin  before  the  third  year  or  after  the 
sixth.  Indoor  life,  constipation,  excitement,  overwork  and  fatigue  are 
both  predisposing  and  exciting  causes.    Overeating  and  fright  are  excitants. 


Disorders  of  Metabolism.  159 

Symptoms. — There  may  be  a  prodromal  period  characterised  by 
anorexia,  offensive  breath,  furred  tongue,  nausea,  gastric  discomfort  and 
constipation  ;  dark  rings  under  the  eyes  and  sallow  complexion  ;  malaise 
and  headache ;  lassitude  and  sleepiness,  or  nervous  irritability  with 
twitching  of  the  eyelids,  stammering,  restlessness,  and  sleeplessness ; 
dyspnoea  and  sighing  respirations,  and  fever.  Some  attacks  are  preceded 
by  the  passage  of  almost  white  stools  or  by  watery  diarrhoea.  A  few  have 
been  ushered  in  by  convulsions.  More  commonly  in  the  midst  of  perfect 
health,  even  while  in  bed  and  asleep,  without  any  definite  exciting  cause, 
without  any  error  in  diet  or  disturbance  of  intestinal  action,  the  child 
is  suddenly  seized  with  vomiting.  Nothing  is  kept  down,  not  even  water. 
Food,  acid,  mucus,  bile  and  possibly  blood  (bright  red  or  coffee-ground 
material)  are  brought  up.  Snow  reported  an  excess  of  free  hydrochloric 
acid  and  mucus,  apparently  pure  gastric  juice,  in  four  cases.  The  vomiting- 
is  frequent,  perhaps  every  quarter  of  an  hour  for  twelve  hours,  projectile, 
without  any  special  nausea,  and  does  not  become  fsecal.  It  may  be  accom- 
panied or  replaced  by  severe  retching.  Perhaps  there  is  a  burning  pain 
in  the  epigastrium,  or  a  "  nasty  "  substernal  pain. 

The  breath  smells  of  acetone,  or  may  be  offensive.  The  tongue  is 
clean,  or  more  or  less  coated.  Thirst  is  sometimes  present  and  intense,  the 
lips  being  dry,  and  the  tongue  parched  and  cracked.  The  eyes  rapidly 
become  sunken,  expression  anxious,  and  the  prostration  great.  Wasting 
is  rapid  and  extreme  ;  the  abdomen  cariniform,  retracted,  and  markedly 
hollowed.  A  girl  of  11  years  weighed  only  24  J  lbs.  (Shaw  and  Tribe). 
Undue  pigmentation  has  been  noted.  The  appetite  may  be  retained,  or 
there  may  be  complete  anorexia.  Sometimes  there  is  a  little  epigastric 
pain  and  tenderness.  Constipation  may  resist  all  treatment  and,  when  the 
bowels  are  moved,  the  stools  are  very  offensive.  The  breathing  is  of  the 
air-hunger  type,  sighing,  or  rapid  and  panting.  The  pulse  is  generally  rapid, 
weak  and  irregular  ;   sometimes  slow,  weak  and  intermittent. 

Fever  may  be  present  during  the  prodromal  stage,  if  any.  The 
temperature  is  usually  raised  at  the  onset  and  during  active  vomiting. 
It  reaches  to  102-103°  F.,  but  may  be  up  to  105°  F.  Hyperpyrexia  has 
occurred  at  the  termination  of  fatal  cases  (Langmead). 

Generally  there  is  great  restlessness,  but  the  mind  is  clear.  Sometimes 
there  is  delirium.  Fatal  cases  develop  drowsiness  and  apathy,  and  die  in 
convulsions  or  coma,  like  that  ol  fatal  diabetes. 

The  urine  is  scanty,  hyperacid,  contains  acetone  bodies,  and  may 
contain  albumin  and  hyaline  casts.  Excess  of  xanthin  bodies,  deficient 
excretion  of  uric  acid,  indicanuria,  haematuria,  and  suppression  have  all 
been  noted  at  times.  Acetonuria  may  be  present  from  the  onset,  or  not 
until  the  end  of  the  attack.  In  Marcy's  fatal  case  indican  and  acetone 
were  absent  in  the  prodromal  stage,  and  present  on  the  second  day 
Howland    and    Richards    found   much   indicanuria,    increased   uric    acid, 


160  Chapter   XIII. 

diminished  sulphuric  acid,  and  an  increase  in  the  unoxidised  sulphur. 
Probably  these  results  indicate  increased  tissue  destruction  and  deficient 
oxidation. 

Course  and  Prognosis. — Between  the  attacks  of  vomiting  the  child 
is  generally  quiet  and  sleeps.  The  ordinary  duration  of  an  attack  is  two 
or  three  days,  and  the  temperature  then  becomes  subnormal.  Six  hours 
is  the  shortest  period.  Attacks  may  be  so  severe  and  prolonged  as  to 
endanger  life  from  cardiac  asthenia.  Nephritis  is  the  most  dangerous 
complication.  Up  to  1908  seven  fatal  cases  had  been  recorded,  four  of  which 
were  examined  after  death,  so  the  prognosis  is  distinctly  favourable. 
Almost  always  the  attack  ends  quite  suddenly.  The  younger  the  child  the 
greater  is  the  prostration  and  the  worse  the  prognosis.  The  attacks  recur 
at  irregular  intervals,  occasionally  regularly  every  month,  and  cease  about 
puberty.  The  intervals  vary  from  a  few  weeks  to  a  year,  usually  one  to  three 
months.  Each  attack  may  prove  the  last.  In  a  few  instances  they  have 
been  replaced  by  migraine.  As  soon  as  the  vomiting  ceases  health  and 
strength  are  rapidly  recovered,  and  between  the  attacks  the  child  is  quite 
well,  except  in  so  far  that  the  younger  children  are  unduly  liable  to  gastric 
and  intestinal  troubles. 

Morbid  Anatomy. — The  liver  presents  the  characteristic  fatty 
appearances  seen  in  acidosis,  to  a  variable  extent.  Fatty  changes  have 
been  found  in  the  kidneys  and  the  heart.  Langmead  obtained  a  definite 
amount  of  acetone  from  the  blood. 

Pathogenesis. — The  worst  cases  closely  resemble  the  late  stages  of 
diabetes.  It  is  almost  certain  that  various  types  of  recurrent  vomiting 
have  been  grouped  together  under  this  title,  and  that  some  of  them  are 
due  to  a  disorder  of  metabolism,  such  as  occurs  in  acid  intoxication  and 
post-anaesthetic  poisoning.  On  the  other  hand  some  may  be  hysterical, 
due  to  a  neurosis,  an  explosion  consequent  on  slight  gastro-intestinal 
disturbance  ;  and  others  associated  with  the  arthritic  diathesis.  In  favour 
of  a  primary  nervous  affection  are  the  hereditary  factors,  the  neurotic 
temperament  of  the  child,  the  occurrence  in  brothers  and  sisters,  the 
effects  of  excitement  and  emotion  as  exciting  causes,  the  sudden  onset  and 
cessation,  and  the  beneficial  results  of  treatment  by  suggestion.  Ace- 
tonuria  in  these  cases  may  be  gastro-intestinal  in  origin,  or  the  effect  and 
not  the  cause  of  the  vomiting.  The  arthritic  cases  may  depend  on  auto- 
toxins  or  intestinal  toxins,  related  to  or  identical  with  purin  bodies,  which 
may  account  for  those  attacks  subsequently  replaced  by  migraine. 

The  most  important  and  dangerous  group  includes  those  dependent 
in  some  way  on  hepatic  inadequacy.  Acetonuria  occurs  before  the  vomiting 
in  some  cases,  so  cannot  always  be  due  to  it.  The  ordinary  bilious  attack, 
consequent  on  error  in  diet,  is  of  this  type.  Perhaps  in  these  cases  we  have 
to  deal  with  a  functional  disorder  of  metabolism,  in  which  the  child  does  not 
ingest    or   is    unable    to    metabolise  a  sufficiency  of  carbohydrate  food, 


Disorders  of  Metabolism.  161 

with  the  result  that  profound  nutritional  disturbance,  hepatic  incompe- 
tence, acid  intoxication  and  autolysis  of  liver  cells  are  induced.  Auto- 
intoxication is  secondary  to  the  inadequacy  of  liver  function.  The  early 
stages  are  hardly  those  of  acid  intoxication,  but  the  later  ones  may  be 
partly  or  entirely  due  to  it.  As  a  rule  there  is  no  deficiency  of  food,  so  the 
defect  must  be  in  the  oxidising  powers  of  the  liver  and  other  organs.  The 
fatal  cases  occur  in  fat  children,  and  any  check  to  oxidation  will  induce 
acid  intoxication  in  a  child  predisposed  to  it  by  an  excessive  fatness  or  an 
undue  quantity  of  fatty  food.  Poisoning  by  the  products  of  intestinal 
putrefaction,  indol  and  skatol,  etc.,  may  be  an  exciting  factor  in  that  they 
reduce  the  oxidising  power  of  the  tissue  cells. 

Hepatic  Inadequacy  gives  rise  to  white  or  clay  coloured  stools,  com- 
plete acholia  without  jaundice,  and  occasionally  cystinuria.  The  excretion 
of  uric  acid  is  decreased  and  indicanuria  increases  as  the  patient  gets 
worse.  Sugar  metabolism  is  unaffected.  Sometimes  the  liver  is  swollen, 
and  jaundice  may  be  present  towards  the  end.  It  may  be  the  first  stage  of 
the  attacks  of  recurrent  vomiting  with  which  it  is  at  times  associated. 

Accurate  diagnosis  is  essential  to  judicious  treatment.  First  attacks 
are  likely  to  be  mistaken  for  ptomaine  or  othar  poisoning,  acute  indigestion, 
acute  gastritis,  gastric  influenza,  appendicitis,  intussusception,  intestinal 
obstruction,  renal  disease,  and  meningitis.  Cases  have  even  been  operated 
on  because  of  the  severe  vomiting  and  constipation.  A  rectal  examination 
should  be  made.  Later,  on  account  of  the  emaciation,  the  affection 
simulates  tuberculosis,  Addison's  disease,  cerebral  tumour,  and  diabetes. 
The  vomit  should  be  examined  for  excess  of  hydrochloric  acid,  and  the 
urine  for  acetone  bodies  and  indican.  The  acetone  odour  of  the  breath 
must  be  looked  for.  Recurrence  of  attacks  and  rapidity  of  recovery  estab- 
lish the  diagnosis. 

Further,  it  is  important  to  try  and  differentiate  the  purely  nervous 
cases  from  those  dependent  on  hepatic  inadequacy  and  associated  with  acid 
intoxication  ;  and  those  in  which  the  gouty  and  arthritic  elements  are 
marked.  A  typical  case,  in  a  girl  of  6  years,  in  whom  the  attack 
occurred  every  4-6  weeks  and  lasted  3  days,  was  partly  neurotic. 
A  sister  had  hysterical  anorexia  at  the  same  age.  Probably  the  neurosis 
was  not  the  sole  factor,  for  the  attacks  came  on  during  sleep,  with  a 
temperature  of  104°  F.  and  marked  constipation. 

The  treatment  of  the  purely  nervous  cases  consists  in  overfeeding, 
massage,  a  darkened  room,  purge,  temporary  starvation,  valerianates  and 
suggestion.  In  the  acetonuric  cases  the  measures  advised  in  the  treatment 
of  acid  intoxication  must  be  adopted  (p.  155).  During  the  prodromal 
stage  give  a  large  enema  ;  calomel  gr.  |-  and  sod.  bicarb,  gr.  v,  half  hourly 
for  10  doses,  followed  by  a  saline  laxative  in  2  or  3  hours  ;  sodium  ben- 
zoate  gr.  v  every  3  hours,  beginning  4-5  hours  later  ;  no  food  ;  water  if 
it  can  be  retained.    Once  the  vomiting  has  begun  nothing  seems  to  controL 

M 


162  Chapter   XIII. 

it.  Iced  sugar  solution,  milk  of  magnesia,  and  sod.  bicarb.,  citrate  or  lactate, 
may  all  be  tried.  After  24  hours  starvation  give  small  amounts  of  broth, 
albumin  water,  cereal  decoctions,  whey  and  peptonised  milk.  Morphia 
and  atropin,  chloral  per  rectum,  strychnia  and  saline  injections  may  be 
useful  or  necessary  to  tide  over  a  crisis.  In  the  intervals  rely  on  a  quiet, 
uneventful  outdoor  life  ;  a  liberal  supply  of  water  ;  a  diet  limited  in  fat, 
and  consisting  chiefly  of  milk,  cocoa,  vegetable  soups,  cereals,  well-cooked 
fruits  and  vegetables,  fish,  chicken,  and  mutton.  Attend  to  the  digestion 
and  bowels  with  rhubarb,  soda,  grey  powder,  calomel,  and  the  sulphate 
and  phospate  of  soda.    Salol  and  other  intestinal  antiseptics  may  be  tried. 

Glycosuria.  Diabetes. — True  diabetes  is  a  very  fatal  disease  in  children, 
and  fortunately  uncommon.  From  1-2  per  cent,  of  all  cases  begin  under 
10  years  of  age.  Bell  (1896)  reported  a  fatal  case  at  the  age  of  3  months. 
It  must  not  be  confused  with  simple  glycosuria,  the  transitory  appearance 
of  sugar  in  the  urine,  such  as  is  seen  in  whooping  cough,  after  anesthesia, 
as  the  result  of  excessive  starchy  or  saccharine  diet,  and  even  in  pneumonia 
and  diphtheria.  Other  copper-reducing  bodies  in  the  urine  can  be  dis- 
tinguished by  their  lack  of  fermentation  power. 

Alimentary  Glycosuria  is  a  defect  in  the  metabolism  and  assimilation 
of  carbohydrate  foods.  It  is  apt  to  occur  in  the  children  of  diabetics. 
The  mildest  type  is  that  in  which  sugar  only  appears  in  the  urine  after  the 
ingestion  of  a  large  amount  of  grape  sugar,  more  than  50  gms.  In  the 
more  marked  cases  the  sugar  appears  after  an  excess  of  starchy  food.  These 
children  can  be  tested  by  a  mixed  dinner  containing  8  oz.  of  carbohydrates, 
and  examining  the  urine  2-4  hours  later.  They  are  liable  to  acne  and 
obesity,  and  may  develop  prematurely. 

True  Diabetes  can  be  divided  into  two  groups,  with  no  strict  line  of 
demarcation.  The  mild  cases  exhibit  a  considerable  and  persistent  amount 
of  sugar,  which  disappears  on  the  reduction  or  omission  of  carbohydrate 
food.  The  severe  cases  are  little  or  not  at  all  affected  by  diet.  Possibly 
they  are  of  pancreatic  origin.  Mild  cases  may  become  severe,  and  occasion- 
ally a  simple  glycosuria  develops  into  a  mild  diabetes,  rarely  into  a  severe 
form. 

A  racial  tendency  is  seen  among  Hindoos  and  Jews,  but  there  is  no 
special  frequency  among  Jewish  children.  In  about  one-fifth  there  is  a 
family  history  of  the  disease,  and  often  a  history  of  neuroses,  gout  or 
tuberculosis.  Several  children  in  a  family  may  be  affected  at  about  the 
same  age.  Cases  have  been  reported  in  the  first  year  of  life,  and  one  is  said 
to  have  been  congenital.  The  yearly  frequency  is  about  the  same  in  the 
first  ten  years  of  life,  and  then  increases.  Both  sexes  are  equally  affected 
Frequently  no  cause  can  be  found.  Some  cases  have  followed  injury 
to  the  head,  convulsions,  operations,  fright,  over-exertion,  rapid  growth, 
dentition,  influenza,  typhoid  and  other  fevers,  sore  throat,  gastric  catarrh, 
and  severe  burns.    A  few  may  be  due  to  a  pancreatic  fibrosis,  consequent 


Disorders  of  Metabolism.  163 

on  congenital  syphilis.  Extirpation  of  the  pancreas  only  produces  glyco- 
suria in  those  birds  which  eat  meat.  Possibly  the  disease  is  dependent  on 
decomposition  of  meat  foods  inducing  hyperactivity  of  the  thyroid 
(Lorand),  especially  if  associated  with  degeneration  of  the  Islands  of 
Langerhans.  An  excess  of  meat  and  carbohydrates  is  more  likely  to  cause 
it  than  if  the  meat  is  omitted. 

Symptomatology. — Usually  the  first  symptoms  are  wasting,  thirst, 
polyuria,  languor  and  joint  pains.  Enuresis  may  be  the  first  sign.  An 
excessive  appetite  is  an  uncommon  feature,  and  there  may  be  no  obvious 
wasting.  An  insidious  early  stage  may  be  overlooked,  and  end  in  death 
from  coma  within  two  days  of  the  first  suspicion  of  illness. 

The  amount  of  urine  varies  greatly,  e.g.,  50  oz.  or  less  in  a  girl  of  10 
years  ;  110  oz.  in  a  boy,  aged  8,  who  looked  quite  well  ;  up  to  10  pints  in 
a  baby  aged  15  months  (Langstein)  ;  up  to  10  quarts  in  a  10  year  old  boy 
(Wegeli).  The  specific  gravity  ranges  from  1025-1050  ;  the  percentage 
of  sugar  from  5-10,  and  the  daily  amount  up  to  3000  grains.  These 
amounts  may  be  exceeded.  In  examining  the  urine  take  a  mixed  specimen 
from  the  total  daily  excretion,  and  not  from  the  morning  urine  only, 
or  an  erroneous  impression  of  the  severity  of  the  disease  will  be  formed. 
Albuminuria  is  not  infrequent,  and  is  generally  present  shortly  before 
death,  with  short  thick  granular  and  cylindrical  casts.  Acetone  bodies  are 
serious  indications.  Diacetic  acid  is  of  grave  import,  and  may  remain 
though  sugar  temporarily  disappears.  The  ammonia  excretion  is  increased. 
Purin  excretion  is  also  increased,  even  though  on  a  purin-free  diet. 

All  the  signs  of  the  disease  in  adults  occasionally  are  seen  in  children, 
viz.,  harsh  dry  skin,  furunculosis,  carbuncles  ;  acetone  breath,  raw  beefy 
tongue,  dryness  of  fauces,  thirst,  toothache,  decayed  teeth,  abnormal 
appetite,  constipation ;  balanitis,  pruritus  vulvae ;  anaemia,  pale  and 
sunken  face,  small  and  frequent  pulse,  subnormal  temperature,  abdominal 
pain,  vomiting,  restlessness,  dyspnoea,  air-hunger,  distress,  heavy  breathing, 
cyanosis,  mental  confusion,  apathy,  progressive  coma,  and  occasionally 
convulsions.     Complications  are  rare  because  of  the  rapid  progress. 

The  diagnosis  is  simple,  if  the  urine  is  examined  and  temporary 
glycosuria  can  be  excluded.  In  infancy  it  may  be  mistaken  for  marasmus 
or  tuberculosis,  for  thirst  and  polyuria  are  not  always  conspicuous.  Lacto- 
suria  may  be  found  in  breast-fed  infants.  Transitory  glycosuria  should 
clear  up  in  a  few  weeks. 

Course  and  Prognosis. — The  onset  is  more  sudden  and  the  course 
more  rapid  than  in  adults.  The  younger  the  child  the  worse  is  the  prog- 
nosis. Few  live  beyond  two  years  and  the  worst  die  within  a  few  weeks, 
or  even  within  a  couple  of  days  of  the  onset  of  acute  symptoms,  the  disease 
being  previously  unsuspected.  Six  months  is  an  average  duration  from 
the  date  of  diagnosis.  Mild  cases  which  yield  to  dietetic  treatment  are 
possibly  curable.     Those  cases  are  most  favourable  which  can  be  thus 


164  Chapter   XIII. 

influenced,  and  have  no  acetonuria.  They  may  live  for  3-6  years.  In 
one  child  glycosuria  persisted  for  8  months,  then  remained  absent 
for  several  months,  but  returned  and  proved  eventually  fatal.  Even  if 
mild  cases  are  doing  well  on  a  limited  diet,  the  carbohydrate  tolerance  is 
liable  to  break  down  on  any  illness  or  indiscretion,  and  generally  fails 
without  such  cause.  Neither  diet  nor  drugs  produce  much  effect  in  severe 
cases.  A  few  die  from  tuberculosis,  pneumonia  or  other  intercurrent 
disease.  The  common  termination  is  that  of  coma,  ushered  in  by  drowsiness 
and  air-hunger,  and  preceded  by  anorexia,  nausea,  vomiting,  and  abdominal 
pain.  A  sudden  fall  in  the  sugar  excretion  often  indicates  the  onset  of 
coma  or  of  an  acute  illness. 

Treatment. — Adopt  careful  hygienic  precautions  against  chill.  Avoid 
excitement  and  overwork,  mental  or  physical.  Allow  prolonged  rest  in 
bed  at  night.  Let  the  child  live  an  ordinary  life,  as  far  as  possible,  with 
change  of  air  and  even  sea-bathing.  Begulate  the  diet  on  the  usual  lines, 
reducing  the  carbohydrates  only  if  the  acetone  reaction  of  the  urine  is 
absent.  Oatmeal  and  potato  seem  to  be  tolerated  best.  The  oatmeal  cure 
consists  in  a  daily  diet  for  adults  of  oatmeal  150  gms.,  butter  150-200, 
roborat  60-70,  eggs  4-5,  and  some  wine.  It  is  given  for  a  week  or  two, 
and  slowly  replaced  by  other  foods.  The  general  principle  of  dietetic 
treatment  is  to  establish  tolerance,  to  keep  within  the  limits,  and  periodically 
to  give  a  carbohydrate-free  diet  for  several  days. 

For  thirst  rely  on  tepid  drinks,  water,  skimmed  milk,  buttermilk, 
water  with  phosphoric  acid  or  cream  of  tartar,  lemonade  made  with  45  grs. 
of  citric  acid  and  3  drs.  of  pure  glycerine  to  the  pint  of  water,  alkalies, 
and  alkaline  mineral  waters. 

For  coma  give  large  doses  of  bicarbonate  of  soda,  and  even  earlier  to 
prevent  its  onset  as  soon  as  there  are  signs  of  acidosis.  Guard  against 
constipation  by  Apenta  water,  Carlsbad  salts  or  Epsom  salts.  Measure 
daily  the  amount  of  urine,  and  estimate  the  quantity  of  sugar  passed. 
The  fermentation  test  is  a  sufficiently  accurate  guide,  in  conjunction  with 
the  weight  of  the  patient,  of  the  effect  of  the  diet  on  the  excretion  of  sugar 
and  the  general  health.  Stimulants  are  often  useful.  Of  drugs  the  chief 
ones  recommended  are  codeine,  opium,  atropine,  bromide  of  arsenic,  liquid 
extract  of  ergot,  aspirin  and  salicylates. 

Scurvy. — Scurvy  is  rarely  seen  in  this  country,  except  in  infants 
brought  up  on  cooked  milk  or  a  proprietary  food  for  a  long  period  of  time. 
It  was  recognised  and  described  by  Glisson  (1651)  as  distinct  from  rickets 
and  having  no  essential  connection  with  it.  Confusion  has  arisen  because- 
it  has  been  called  at  different  times,  acute,  scurvy,  or  hemorrhagic  rickets. 
These  names  should  be  given  up.  Cases  have  been  described  by  Sir  Thomas 
Smith  (1876)  as  "  hsemorrhagic  periostitis  "  ;  by  Gee  (1881)  as  "  periosteal 
cachexia  "  ;  by  Cheadle  (1878)  as  "  scurvy  supervening  on  rickets,"  and 
(1882)   as   "  osteal  or  periosteal  cachexia  and  scurvy,"  recognising  that. 


Disorders  of  Metabolism. 


165 


the  affection  was  true  scurvy.  As  the  result  of  a  full  description  by  Sir 
Thomas  Barlow  (1883),  who  showed  that  the  scurvy  was  the  central  factor, 
and  the  rickets  variable  and  unimportant,  it  has  been  known  as  Barlow' 's 
Disease.  Subperiosteal  hemorrhage  is  not  common  in  the  scurvy  of  adults. 
In  infants  the  actively  growing  tissue  is  very  vascular  and,  therefore,  more 
liable  to  haemorrhage. 

It  is  by  no  means  uncommon,  though  often  unrecognised,  in  infants. 
The  mildest  cases  may  be  entirely  overlooked,  the  child  recovering  by 
reason  of  some  change  in  the  diet.  An  individual  susceptibility  may  show 
itself  in  twins,  one  only  being  affected.  Three-fourths  of  the  cases  occur 
between  6  and  12  months  of  age.  It  is  rare  under  6  months  and  after 
15  months  of  age.  A  few  cases  have  been  recorded  in  breast-fed  infants, 
even  as  early  as  the  fourth  or  fifth  week  of  life,  but  they  are  open  to  criticism. 
The  disease  occurs  rather  more  often  in  boys,  in  fat  anaemic  babies  and  in 
the  ill-nourished,  at  any  period  of  the  year,  in  town  or  country,  and  in 
any  climate.  Possibly  plenty  of  fresh  air  may  postpone  the  onset.  It  occurs 
in  every  grade  of  the  social  scale,  but  more  frequently  in  private  than  in 
hospital  practice,  for  the  children  of  the  poor  are  rarely  brought  up  for  a 
sufficiently  long  period  on  cooked  milk  and  often  receive  tastes  of  various 
antiscorbutic  foods.  The  following  table  shows  the  diet  of  a  large  number 
of  collected  cases  : — 


Breast  Milk 

21 

Breast  Milk  with  additional  food 

2 

Uncooked  Cow's  Milk 

5 

Pasteurised  Milk 

40 

Boiled  Milk 

14 

Sterilised  Milk 

122 

Condensed  Milks 

72 

Proprietary  Foods 

.       250 

Dried  Milk  Foods  with  water  only 

21 

Some  of  the  proprietary  foods  produced  the  disease  although  given 
with  fresh  milk.  Long  continuance  of  the  particular  diet  is  an  important 
factor.  Thus,  a  mild  case  developed  in  a  child,  aged  10  months,  who  for 
8  months  had  been  fed  upon  a  mixture  of  cream,  milk,  sugar  and  water, 
sterilised  for  20  minutes.  Another  child,  aged  15  months,  had  taken 
pasteurised  milk  only  for  a  year. 

Pathology. — A  change  is  produced  in  milk  by  heat,  reducing  or 
destroying  its  antiscorbutic  property.  It  is  no  longer  a  fresh  food.  The 
greater  the  heat  and  the  longer  the  duration  of  heating,  the  greater  is  this 
destruction.  For  this  reason  condensed  milks  and  patent  foods  are  par- 
ticularly injurious.  Possibly  it  is  connected  with  the  destruction  of 
enzymes  ;  changes  in  the  protein  ;  or  the  conversion  of  soluble  salts  of 
lime  into  insoluble  forms,  e.g.,  the  formation  of  insoluble  calcium  phosphate, 


166  Chapter   XIII. 

and  of  the  crystalline  and  less  soluble  calcium  citrate  from  the  more  soluble 
amorphous  salt  (Citric  Acid  Theory).  Nevertheless,  the  addition  of 
citrates  to  the  food,  or  of  alkaline  phosphates  to  keep  the  citrate  in  solution, 
has  apparently  no  remedial  action.  Nor  is  it  due  to  the  absence  of  potash 
salts  in  organic  form,  for  these  salts  are  not  curative.  Cooking  does  not 
affect  the  antiscorbutic  property  of  potatoes  and  greens.  The  theory  that  it 
it  is  clue  to  tainted  food  or  ptomaines  (Tainted  Food  Theory)  is  certainly 
not  supported  by  evidence  derived  from  cases  in  infancy  ;  for  it  arises 
occasionally  in  the  breast-fed  and  on  diets  in  which  neither  animal  food 
nor  microbes  are  present ;  and  there  is  no  evidence  of  ptomaine  poisoning. 
Sir  Almroth  "Wright  ascribes  it  to  an  Acid  Intoxication,  very  similar  to 
that  produced  experimentally  in  herbivora  by  the  ingestion  of  a  surplus 
of  mineral  acids  over  bases.  Thus,  a  diet  of  meat  and  cereals  with  the 
exclusion  of  green  vegetables  and  fruits  will  produce  it.  Meat  and  cereals 
contain  a  large  excess  of  minerals  acids,  especially  phosphoric  acid,  while 
vegetables  and  fruits  contain  an  excess  of  bases.  Wright  divides  foods 
into  :  (1)  Acid  or  scorbutic,  viz.,  eggs,  fresh  and  salt  meat,  and  many 
cereals ;  (2)  Neutral  or  non-scorbutic,  viz.,  sugar,  vegetable  oils,  and 
animal  fats  ;  (3)  Alkaline  or  antiscorbutic,  viz.,  milk,  blood,  lime-juice, 
orange  juice,  potatoes,  green  vegetables,  etc.  In  adults  he  found  the 
alkalinity  of  the  blood  was  decreased,  and  he  advises  the  administration 
of  the  salts  of  the  oxidizable  organic  acids,  e.g.,  sodium  lactate,  to  restore 
the  normal  blood  alkalinity.  But  the  reduced  alkalinity,  if  present,  is  due 
to  anaemia.  Moreover,  scurvy  does  not  occur  in  Acidosis,  and  lime-juice 
raises  the  acidity  of  the  urine,  yet  cures  the  disease.  According  to  Hut- 
chison, "Wright's  division  of  food-stuffs  is  based  on  inaccurate  chemistry, 
and  only  eggs  and  meat,  deprived  of  all  blood,  leave  an  acid  ash.  Recent 
experiments  by  Axel  Hoist  of  Christiania  (1908)  upset  Wright's  theory. 
Scurvy  was  produced  in  guinea  pigs  by  a  diet  of  bread  and  dry  cereals, 
but  not  if  fresh  raw  carrot  was  added  ;  on  a  diet  of  compressed  dried  potato 
and  water,  but  not  if  cabbage  juice  was  added  ;  on  a  diet  of  dried  carrot, 
even  if  soaked  in  a  solution  of  bicarbonate  of  soda  ;  and  on  a  diet  of  dried 
barley  and  water,  but  not  if  the  barley  was  allowed  to  sprout  first.  Yet 
in  the  sprouted  and  unsprouted  barley  the  same  amounts  of  acid  and  salts 
were  present.  Nor  did  the  addition  of  sodium  citrate  and  calcium  carbonate 
to  these  diets  prevent  the  disease.  It  may,  therefore,  be  accepted  that 
scurvy  is  not  due  to  acid  intoxication  or  reduced  alkalinity  of  the  blood. 
All  that  we  can  say  at  present  is  that  it  is  the  result  of  the  lack  of  some 
property  in  fresh  food,  which  is  destroyed  by  heat,  or  an  inadequate  supply 
of  fresh  food,  and  that  it  may  be  accentuated  by  unsuitable  diet  con- 
taining an  excess  of  starch. 

Symptoms  and  Course. — The  onset  is  gradual,  with  fretfulness,  impaired 
appetite,  malaise,  ansemia  and  loss  of  weight.  Sometimes  immobility  of  a 
limb  is  the  first  sign  to  attract  attention,  or  some  general  tenderness,  the 


Disorders  of  Metabolism.  167 

child  crying  when  handled  or  even  approached,  for  fear  of  being  moved. 
There  may  be  a  history  of  a  previous  attack,  lasting  for  a  week  or  two  and 
ending  in  recovery.  If  so,  it  will  be  found  that  the  actual  cause  was  not 
recognised,  and  the  improvement  was  due  to  some  temporary  change 
in  the  diet.  Not  infrequently  haematuria  is  the  first  sign.  In  the  mildest 
cases,  although  some  of  the  teeth  are  cut,  the  gums  may  be  unaffected  or 
exhibit  swelling,  hyperaemia  and  slight  purplish  discolouration.  They 
show  no  change  unless  the  teeth  are  cut  or  almost  through.  In  severe  cases 
they  are  swollen,  bulbous,  ecchymotic,  varying  in  colour  from  dusky  to 
purple,  and  may  ulcerate  and  bleed  freely  (haemorrhagic  gingivitis).  The 
swelling  may  form  a  fungating  mass  so  great  as  to  hide  the  teeth,  sloughs 
form,  and  the  breath  becomes  very  offensive.  Sometimes  there  is  haemor- 
rhagic  discolouration  of  the  hard  palate.  The  tenderness  and  pain  cause  com- 
plete immobility  of  the  limbs,  especially  the  legs,  with  extension,  eversion, 
and  pseudo-paralysis  ;  or  the  legs  may  be  kept  partially  flexed  and  rigid. 
This  is  due  to  local  pathological  changes,  not  necessarily  causing  a  visible  or 
palpable  swelling.  Generally  on  examination  there  are  found  one  or  more 
colourless,  painful,  tender  swellings,  often  symmetrical.  The  most  common 
site  is  the  lower  third  of  the  thigh,  and  the  least  common  is  the  upper  limb  ; 
occasionally  the  clavicles,  scapulae  and  ribs.  The  swelling  is  due  to  sub- 
periosteal effusion  of  blood,  taking  place  over  the  long  bones,  and  some- 
times causing  separation  of  the  epiphysis  and  soft  crepitus.  The  super- 
jacent skin  is  smooth,  tense,  shiny,  sometimes  bluish,  not  hot,  and  rarely 
pits  of  pressure.  Haemorrhages  may  occur  over  the  flat  bones  of  the  skull, 
forming  large  bluish  swellings,  like  sarcoma.  The  thorax  is  often  tender. 
The  sternum  may  sink  in  from  fracture  or  separation  at  the  costo-chondral 
junction,  and  cause  a  peculiar  flattening  of  the  front  of  the  chest.  Bleeding 
often  takes  place  from  the  nose,  and  occasionally  from  the  ear,  into  the 
eyelid,  behind  the  eyeball,  from  any  mucous  surface,  into  the  muscles, 
under  the  skin,  and  into  various  serous  cavities,  the  cranial  cavity,  joints, 
and  any  organ  of  the  body.  Anaemia  is  independent  of  haemorrhage  and 
often  marked  ;  the  blood  is  deficient  in  red  cells  and  percentage  of  haemo- 
globin. Muscular  pains  are  severe  and  cause  loss  of  rest ;  fainting  attacks 
are  not  uncommon  ;  occasionally  the  long  bones  get  broken.  Fever  is 
due  to  complications,  or  to  disturbed  sleep  and  general  malaise  from  pain. 
In  older  children  similar  symptoms  occur,  but  the  disease  as  a  whole 
approximates  more  closely  to  the  adult  type.  It  is  generally  due  to 
deficiency  of  vegetable  and  meat  foods. 

Morbid  Anatomy. — The  bone  symptoms  are  due  to  extravasation 
between  the  actively  growing  periosteum  and  the  diaphysis,  leaving  the 
bone  bare  and  impairing  its  nutrition.  The  periosteum  may  be  completely 
separated,  the  epiphyses  detached,  and  the  shaft  free  in  a  cavity  con- 
taining blood  and  clot.  Bone  forms  in  the  detached  periosteum,  for  its 
osteogenetic  power  is  not  destroyed.      Lymphoid   cells  in  the   marrow, 


]68  Chapter   XIII. 

at  the  junction  of  the  cartilage  and  shaft  of  long  bones,  are  replaced  by  a 
reticular  tissue,  poor  in  cells  and  often  the  scat  of  haemorrhages.  The 
changes  in  the  bone  marrow  and  the  destruction  of  osteoblasts  lead  to 
inefficient  formation  of  new  bone.  Consequently  the  normal  bone  absorp- 
tion causes  thinning  of  the  bone  in  these  regions,  rarefaction,  partial 
dislocation  at  the  epiphyseal  line  and  fractures,  partial  or  complete, 
from  very  slight  violence.  There  is  no  severe  displacement  for 
the  periosteum  is  untorn.  It  is  rare  for  necrosis  of  the  bone  to  take 
place. 

Complications  are  such  as  are  due  to  haemorrhages  in  various  situations, 
rather  to  be  regarded  as  symptoms,  and  those  due  to  associated  rickets. 
Intrarenal  haemorrhage  may  give  rise  to  blood,  albumin  and  casts  in  the 
urine,  and  may  be  mistaken  for  acute  nephritis.  Albuminuria  may  occur 
alone.  Acute  nephritis  is  rare.  Diarrhoea  is  a  serious  complication  ;  pye- 
litis prolongs  the  illness  ;  broncho-pneumonia  may  prove  fatal.  Feeding 
may  be  difficult  on  account  of  the  condition  of  the  gums. 

Diagnosis  is  only  difficult  in  mild  cases  in  very  young  infants  before 
any  teeth  are  cut.  The  disease  is  often  unsuspected  for  the  child  may  be 
very  fat,  sometimes  abnormally  so,  and  the  suspicion  of  scurvy  not  aroused. 
The  fatness  also  renders  it  difficult  to  recognise  a  moderate  subperiosteal 
swelling,  especially  if  it  is  symmetrical  on  the  two  sides.  The  child  may  have 
been  brought  up  amid  most  excellent  surroundings.  The  cardinal  signs 
are  anaemia  pain  and  tenderness,  all  of  which  commonly  occur  before  the 
swelling  of  the  gums.  Fretfulness  and  spongy  gums,  or  haematuria,  may 
be  the  only  symptoms.  "Whenever  an  infant  suffers  from  pain  and  tender- 
ness in  the  limbs,  it  should  be  carefully  examined  for  scurvy  and  inquiry 
made  into  the  diet.  The  affection  is  often  mistaken  for  rickets,  when  rickets 
is  present,  but  it  is  doubtful  whether  this  disease  is  ever  painful.  The 
pseudo-paralysis  of  the  lower  limbs  in  a  rachitic  child  with  marked  kyphosis 
may  be  erroneously  diagnosed  as  pressure  paraplegia  due  to  spinal  caries. 
The  rarity  of  rheumatism  at  this  age  ought  to  prevent  such  a  diagnosis 
being  made.  A  swelling  limited  to  one  limb  or  epiphysis  has  been  mistaken 
for  sarcoma,  acute  periostitis  or  epiphysitis.  Syphilitic  epiphysitis  occurs 
in  wasted  infants  under  six  months  of  age.  Multiple  osteomyelitis  is 
extremely  rare  and,  like  localised  osteomyelitis,  is  accompanied  by  high 
fever.  Epistaxis  may  be  regarded  as  accidental ;  renal  haemorrhage 
ascribed  to  sarcoma;  subcutaneous  haemorrhages  mistaken  for  purpura; 
and  the  condition  of  the  gums  put  down  to  acute  leukaemia.  If  there 
is  no  swelling  and  the  gums  are  unaffected,  the  pseudo-paralysis  can  be 
distinguished  from  that  of  infantile  palsy  by  the  tenderness  and  pain. 
Orbital  haemorrhage,  usually  in  the  upper  lid,  is  very  suggestive.  In  only 
one  case  have  I  found  marked  tenderness  and  dusky  gums  unassociated 
with  anaemia.  Ulcerative  stomatitis  is  differentiated  by  its  not  being 
limited  to  the  gums. 


Disorders  of  Metabolism.  169 

Prognosis. — Mild  cases  get  rapidly  well,  and  show  definite  improvement 
as  regards  the  tenderness  in  a  day  or  two,  if  put  on  appropriate  treatment. 
In  bad  cases  the  prognosis  must  be  guarded  because  of  the  liability  to  severe 
haemorrhage,  syncope  from  the  profound  anaemia,  and  death  from  diarrhoea 
and  exhaustion.  Convalescence  is  prolonged  ;  absorption  of  haemorrhage 
and  thickening  slow  ;  the  separated  periosteum  may  form  a  bony  sheath. 
Treatment  may  fail  in  advanced  cases  of  anaemia,  with  extreme  cachexia, 
and  enteritis  or  broncho-pneumonia. 

Treatment. — Rapid  recovery  on  an  antiscorbutic  diet  is  strong  con- 
firmatory evidence  of  the  accuracy  of  the  diagnosis.  Put  the  child  on  a 
diet  of  uncooked  milk  and  the  juice  of  oranges  or  grapes,  if  it  is  under 
six  months  of  age,  with  the  addition  of  cream  and  meat  juice  if  necessary. 
Over  this  age  add  potato  cream  to  the  diet ;  it  is  made  by  adding  2  tea- 
spoonfuls  of  the  outer  part  of  a  baked  floury  potato  to  1  oz.  of  milk,  and 
from  1-2  teaspoonfuls  is  given  alone,  or  in  the  first  part  of  the  milk  feed, 
3  or  4  times  a  day.  If  given  to  very  young  infants,  or  for  long,  it  is  liable 
to  upset  the  digestion.  In  mild  cases  the  milk  need  not  be  given  fresh. 
It  can  be  just  brought  to  a  boil,  mixed  with  fresh  barley  water,  and  the 
juice  of  fruit,  vegetables  or  meat  added,  or  given  independently.  Older 
infants  may  have  vegetable  soups  or  purees  made  with  carrots  or  potatoes. 
The  child  should  be  handled,  moved,  and  dressed  as  little  as  possible  ; 
affected  legs  placed  between  sandbags,  and  an  affected  arm  bandaged 
gently  to  the  side.  In  rare  instances  extreme  periosteal  swelling  must  be 
relieved  by  a  small  incision  and  packing.  The  gums  can  be  painted  with  an 
antiseptic  astringent  lotion  of  tincture  of  myrrh  and  Listerine.  Drugs  are 
unnecessary.  Sodium  lactate  can  be  given  and  is  harmless.  Iron,  arsenic, 
and  cod-liver  oil  are  useful  in  convalescence. 


Chapter  XIV, 

INFANTILE    ATROPHY. 

Syn.  :    Athrepsia  (Parrot,  1877) — Malnutrition — Marasmus — Inanition. 

The  Registrar- General  divides  wasting  diseases  into  those  due  to 
premature  birth,  congenital  defects,  injury  at  birth,  atelectasis  and 
atrophy.  It  is  a  curious  and  inexplicable  fact  that  the  mortality  is  much 
greater  among  males  than  females.  The  total  mortality  rate  for  wasting 
diseases  has  increased  during  the  last  thirty  years,  although  there  is  a 
considerable  decrease  in  the  number  of  cases  ascribed  to  atrophy  alone. 
This  may  be  the  result  of  stricter  methods  of  registration  and  more  accurate 
diagnosis  of  the  causes  of  atrophy.  Many  stillborn  infants  formerly 
escaped  registration,  but  now  appear  in  statistics  as  prematurely  born. 
Nevertheless,  it  seems  that  there  is  an  increase  in  the  inherent  predis- 
position to  death  in  early  life  from  defective  vitality,  congenital  defects, 
and  similar  causes. 

Physical  Deterioration. — There  is  little  evidence  that  the  race  as  a 
whole  is  progressively  degenerating.  Without  doubt  a  very  large  number 
of  imperfectly  developed  children  and  adults  are  in  existence.  Relative 
statistics  of  age,  weight  and  height  in  different  decades,  are  of  compara- 
tively little  value,  for  the  proportion  of  the  unfit  or  badly  grown  is  large 
and  tends  to  increase  yearly.  This  is  the  natural  result  of  improved 
hygiene,  sanitation,  cheap  food,  and  medical  science.  Many  infants,  who 
in  former  days  succumbed  to  the  stress  of  existence,  now  survive,  grow  up, 
and  propagate  the  species.  A  great  amount  of  good  can  be  done  by 
directing  attention  to,  and  counteracting  as  far  as  possible,  those  causes 
which  prevent  proper  growth  and  development  without  actually  causing 
deterioration. 

Imperfect  development  depends  upon  ante-natal  conditions,  diet, 
and  environment.  About  80  per  cent,  of  all  children  are  born  healthy. 
The  debility  of  the  remainder  is  due  to  morbid  heredity  or  conditions 
affecting  the  mother  during  pregnancy.  The  main  hereditary  factors  are 
tuberculosis,  syphilis,  alcoholism,  neuroses  and  general  debility.  The 
influence  of  morbid  heredity  tends  to  die  out  by  extinction  of  the  family, 
or  is  corrected  by  marriage  with  healthy  subjects.  The  factors  affecting 
the  mother  during  pregnancy  are  referred  to  in  a  previous  chapter  (p.  21). 


Infantile    Atrophy.  171 

Anything  that  impairs  the  health  of  the  mother  is  more  or  less  injurious 
to  the  child.  After  birth  development  is  mainly  a  question  of  suitable  diet. 
Other  factors  being  equal,  breast-fed  infants  are  stronger,  healthier  and 
less  prone  to  disease  than  those  artificially  fed.  Hebrew  children  are  better 
grown,  heavier,  less  rachitic,  and  have  sounder  teeth  than  those  of  the 
Gentiles.  This  is  due  to  the  fact  that  the  Jewish  mother  is  better  fed  and 
cared  for  during  pregnancy,  and  that  her  child  is  almost  always  breast-fed 
during  infancy,  and  gets  a  more  suitable  diet  during  early  childhood. 

The  advantages  of  cheap  food  have  been  rather  overrated.  The  craze 
for  cheapness  has  led  to  the  adulteration  of  food  and  the  provision  of 
cheap,  tinned,  savoury  and  unwholesome  foods,  which  form  an  injudicious 
and  unsuitable  diet  for  young  children.  It  is  by  no  means  uncommon  to 
find  a  child  fed  on  condensed  milk,  proprietary  foods,  tinned  meats  and 
fish,  sausages,  and  pickles ;  tasty  articles  of  diet  which  deprave  the  appetite 
for  simpler  food,  and  give  rise  to  gastro-enteritis  and  malnutrition,  and 
predispose  to  tuberculous  infection.  Tea,  alcohol  and  smoking  in  early 
life  are  also  distinctly  harmful ;  so,  too,  the  use  of  drugs,  such  as  opiates 
and  white  bryony,  and  patent  medicines. 

Other  deleterious  factors  are  overcrowding,  bad  hygiene,  insufficient 
clothing,  exposure  to  inclement  weather,  insufficient  sleep,  over-fatigue, 
and  general  neglect.  Education  is  by  no  means  an  unmixed  blessing. 
Children,  who  in  former  days  added  to  the  family  exchequer,  are  kept  at 
school,  and  the  parents  have  difficulty  in  providing  for  them.  Many  of 
them  suffer  from  over-pressure  and,  in  winter  especially,  from  insufficient 
fresh  air,  light  and  exercise. 

The  general  effects  of  these  various  causes  are  the  production  of 
undersized,  weakly  adults.  They  are  small,  stunted,  and  have  bad  diges- 
tion, which  is  further  impaired  by  indulgence  of  the  craving  for  tasty  and 
stimulating  foods  and  drink.  Little  prospect  is  there  of  such  people 
becoming  parents  of  strong  and  healthy  children.  Morally,  physically  and 
mentally  they  are  ill-developed,  and  their  children  are  likely  to  be 
congenitally  feeble  and  liable  to  atrophy. 

Atrophy. — Although  malnutrition,  atrophy,  wasting  and  marasmus 
are  merely  symptoms  or  names  for  various  degress  of  wasting,  there  is  a 
general  condition  deserving  the  name  of  Infantile  Atrophy.  It  must  not 
be  confounded  with  simple  wasting  and  inanition  due  to  starvation, 
though  it  can  be  produced  by  insufficient  or  unsuitable  diet.  Malnutrition 
indicates  that  constructive  metabolism  is  not  greater  than  destructive. 
It  varies  in  degree  and  rapidity  of  progress.  It  may  occur  at  any  age,  but 
is  a  most  marked  feature  during  the  first  year. 

It  can  be  ascribed  to  defective  diet,  inability  to  suck,  indigestion,  bad 
hygiene  and  neglect,  an  inherited  defect  of  tissue,  an  inherited  taint,  pre- 
maturity, defect  in  the  digestive  organs,  malformation  and  organic  disease. 


172  Chapter   XIV. 

Tke  dietetic  factors  are  over-feeding,  food  insufficient  in  quality  or 
quantity,  an  unsuitable  breast-milk  or  artificial  mixture,  bacterial  con- 
tamination, and  failure  of  assimilation. 

Inability  to  suck  or  swallow  may  depend  upon  structural  defects  or 
organic  disease,  suck  as  kare-lip,  cleft  palate,  large  tonsils,  palatal  palsy,  or 
inflammatory  affections  of  tke  moutk  and  throat.  It  may  depend  upon 
nasal  obstruction,  from  snuffles  or  adenoids  ;  upon  small  and  retracted 
nipples  or  an  unsuitable  teat ;  on  complete  anorexia  or  unsatisfactory 
food.  Occasionally  tkere  is  no  obvious  explanation,  and  in  suck  instances 
it  kas  been  ascribed  to  imperfect  co-ordination  or  development  of  tke 
nerve  centres  for  suction  or  deglutition.  Sometimes  suck  infants  will 
begin  suddenly  to  suckle  normally.  Pinard  reported  a  remarkable  case 
in  wkick  tke  reflex  area  for  suckling  receded  gradually  from  tke  tip  to  tke 
base  of  tke  tongue.  Tke  ckild  died  from  kydrocepkalus.  In  otker  infants 
tke  refusal  of  food  depends  on  mental  defect  or  on  temper.  If  tke  use  of 
tke  bottle  kas  been  unduly  prolonged,  tke  ckild  may  refuse  semi-solid  food. 

Of  tke  general  causes  most  importance  must  be  attacked  to  pre- 
maturity and  a  family  kistory  of  tuberculosis  or  syphilis.  Even  apart  from 
actual  disease  tkere  results  a  feeble  vitality,  due  to  tke  inkeritance  of 
imperfect  tissues  wkick  are  incapable  of  efficiently  carrying  out  tke  functions 
of  digestion,  absorption  or  assimilation.  By  far  tke  most  important  factor 
is  tke  diet  of  tke  ckild,  eitker  alone  or  in  conjunction  witk  otker  causes. 
Hence  arise  tke  intestinal  troubles,  e.g.,  persistent  indigestion,  wkick  are 
tke  ckief  cause  of  atropky. 

Morbid  Anatomy. — Post  mortem  examination  reveals  sometimes 
congestion  or  oedema  of  tke  meninges  and  brain,  kypostatic  congestion  of 
tke  lungs,  collapse  and  pleural  ecckymoses,  and,  rarely,  sinus  tkrombosis. 
Tke  gastric  and  intestinal  mucosa  is  pale,  sometimes  swollen,  and  may 
skow  patckes  of  congestion,  erosions  and  sub-epitkelial  kaemorrkage. 
Tke  kidneys  are  almost  always  pale  ;  tke  glomeruli  injected,  cortex  swollen, 
pyramids  kypera^mic  ;  witk  cloudy  swelling  and  fatty  degeneration  of  tke 
epitkelium,  especially  in  tke  convoluted  tubes.  In  prolonged  cases  tke 
liver  skows  fatty  and  parenckymatous  degeneration.  Tke  organs  are 
generally  pale  ;  tke  lympk  nodes,  follicles  and  Peyer's  patckes  may  be  a 
little  enlarged. 

Pathology. — Tke  anatomical  ckanges  are  tke  effect,  not  tke  cause  of 
tke  wasting.  Tke  atropky  of  tke  intestinal  mucosa,  to  wkick  tke  wasting 
kas  been  ascribed,  is  part  of  tke  general  wasting  ;  wkile  tke  microscopical 
appearances  are  due  to  gaseous  distension  of  tke  gut  and  post  mortem 
ckanges.  In  otker  words  tke  disorder  is  one  of  functional  impairment  of 
digestion,  absorption  or  assimilation.  In  tkose  instances  in  wkick  a 
sufficient  and  nutritious  diet  is  apparently  digested,  and  yet  tke  ckild 
wastes,  tke  functions  of  assimilation  are  in  abeyance,  defective  or  destroyed. 
Witk   increasing   feebleness   tke    circulation    becomes    weaker,    tke   lung 


Infantile   Atrophy.  173 

expansion  imperfect,  and  oxidation  incomplete.  On  insufficient  evidence 
the  condition  has  been  ascribed  to  acid-intoxication  ;  to  auto-intoxication 
from  decomposing  food  ;  to  deficient  activity  of  nutritive  ferments,  due 
to  intestinal  infection  ;  to  defect  in  Paneth's  cells,  found  in  Lieberkuhn's 
crypts  ;    and  to  sub-acute  or  chronic  infection  of  the  intestinal  tract. 

Symptoms  vary  according  to  the  age,  the  rapidity  of  the  wasting  and 
its  duration.  The  most  typical  cases  are  seen  in  infancy.  After  the  first 
year  acute  inanition  and  marasmus  are  less  frequent,  though  they  result 
from  acute  illness  and  from  causes  similar  to  those  acting  during  the  first 
year  of  life. 

Acute  Inanition  or  Acute  Atrophy  is  characterised  by  rapid  loss  of 
weight,  and  is  almost  invariably  associated  with  a  deficient  supply  or  an 
excessive  loss  of  fluid.  It  may  be  due  to  unsuspected  starvation.  The 
child  is  pallid  and  prostrated.  The  extremities  are  cold,  and  the  skin  dry 
or.  occasionally,  covered  with  clammy  sweat.  The  pulse  is  weak  and  frequent, 
breathing  shallow  and  irregular,  and  temperature  subnormal.  The  fon- 
tanelle  is  sunken,  sutures  overlapping,  pupils  small  or  pin-point,  and  the 
mental  condition  one  of  irritability  or  fretfulness,  passing  into  a  state  of 
semi-stupor.  The  appetite  is  lost.  Vomiting  may  be  absent,  or  occur  after 
several  feeds  have  been  taken,  because  of  distension  of  the  stomach  due 
to  loss  of  its  motor  power.  The  stools  are  sometimes  normal,  but  usually 
contain  undigested  food,  and  frequently  mucus.  If  no  food  is  taken,  they 
consist  of  epithelial  debris,  mucus  and  bile,  and  look  like  meconium. 
The  asthenia  increases.  It  may  be  associated  with  diarrhoea  and  slight 
cyanosis  of  the  lips,  and  prove  fatal  in  a  few  clays.  The  younger  the  infant 
the  more  rapid  is  the  progress.  In  less  severe  cases  life  may  be  prolonged 
from  three  to  six  weeks. 

An  infant  is  said  to  be  in  a  state  of  Malnutrition  when  it  is  much 
below  its  proper  weight,  remains  stationary  in  weight,  or  gains  very  slowly 
for  some  considerable  time.  In  addition  there  is  a  deficiency  in  the  other 
vital  processes  of  development,  such  as  growth  in  length,  acquirement  of 
the  functions  of  sitting,  standing  and  walking,  and  mental  development. 
The  muscles  are  flabby,  the  ligaments  weak,  and  the  joints  lax  and 
insufficiently  supported.  The  fontanelle  is  depressed.  Dentition  may  be 
delayed,  but  it  is  often  accomplished  without  trouble  or  discomfort.  Such 
infants  are  more  or  less  anaemic,  sharp-featured  and  emaciated,  with  cold 
extremities,  dark  rings  under  the  eyes,  deficient  elasticity  of  the  skin,  and 
a  temperature  which  readily  sinks  below  normal.  They  are  fretful,  irri- 
table, restless  and  sleep  badly.  Especially  are  they  subject  to  gastro- 
intestinal and  pulmonary  troubles,  and  frequently  die  from  an  attack  of 
bronchitis.  The  appetite  is  poor  or  capricious.  Indigestion  is  readily  £et 
up  and  attacks  of  diarrhoea  are  frequent.  Sometimes  there  is  an  actual 
catarrhal  enteritis  or  entero-colitis. 


174  Chapter   XIV. 

As  the  process  continues  it  passes  into  the  more  serious  stage  of 
wasting,  to  which  the  name  of  Marasmus  has  been  given.  It  must  be 
clearly  understood  that  marasmus  is  not  a  disease,  but  is  merely  a  late 
stage  in  the  course  of  malnutrition  from  various  causes.  It  is  conse- 
quently  common  during  the  first  year  of  life,  not  infrequent  in  the  second 
year,  and  may  occur  at  later  ages  as  a  sequel  of  prolonged  wasting  diseases, 
such  as  persistent  vomiting,  tuberculous  affections  and  cirrhosis  of  the  liver. 

In  infancy  the  general  history  is  that  the  child  has  been  always 
delicate  or  that  it  was  apparently  healthy  at  birth  and  while  breast-fed  ; 
that  it  began  to  waste  when  it  was  weaned  ;  that  the  wasting  has  steadily 
persisted  in  spite  of  various  methods  of  feeding,  tried  by  the  mother, 
recommended  by  the  neighbours,  or  suggested  by  specious  advertisements  ; 
and  that  in  spite  of  all  treatment  the  baby  has  got  thinner  and  thinner, 
and  has  had  frequent  attacks  of  vomiting  and  diarrhoea. 

In  a  typical  case  the  facial  aspect  is  that  of  old  age.  The  skin  of  the 
face  is  wrinkled,  thrown  into  folds  on  the  forehead  and  between  the  eyes, 
has  lost  its  elasticity  and  is  devoid  of  subcutaneous  fat.  All  over  the 
body  and  limbs  it  is  lax  and  easily  raised  from  the  subcutaneous  tissues. 
It  is  harsh,  dry,  and  hangs  in  folds.  The  bones  stand  out  sharply,  giving 
the  features  a  pinched  look  ;  the  eyes  and  temples  are  sunken,  and  the 
pupils  small ;  the  chest  and  extremities  show  little  more  than  skin  and 
bone  ;  the  abdomen  is  protuberant  and  tympanitic  ;  and  the  terminal 
phalanges  bluish.  The  temperature  is  low,  and  may  fall  below  95°  F., 
even  to  90°  F.  The  blood  is  deficient  in  haemoglobin  ;  the  circulation 
feeble  ;  and  the  face  pallid,  earthy  or  ashen  in  colour.  The  tongue  is  red 
and  dry,  and  both  it  and  the  mouth  are  often  covered  with  patches  of 
aphthae.  The  appetite  may  be  completely  lost  or  abnormal,  and  the 
state  of  the  stomach  and  bowels  as  in  malnutrition.  Even  water  may  be 
vomited,  and  if  the  stools  are  apparently  well  digested  they  are  unduly 
large  for  the  amount  of  food  taken.  The  mental  condition  is  one  of  fret- 
fulness  and  irritability,  or  of  listlessness  and  apathy. 

As  the  child  gets  worse,  it  is  very  liable  to  develop  oedema  of  the  dorsum 
of  the  feet  and  hands,  and  later  of  the  eyelids,  face  and  rest  of  the  body. 
Effusions  into  serous  cavities  are  absent.  Diarrhoea  may  become  less  or 
cease.  Petechial  haemorrhages  are  apt  to  appear  on  the  lower  part  of  the 
abdomen,  the  whole  abdomen,  or  on  the  trunk,  upper  part  of  the  thighs, 
and  elsewhere. 

In  simple  malnutrition  and  acute  inanition  complications  are  usually 
absent.  Aphthous  stomatitis  may  occur  at  any  stage  of  wasting,  and 
helps  to  maintain  or  increase  the  malnutrition.  Herpetic  stomatitis  is 
less  frequent,  but  is  liable  to  occur  in  repeated  attacks  in  chronic  cases. 
Temporary,  mild  or  severe,  enteritis  or  entero-colitis  is  common.  In  pro- 
longed wasting  redness  of  the  skin  appears  over  the  sacrum,  heels,  occiput, 
and   other   bony    prominences,   and    may   proceed   to   the   formation    of 


Infantile   Atrophy.  175 

bed-sores.  Erythema  and  superficial  ulceration  of  the  buttocks  arise  from 
irritant  discharges.  Pustular  boil-like  spots  appear  on  the  scalp,  and 
similar  boils  or  subcutaneous  abscesses  on  the  trunk  and  limbs.  The 
glands  are  susceptible  to  enlargement,  and  may  reach  the  size  of  large  peas 
or  small  nuts  in  the  neck,  groins  and  axillae.  Reflex  opisthotonos  is  not 
uncommon,  and  the  babe  may  lie  continually  with  its  head  thrown  back, 
spine  bent  and  heels  drawn  up.  Vomiting  and  enteritis  are  serious 
complications. 

Improvement  is  indicated  by  gain  in  weight,  provided  there  is  no 
oedema,  better  appetite  and  digestion,  less  fretfulness,  and  a  temperature 
nearer  the  normal  level.  The  downward  course  is  usually  gradual,  and 
death  results  from  asthenia,  sometimes  in  convulsions.  It  may  be  preceded 
by  a  period  of  unconsciousness  of  more  or  less  sudden  onset.  It  may  take 
place  quite  suddenly,  although  no  change  has  been  noted  in  the  state  of 
the  child  ;  due  to  cardiac  syncope,  perhaps  the  result  of  flatulent  distension 
of  the  stomach.  Quite  sudden  collapse  may  also  be  induced  by  pulmonary 
collapse,  broncho-pneumonia,  vomiting,  diarrhoea  or  fits. 

Diagnosis. — Acute  inanition  is  usually  recognised  easily  when  due 
to  insufficient  food,  if  the  possible  cause  is  suspected.  A  baby,  seen  on  the 
thirteenth  day  of  life,  was  dying  from  starvation.  It  had  lost  2  lbs.  in 
weight  and  its  stools  contained  no  faecal  matter.  The  mother's  breasts 
were  large  and  fat,  and  the  milk  supply  had  been  supposed  to  be  efficient. 
On  extra  food  the  child  rapidly  recovered.  The  subnormal  temperature 
generally  enables  acute  diseases  to  be  excluded,  and  the  rapid  onset  of  the 
wasting  distinguishes  it  from  that  of  marasmus,  except  when  it  occurs  as 
a  termination  of  chronic  wasting. 

The  differentiation  between  malnutrition  and  marasmus  in  infancy 
is  merely  one  of  degree.  Before  making  a  diagnosis  of  simple  malnutrition, 
care  must  be  taken  to  exclude  the  common  causes  of  wasting  in  which 
there  is  organic  or  constitutional  disease,  such  as  pyloric  stenosis  and 
other  malformations  of  the  alimentary  tract,  gastric  and  intestinal  catarrh, 
pulmonary  troubles,  empyema,  morbus  cordis,  rickets,  congenital  syphilis, 
and  tuberculosis.  Time  after  time  one  sees  infants  in  whom  tuberculous 
disease  is  suspected,  and  no  evidence  thereof  found  after  death.  Less 
often,  at  the  autopsy  on  a  "  waster,"  extensive  tuberculosis  is  found, 
although  there  has  been  no  suspicion  thereof  during  life  and  the  tem- 
perature has  remained  continuously  subnormal. 

Methods  of  diagnosis  in  infancy  include  regular  weighing  ;  examination 
of  the  breast-milk  or  the  artificial  food  ;  the  passage  of  a  stomach  pump 
and  examination  of  the  contents  of  the  stomach  for  mucus,  hydrochloric 
and  organic  acids,  and  bacteria,  and  estimation  of  its  motility  ;  examination 
of  the  faeces  ;  examination  of  the  urine  for  albumin  and  indican,  and  less 
often  of  the  blood  and  cerebro-spinal  fluid. 


176  Chapter  XI  V. 

In  older  children  the  suspicion  of  tuberculosis  is  very  difficult  to  get 
rid  of.  The  history,  diet  and  mode  of  life  must  be  carefully  investigated, 
and  the  child  examined  thoroughly  for  evidence  of  lung  disease  and 
glandular  enlargement  in  the  neck,  chest  or  abdomen.  Chronic  dyspepsia 
at  the  time  of  the  second  dentition  is  often  a  cause  of  marked  wasting,  with 
cough,  anorexia,  and  sometimes  headache  and  restlessness.  It  is  gastric 
or  intestinal  in  origin,  and  may  be  associated  with  pharyngitis,  enlarged 
tonsils  and  adenoids.  Do  not  forget  that  as  the  child  grows  in  height  it 
commonly  loses  weight,  but  that  malnutrition  associated  with  rapid 
growth  is  not  always  due  to  growth.  Lack  of  development  may  also 
result  from  naso-pharyngeal  obstruction  or  deficiency  of  thyroid  secretion. 

Treatment. — The  prophylaxis  of  infantile  atrophy  includes  all  that 
is  conducive  to  healthy  growth  and  development.  In  treating  a  wasted 
infant  the  diet  should  be  that  appropriate  for  an  infant  younger  in  age. 
and  the  intervals  between  the  meals  shorter.  For  infants  under  4  months 
a  wet  nurse  is  advisable.  The  diet  should  be  weak  in  quality,  and  altered 
in  accordance  with  the  progress  of  the  case.  Changes  must  be  made  with 
extreme  care.  A  slight  excess  of  food  may  bring  on  acute  indigestion  or 
diarrhoea,  and  undo  in  24  hours  the  good  of  weeks  of  careful  treatment  or 
even  prove  fatal.  Breast-feeding  may  be  prolonged,  entirely  or  partially, 
up  to  the  age  of  18  months  if  the  child  is  small  and  like  a  much  younger 
infant.  If  it  is  not  available,  or  is  inadvisable,  reliance  must  be  placed  on 
whey,  cream  and  whey,  peptonised  and  modified  milk,  condensed  milk, 
albumin  water,  various  malted  and  partly  malted  foods,  and  Benger's 
food.  At  first  cow's  milk  must  be  much  diluted  and  given  very  cautiously. 
The  digestive  capacity,  not  the  age  or  weight,  is  to  be  taken  as  the  guide 
to  the  diet  selected.  In  mild  cases  the  ordinary  principles  of  feeding, 
suitable  for  a  rather  younger  infant,  can  be  adopted.  In  more  severe  ones 
the  yolk  of  egg,  bone  marrow,  raw  meat  juice,  and  cod-liver  oil  may  be 
given,  bearing  in  mind  that  marasmic  infants  digest  fat  with  difficulty 
and  may  get  diarrhoea.  A  suitable  mixture,  consisting  of  the  yolk  of  one 
egg,  glycerine  1  oz.,  olive  oil  or  cod-liver  oil  1  oz.,  and  creosote  10  m.,  in 
doses  up  to  1  dr.,  can  be  given  4  times  a  day.  In  very  severe  cases  the 
infant  must  be  kept  warm,  rubbed  with  oil,  wrapped  in  cotton  wool,  and 
surrounded  with  hot  bottles,  or  put  in  an  incubator. 

The  general  measures  suitable  for  all  cases,  modified  according  to  the 
age,  include  a  liberal  supply  of  fresh  air  ;  general  friction  or  massage  with 
olive  oil  or  cocoa  butter  ;  regularity  in  diet,  sleep  and  bathing  ;  and  spon- 
ging with  cold  water,  about  60-70°  F.,  after  the  morning  bath.  If  these 
cases  are  accumulated  in  institutions,  ventilation  must  be  free  and  each 
child  allowed  800  c.f.  air  space.  Alcohol,  saline  injection  and  gavage  are 
sometimes  needed. 

No  cases  exercise  the  skill  of  the  physician  to  a  greater  extent  than 
some  of  these  wasters.     The  longer  the  duration  of  wasting,  the  greater 


Infantile   Atrophy.  177 

is  the  care  required  and  the  more  tedious  is  the  cure.  Much  depends  on  the 
faithful  carrying  out  of  instructions,  which  should  invariably  be  written 
down  fully  and  clearly.  The  parents  must  have  faith  in  the  physician 
to  whose  charge  they  entrust  the  treatment,  and  above  all  must  realise 
that  the  progress  will  be  very  slow.  Experiments  in  diet  are  often  fatal, 
especially  in  hot  weather,  and  frequently  bad  results  are  due  to  changes  in 
the  food  ordered  by  competent  physicians  successively  called  in  con- 
sultation. No  case  is  hopeless  and  no  pains  are  wasted  in  trying  to  bring 
about  a  better  state  of  health,  for  these  babies  ultimately  become  strong 
and  healthy,  if  the  atrophy  is  due  to  dietetic  causes  and  not  of  constitu- 
tional origin.  The  utmost  care  is  necessary,  and  plenty  of  fluid  given. 
Water  can  do  no  harm.  The  stools  must  be  examined  daily  and  the 
child  weighed  twice  a  week  or  daily  in  the  worst  cases. 

In  older  children  the  treatment  consists  of  simple  diet,  regular  meals, 
regular  habits,  and  open-air  life,  cold  sponging,  limited  studies,  and  no 
excitement.  Forced  feeding  is  inadvisable.  Iron,  arsenic  and  cod-liver 
oil  are  the  best  drugs,  if  the  alimentary  tract  is  in  a  satisfactory  condition. 

In  every  case  of  simple  atrophy  the  prognosis  improves  with  the  age 
of  the  child,  and  varies  directly  as  the  care  devoted  to  its  treatment  and 
its  environment.  It  is  worst  in  those  instances  of  inherited  constitutional 
delicacy,  and  is  increased  in  gravity  by  hot  weather.  The  mortality  is 
high  in  hospitals,  because  only  the  worst  and  most  prolonged  cases  are 
admitted,  and  the  power  of  assimilation  in  many  of  them  is  apparently 
completely  lost. 


N 


Chaptek  XV. 

RICKETS. 

Rickets  was  described  by  Glisson  (1681),  who  gave  it  the  name  of 
"Rachitis"  from  a  Greek  word  for  the  spine,  on  account  of  the  deformity 
of  the  spine  so  commonly  present  and  its  similarity  to  the  popular  name 
"Rickets"  which  was  probably  a  corruption  of  the  Norman-French  word 
"  Riquets  "  for  deformities.  It  is  a  common  chronic  disease  of  malnutrition, 
occurring  early  in  life  from  faulty  diet.  Its  increasing  prevalence  is  due 
to  the  increasing  inability  of  women  to  nurse  their  children  and  to  aggre- 
gation in  industrial  centres.  It  affects  the  whole  system,  but  the  most 
evident  effects  are  produced  on  the  cartilages  and  bones.  The  osteogenetic 
tissues  undergo  abnormal  proliferation  and  either  lose  or  have  never 
possessed  the  power  of  making  good  bone.  The  general  disturbance  of 
metabolism  involves  the  nervous  system,  mucous  membranes,  muscles, 
and  ligaments.  The  disease  is  not  fatal  in  itself,  but  predisposes  to  illness 
which  may  be  fatal,  or  would  not  be  serious  apart  from  the  effects  of  the 
rachitic  process.  It  is  a  grave  source  of  alimentary  and  respiratory 
affections  in  infancy,  of  nervous  phenomena  less  directly,  and  of  deformities 
which  may  affect  the  individual  throughout  life  and  in  the  future  mother 
prove  a  source  of  disaster  during  confinement. 

Some  cases  are  much  more  acute  than  others,  and  are  associated  with 
visceral  lesions,  profuse  sweating  and,  possibly,  some  bony  tenderness. 
In  others  the  bone  symptoms  and  resulting  deformities  predominate. 
In  a  third  type  the  catarrhal  symptoms  are  the  chief  feature.  In  a  fourth 
variety,  known  as  the  "  Acrobatic  "  type,  there  is  a  remarkable  laxity  of 
ligaments  and  muscles. 

Etiology. — It  exists  everywhere,  although  it  has  been  called  "The 
English  Disease."  Climate  and  confined  life  encourage  its  production.  It 
is  common  in  the  temperate  zone  ;  rare  in  the  tropics,  China,  Japan,  and 
the  southern  parts  of  Italy  and  Spain  ;  almost  unknown  near  the  equator, 
infrequent  in  Iceland,  Greenland,  Norway,  and  Denmark.  It  is  rare  at  high 
altitudes  ;  more  common  in  towns  than  country  districts  ;  rare  among 
negroes  ;  almost  as  common  among  the  rich  as  the  poor,  though  in  a  less 
severe  form.  The  worst  cases  are  seen  in  the  spring,  as  the  result  of  the 
climatic  conditions  and  confined  life  of  an  English  winter.  Yet  they 
do  not  occur  in  some  more  northern  countries  where  winter  is  longer  and 


Rickets.  179 

the  child  more  indoors.  If  slight  beading  of  the  ribs  or  craniotabes  be 
regarded  as  sufficient  evidence  of  the  disease,  it  will  be  found  in  50  per  cent. 
of  all  children  living  in  towns. 

The  disease  is  not  transmitted  from  the  parents.  Hausen  states  that 
a  stallion  begat  seven  rachitic  foals,  and  that  two  of  the  mares  subsequently- 
had  healthy  foals  by  other  sires.  Possibly  the  mother's  diet  during 
pregnancy,  if  deficient  in  protein  and  fat,  and  deterioration  of  her  health 
from  any  cause,  such  as  frequent  pregnancies,  may  act  as  predisposing 
and  exciting  causes,  through  the  child  being  born  delicate  and  with  less 
resisting  power,  and  the  maternal  milk  supply  being  of  poor  quality. 
Sex  has  no  influence.  It  begins  at  some  period  of  the  first  dentition,  does 
not  often  become  evident  before  the  age  of  6  months — a  fact  suggestive 
•of  post-natal  causes — and  by  the  eighteenth  month  is  distinctly  marked  ; 
usually  it  begins  at  the  age  of  6-12  months.  Intra-uterine  cases  have  been 
reported,  and  a  few  in  later  childhood.  It  may  occur  in  breast-fed 
infants  because  of  a  deficiency  in  the  mother's  milk.  In  bottle-fed  infants 
it  results  from  a  diet  deficient  in  fat,  still  more  if  it  is  also  deficient  in  protein, 
and  even  more  if  carbohydrate  is  in  excess.  The  food  may  contain  the 
requisite  percentages  of  the  different  constituents,  but  the  assimilative 
powers  of  the  child  be  impaired  by  its  unsuitable  character.  It  is  very 
unusual  to  find  a  baby  brought  up  on  condensed  milk,  alone  or  in  combination 
with  a  proprietary  food,  who  is  not  definitely  rachitic  ;  these  foods  are 
deficient  in  protein  and  fat.  The  breast-fed  infant  may  develop  the  disease 
and  the  bottle-fed  one  remain  healthy.  In  the  breast-fed,  however,  it  is 
generally  of  a  mild  type.  The  importance  of  food  must  not  be  overrated  ; 
some  infants  will  thrive  upon  almost  anything,  and  not  develop  rickets. 

Puppies  fed  by  Guerin  on  a  meat  diet  for  4-5  months  became  rachitic 
while  others  of  the  same  litter,  suckled,  showed  no  sign  of  the  disease. 
Bland  Sutton  found  that  young  lions  at  the  Zoological  Gardens  became 
very  rachitic,  if  weaned  early  and  fed  on  raw  meat  only.  The  addition  of 
milk  and  cod-liver  oil  to  the  diet  cured  them  in  3  months.  Two  young 
monkeys  fed  on  a  vegetable  diet  developed  rickets.  On  the  other  hand 
.similar  feeding  experiments  on  young  animals  have  produced  profound 
marasmus  and  death  without  causing  rickets.  These  experiments  show 
that  an  improper  diet  will  produce  the  disease,  though  it  fails  to  show 
itself  under  conditions  which  produce  marasmus.  The  defect  in  the  diet 
is  a  deficiency  in  fat. 

Kecent  experiments  by  Findlay  (1908)  show  that  confinement  and 
lack  of  exercise  have  an  important  bearing  on  rickets  ;  so  much  so  that 
he  ascribes  the  disease  to  lack  of  exercise.  Oxidation  is  diminished  or 
■carbonic  acid  excretion  defective.  He  found  that  experimental  animals 
and  birds  kept  in  cages  often  developed  rickets,  although  they  got  sun  and 
fresh  air;  and  he  induced  it  in  puppies  by  confinement  only,  and  could  not 
do  so  by  any  diet  if  free  exercise  was  allowed.     In  support  of  his  views 


180  Chapter  XV. 

it  may  be  urged  that  the  disease  is  common  in  towns  and  the  winter  months  ; 
that  it  is  rare  in  hot  countries  ;  and  that  it  does  not  occur  in  Japan  in  spite 
of  prolonged  lactation.  Maternal  nursing  and  an  open-air  life  in  a  mild 
climate  have  a  greater  prophylactic  effect  than  mere  locality. 

Associated  digestive  disorders  also  indicate  that  the  diet  is  unsuitable. 
If  such  disorder  is  severe  or  prolonged,  the  marasmic  state  hides  the 
rachitic  one.  Marked  evidence  of  the  disease  is  rare  in  marasmic  infants. 
This  probably  means  that  assimilation  and  growth  must  take  place  in 
order  to  produce  the  characteristic  physical  signs.  Syphilis  has  no  influence 
beyond  interfering  with  digestion  and  assimilation,  and  reducing  the 
resisting  power  of  the  infant.  Tuberculosis  has  a  similar  effect.  The 
malformation  of  the  thorax  induced  by  rickets,  and  the  catarrhal  affections 
of  the  lungs  to  which  a  rachitic  baby  is  liable,  render  it  more  susceptible  to 
tuberculosis.  Only  wasting  disorders  can  be  regarded  as  antagonistic,  and 
they  are  merely  so  because  the  child  has  not  sufficient  vitality  left  for  the 
production  of  the  characteristic  proliferative  processes  in  the  cartilages 
and  bones. 

Morbid   Anatomy. — Changes  take  place  in  the  bones  as  the  result  of 
imperfect  nutrition   or  chronic  inflammation,   or   a   combination  of  the 
two  processes.     There  is  increased  vascularity  of  the  medulla  and  perios- 
teum, and  increased  cell  proliferation,  but  ossification  is  imperfect  in  spite 
of  the  excessive  preparation  made  for  it.     The  bones  become  soft  and 
flexible,  and  the  epiphyses  enlarged.     At  the  epiphyseal  line  of  the  long 
bones  there  are  found  excessive  vascularity  of  the  cartilage  and  abnormal 
proliferation  and  irregularity  of  the  cartilage  cells,  and  of  the  osteoblasts- 
in  the  deep  layer  of  the  periosteum.    The  process  of  ossification  is  imperfect,, 
slow  or  arrested,  and  the  normal  absorption  of  the  inner  layers  of  the  bone 
in  the  medullary  cavity  is  increased.     At  the  growing  zone  calcification 
is  deficient  and  much  osteoid  tissue  formed.    The  cartilage  at  the  epiphy- 
seal line  is  thickened,  bluish-white,  softer  than  normal,  and  almost  gela- 
tinous.    On  one  side  it  blends  with  the  cartilage  of  the  epiphysis,  and  on 
the  other  has  an  irregular  dentate  border  and  contains  scattered  irregular 
calcified  areas.     This  causes  beading  of  the  ribs  and  enlargement  of  the 
epiphyseal  line  at  the  ends  of  the  bones.    In  more  severe  cases  the  whole  of 
the  epiphysis  is  involved,  for  the  ossifying  centres  become  softer,  larger  and 
unduly  vascular.     The  shafts  are  abnormally  flexible,  because  of  deficient, 
periosteal  bone  formation  and  increased  medullary  absorption.     Normal 
bone  contains  37  parts  of  organic  and  63  of  inorganic  matter  ;    the  worst 
rachitic  bone,  79  organic  and  21  inorganic,  in  consequence  of  the  absorption 
of  phosphate  of  lime.     Kassowitz  states  that  the  deficiency  of  lime  salts- 
is  20-30  per  cent.    The  shafts  become  rounded  and  abnormal  curves  form. 
These  curves  are  simple  exaggerations  of  normal  curves,  produced  by  the 
weight  of  the  trunk  and  limbs.     Abnormal  curves  are  due  to  unnatural 
positions  and  abnormal  muscular  action.     Premature  union  of  the  shaft 


RicJcets.  181 

with  the  epiphysis  may  arrest  growth.  Fractures  result  from  trivial  causes 
on  account  of  the  fragility  of  the  bones.  They  are  usually  of  the  green- 
stick  variety,  at  the  point  of  the  greatest  curvature  of  the  bone,  and  most 
common  in  the  radius,  ulna,  clavicle  and  ribs  in  the  order  named  ;  much 
•callus  is  thrown  out. 

The  enlargement  of  the  cartilages  at  their  junction  with  the  ribs 
produces  the  "Beading"  or  rickety  "Rosary."  It  is  first  felt  at  the  ends 
of  the  fifth  and  sixth  ribs,  and  is  most  marked  on  the  pleural  surface.  The 
so-called  beading  at  the  back  of  the  thorax  is  due  to  partial  fracture  of  the 
ribs  at  or  near  the  angles.  These  beads  are  angular,  rather  than  nodular, 
projections  on  the  external  surface  ;  single  or  unilateral,  asymmetrical, 
and  variable  in  position.  In  front  of  the  chest  grooves  are  situated  outside 
the  beads,  extending  from  above  obliquely  downwards  and  outwards,  and 
are  due  to  the  atmospheric  pressure  on  the  ribs  which  are  softer  than  the 
•cartilages. 

Harrison's  sulcus  is  a  transverse  groove  at  the  level  of  the  upper 
limits  of  the  liver,  spleen  and  stomach,  which  prevent  the  lower  parts  of  the 
chest  wall  falling  in  as  much  as  the  upper.  The  liver  renders  it  more 
marked  on  the  right  than  on  the  left  side.  The  unyielding  abdominal 
viscera  cause  eversion  of  the  lower  ribs.  On  the  left  side  the  ribs  may  be  a 
little  more  convex  on  account  of  the  underlying  heart.  The  apex  of  the 
heart  may  be  displaced  outwards  ;  and  the  left  ventricle  be  more  exposed 
and  exhibit  a  white  patch  due  to  attrition  against  a  bead.  There  is  partial 
collapse  of  the  lung  under  the  deep  antero-lateral  furrows,  with  emphysema 
of  the  anterior  portions.  Bronchitis,  broncho-pneumonia  and  patches 
of  collapse  are  often  present. 

The  abdomen  is  "  pot-bellied "  from  flatulent  distension  due  to 
intestinal  catarrh,  excess  of  carbohydrate  food  and  muscular  weakness. 
The  liver  is  sometimes  enlarged,  and  still  more  often  appears  so,  for  the 
•deformity  of  the  chest  exposes  more  of  its  surface.  The  spleen  and  lym- 
phatic glands  may  be  larger  than  normal.  The  pelvis  is  more  triangular 
than  oval  in  shape,  but  this  depends  partly  on  the  age  at  which  the  disease 
is  active  and  the  position  assumed  by  the  child.  The  bodies  of  the  verte- 
bras are  softer  and  more  vascular  than  normal.  Between  them  and  the  discs 
is  a  bluish-white  proliferating  zone  of  cartilage. 

The  cranium  may  show  extensive  craniotabes  from  delayed  ossification 
or  a  patchy  variety  due  to  re-absorption  of  already  formed  bone.  Ossifica- 
tion of  the  fontanelles  is  commonly  delayed.  In  mild  cases  the  edges  only 
of  the  cranial  bones  show  periosteal  thickening;  in  more  severe  ones  cranial 
bosses  or  hyperostoses  are  formed.  These  are  soft,  red,  vascular  masses  of 
spongioid  bone,  as  much  as  half-an-inch  thick,  and  can  be  indented 
with  the  finger  or  cut  with  a  knife,  blood  and  serum  being  easily  squeezed 
out.  They  are  due  to  thickening  of  the  bone,  chiefly  the  outer  table,  about 
the  centres  of  ossification.     In  the  course  of  time  thev  are  absorbed  or 


182  Chapter    X  T. 

organised  into  light  porous  bone,  or  form  diffuse  laminae  of  dense  ivory-like 
bone.  The  abnormal  ossification  makes  the  appearance  of  the  skull 
suggestive  of  hydrocephalus. 

Pathology. — The  cardinal  factor  is  increased  vascularity  of  the 
growing  portions  of  the  bones,  giving  rise  to  excessive  cell  proliferation  and 
irregularities  of  calcification  and  ossification.  When  it  subsides  the  vessels 
diminish  in  size  and  normal  bone  is  formed.  The  process  may  be  regarded 
as  analogous  to  that  of  a  chronic  inflammation.  In  support  of  this  view 
it  may  be  pointed  out  that  artificially  produced  hyperaemia  causes  prolifera- 
tion of  cartilage  cells,  absorption  of  newly-formed  bone,  and  deficiency  of 
lime  salts  ;  and,  further,  that  bones  affected  with  chronic  inflammation  are 
deficient  in  lime  salts. 

Undoubtedly  there  is  perversion  of  tissue  metabolism.  The  deficiency 
of  lime  salts  in  the  bones  has  been  ascribed  to  deficiency  of  lime  and 
phosphoric  acid  in  the  diet,  and  defective  absorption  or  increased  katabolism 
( The  Lime  Theory).  Experiments  on  animals  show  that  a  diet  deficient 
in  lime  produces  osteoporosis  and  rachitic-like  changes  in  the  growing 
cartilages  and  the  periosteum.  This  condition,  however,  differs  from  rickets, 
in  that  the  soft  tissues  are  also  deficient  in  lime  and  that  it  can  be  cured 
by  giving  calcium  chloride.  It  may  also  be  urged  against  the  lime  theory 
that  uncalcified  cartilage  is  in  excess  in  rickets,  that  such  cartilage  con- 
tains a  high  percentage  of  lime  salts,  and  that  marked  proliferation  of  the 
cells  is  impossible  without  a  supply  of  lime.  Both  cow's  milk  and  fari- 
naceous foods  contain  much  lime. 

According  to  the  "  Lactic  Acid  Theory,"  lime  is  absorbed  from  the 
bones  by  lactic  acid  circulating  in  the  tissues,  and  there  is  an  excess  of 
lactic  acid  and  other  inorganic  acids  in'the  blood.  These  organic  acids  are 
produced  by  an  excess  of  carbohydrate  food  and  deficient  oxidation.  Conse- 
quently rickets  develops  in  infants  over-fed  on  carbohydrate  food  and 
deprived  of  sufficient  exercise  and  fresh  air.  Deficient  metabolism  of 
carbohydrates  leads  to  the  production  of  by-products  which  affect  cartilage 
and  bone,  as  well  as  the  general  metabolism  of  the  body.  The  administra- 
tion of  lactic  acid  to  flesh  eating  animals  produced  rickets,  and  subse- 
quently osteomalacia,  and  in  herbivorous  animals  osteomalacia  without 
antecedent  rickets  (Heitzmann).  These  experiments  and  conclusions  are  of 
doubtful  value,  for  the  food  was  deficient  in  lime  salts  and  marasmus  and 
other  complications  occurred.  Korsakow  repeated  them  on  dogs  without 
success.  Wegner  produced  rickets  by  giving  small  doses  of  phosphorus, 
probably  through  its  action  as  an  irritant.  We  may  conclude,  therefore, 
that  the  various  theories,  viz.,  (1)  errors  of  lime  metabolism  ;  (2)  excess 
of  lactic  acid  ;  (3)  deficient  blood  alkalinity  ;  (4)  retention  of  carbonic  acid, 
are  all  unconfirmed.  Our  knowledge  is  at  present  limited  to  the  fact 
that  the  disease  is  the  result  of  an  improper  diet,  apparently  one  defective 
in  fat,  which  gives  rise  to  increased  vascularity  ;    and  that  both  this  and 


Rickets.  183 

the  bone  changes  are  due  to  the  circulation  in  the  blood  of  some  irritant, 
which  leads  to  absorption  of  lime  and  other  changes.  This  is  seen  in  the 
production  of  craniotabes  by  softening  of  previously  ossified  bone.  If 
from  deficiency  of  lime  in  the  food,  or  from  mal  assimilation  of  lime,  the 
blood  is  defective  in  this  salt,  it  is  reasonable  to  assume  that  it  re-absorbs 
lime  from  bone  in  order  to  maintain  its  normal  equilibrium. 

Symptoms. — The  indications  of  rickets  consist  of  certain  constitu- 
tional symptoms  and  the  anatomical  effects,  softening  and  deformity,  on 
the  skeletal  system.  The  first  signs  are  fretfulness,  restlessness,  disturbed 
sleep,  throwing-off  the  bed-clothes,  sweating  of  the  head,  beading  of  the 
ribs,  craniotabes,  constipation,  and  disinclination  to  move  about  if  able 
to  do  so.  Later  on  there  develop  enlargement  of  the  epiphyses,  especially 
the  radial ;  deformities  of  the  head,  limbs  and  thorax  ;  protuberant  ab- 
domen ;  weakness  of  the  muscles,  ligaments  and  other  tissues  of  the  body  ; 
an&'mia  ;  irritability  of  the  nervous  system  ;  liability  to  catarrh  of  the 
respiratory  and  the  alimentary  mucous  membranes  ;  irregular  and  delayed 
dentition  ;   and  perhaps  enlargement  of  the  liver  and  spleen. 

The  blood  shows  nothing  characteristic,  though  anaemia  is  often 
present  and  the  haemoglobin  may  amount  to  only  60  per  cent.  The  anaemia 
must  be  regarded  as  due  to  adventitious  causes,  or  as  a  result  of  the  same 
cause  that  produces  the  rickets.  It  is  not  due  to  rickets  itself,  for  ordin- 
arily the  number  of  red  cells  and  percentage  of  haemoglobin  is  increased. 
Nucleated  red  cells,  polychromatophilia  and  myelocytes  are  rare  ;  and  the 
white  cells  show  no  definite  change.  Pyrexia,  if  present,  is  due  to  some 
complication.  Some  children  are  rosy  and  well  nourished  ;  others  are  pale, 
fat  and  flabby,  with  very  little  resisting  power,  and  liable  to  acute  affections 
of  the  mucous  membranes.  These  are  spoken  of  as  cases  of  "  fat  rickets," 
as  opposed  to  "  thin  rickets,"  in  which  there  is  considerable  wasting.  The 
appetite  is  generally  good,  sometimes  it  is  excessive,  and  there  is  a  great 
desire  for  salt.  Constipation  is  frequent  in  the  early  stages  and  still  more 
so  in  the  later  ones.  It  is  due  to  lack  of  muscular  tone  and  sometimes 
chronic  intestinal  catarrh  ;  it  may  alternate  with  diarrhoea,  for  the  hard 
dry  stools  set  up  a  chronic  catarrh  in  the  colon,  with  passage  of  large 
quantities  of  mucus  ;  the  stools  are  often  deficient  in  pigment.  Diarrhoea 
is  liable  to  be  acute.  The  urine  is  faintly  acid  and  deficient  in  calcium,  but 
no  marked  differences  have  been  noticed.  Neither  lactic  acid  nor  phos- 
phoric aoid  has  been  found  in  excess.  Various  symptoms  arise  from 
defective  nutrition  of  the  central  nervous  system.  Sweating  is  profuse 
during  sleep  ;  the  sweat  is  acid,  stands  out  in  drops  on  the  forehead  and 
may  soak  the  pillow.  Sometimes  there  is  increased  general  sweating, 
with  sudamina.  Insomnia  is  common.  While  asleep  the  child  is  restless, 
rolls  the  head  from  side  to  side,  rubs  the  hair  off  the  occiput,  burrows  in 
the  pillows,  tosses  about  and  throws  off  the  clothes.  These  symptoms  are 
not  always  due  to  rickets.     There  is  increased  susceptibility  to  reflex 


184  Chapter   XV. 

irritation  ;  increased  liability  to  muscular  spasm  in  the  form  of  laryngo- 
spasm,  tetany  and  general  convulsions.  These  affections  are  most  common 
at  3-9  months  of  age,  and  often  induced  by  stomach  or  intestinal  disturbance. 
In  some  cases  facial  irritability  is  the  only  sign  ;  it  must  be  regarded  as  a 
danger  signal. 

The  head  appears  too  large  actually  or  in  proportion  to  the  rest  of  the 
body.  Occasionally  it  is  dolichocephalic,  elongated  fore  and  aft,  with 
raised  prematurely  ossified  sutures  ;  a  type  more  common  in  the  degenerate 
than  the  rachitic.  Usually  it  is  an  irregular  square  with  flattened  crown 
and  broad  square  forehead  ;  sometimes  the  frontal  and  parietal  bosses 
are  so  marked  as  to  stand  up  above  the  median  and  transverse  grooves, 
due  to  the  sagittal  and  coronal  sutures,  forming  the  "  hot-cross  bun  "  type, 
or  "  tete  carree."  These  bosses  may  have  a  pale  bluish  tinge,  as  seen  through 
a  thin  scalp.  They  are  a  possible  source,  while  growing,  of  local  discomfort 
and  irritability,  leading  to  head  banging,  rolling,  etc.  The  occipital  pro- 
tuberance is  prominent,  for  the  whole  of  the  upper  part  of  the  bone  may  be 
flattened  from  pressure,  so  as  to  appear  nearly  vertical  on  side  view. 
Marked  asymmetry  is  due  to  flattening  of  the  parieto-occipital  region 
on  the  one  side,  and  prominence  of  the  frontal  region  on  the  other.  The 
anterior  fontanelle  is  large,  and  may  remain  open  until  the  end  of  the 
first  dentition,  instead  of  being  closed  by  the  end  of  the  eighteenth  month. 
Even  at  the  age  of  2  years  it  may  measure  2  ins.  across,  and  there  is  a 
depression  sometimes  in  its  place  up  to  the  age  of  5  years.  The  other 
fontanelles  and  sutures  remain  open  an  unduly  long  time,  and  there  is 
delay  in  ossification  of  the  bones  along  the  edges  of  the  sutures,  giving  rise 
to  one  variety  of  craniotabes.  The  superficial  veins  of  the  scalp  are 
prominent  and  easily  seen  through  the  thin  skin.  They  may  form  definite 
grooves  in  the  bone,  distinguishable  with  difficulty  from  irregular  sutures. 
The  hair  is  thin  and  often  worn  off  the  occiput,  and  sometimes  off  the 
sides,  from  sweating  and  friction. 

The  face  looks  small  by  contrast  with  the  prominent  forehead  and 
large  head.  The  antero-posterior  diameter  of  the  upper  jaw  is  lengthened, 
and  gives  it  a  beak-like  aspect ;  that  of  the  lower  jaw  is  shortened,  and  the 
shape  is  irregular. 

Craniotabes. — There  are  two  distinct  forms  of  this  condition.  The 
first  is  uncommon  ;  is  seen  in  infants  under  6  months  of  age  ;  and  consists 
of  small  soft  spots,  round  or  oval,  J-l  in.  in  diameter,  and  chiefly  in  the 
posterior  half  of  the  parietals  and  the  membranous  half  of  the  occipital 
bone.  On  pressure  they  yield  with  parchment-like  crackling.  This 
variety  is  seen  in  congenital  syphilis,  with  or  without  rickets.  In  the  other 
type  the  free  margins  of  the  flat  bones  of  the  skull,  especially  the  parietal 
and  the  occipital,  are  soft  and  late  in  ossifying,  and  remain  membranous 
for  a  long  time.  It  is  quite  common  to  find  softening  along  the  margins 
of  the  parieto-occipital  suture,  and  in  severe  cases  along  the  margins  of 


Rickets.  185 

each  cranial  suture,  and  round  each  fontanelle.  In  the  latter  instances 
there  may  be  isolated  soft  spots,  due  to  surrounding  ossification.  The 
occiput  is  flattened.  The  condition  is  rather  one  of  marked  flexibility 
than  true  softening.  This  flexibility  is  found  from  the  third  to  the  twelfth 
month  of  life,  rarely  earlier  and  never  later.  It  is  most  common  in  infants 
brought  up  on  condensed  milk,  and  in  those  seen  in  the  early  months  of  the 
year.  It  is  due  to  delayed  ossification  or  to  re-absorption  of  lime  salts 
from  the  newly  ossified  bone,  in  consequence  of  deficiency  of  lime  salts  in 
the  food  or  their  presence  in  an  unsuitable  form.  It  may  exist  without 
any  other  evidence  of  rickets,  or  with  very  slight  beading.  Consequently, 
it  cannot  be  regarded  as  a  definite  proof  of  rickets,  but  it  shows  that  the 
diet  is  unsuitable.  On  the  other  hand,  it  is  cured  by  anti-rachitic  remedies 
and  is  often  associated  with  laryngospasm.  The  cranial  bones  may  be 
membranous  at  birth  and  remain  so,  or  undergo  softening  from  cerebral 
tumour  or  hydrocephalus. 

Variations  in  teething  depend  on  the  date  of  origin  of  the  disease.  The 
first  teeth  are  often  cut  at  the  usual  time,  and  the  subsequent  ones  are 
delayed,  cut  irregularly,  or  "  cut  on  the  cross,"  or  follow  each  other  in 
rapid  succession.  Delayed  dentition  is  by  no  means  a  proof  of  rickets,  for 
infants  of  12  months  without  teeth  may  show  no  signs  or  symptoms  of 
the  disease.  On  account  of  malformation  of  the  jaws  and  impaired 
alveolar  development,  the  crowns  of  the  teeth  are  not  properly  adjusted 
and  the  incisors  often  bend  inwards.  The  teeth  seem  especially  liable  to 
decay  and  discoloration,  and  often  show  horizontal  ridges  and  depressions 
on  the  enamel.  It  is  uncertain  that  this  dental  state  is  of  rachitic  origin. 
The  milk  teeth  ought  not  to  suffer,  for  calcification  is  advanced  at  birth, 
yet  early  decay  of  these  teeth  is  common.  The  permanent  teeth  calcify 
during  the  first  year  of  life  and  are  more  likely  to  be  affected.  Teething 
is  more  likely  to  cause  illness  than  in  normal  children,  because  of  the 
nervous  instability  and  liability  to  catarrh  of  the  mucous  membranes. 

The  beading  or  rachitic  rosary  is  the  first  and  most  constant  anatomical 
change.  The  beads  or  nodules  are  most  obvious  on  the  fifth  or  sixth  ribs, 
easily  felt  if  not  visible  to  the  eye,  and  vary  in  size.  They  are  rarely  felt 
before  the  third  month,  sometimes  at  1  month,  and  occasionally  are 
present  in  the  newborn  and  on  the  pleural  surface  in  stillborn  infants. 
Slight  projections  at  birth  must  not  be  regarded  as  rachitic.  In  untreated 
cases  the  beads  increase  in  size  up  to  the  end  of  the  second  year  and  then 
slowly  disappear.  Except  in  recrudescent  or  late  rickets,  there  is  little 
trace  of  them  after  the  age  of  4  or  5  years,  and  none  at  all  in  adults.  A 
spurious  beading  on  the  pleural  surface  is  due  to  partial  dislocation  of  the 
ribs  backward,  at  the  costo-chondral  junction.  Posterior  beads  on  the 
back  of  the  thorax  are  due  to  green-stick  fracture  of  the  ribs  near  the 
posterior  angles. 

The  chest  appears  very  small  in  its  upper  part,  in  comparison  with  the 


186  Chapter   XV. 

large  square  head  and  protuberant  belly.  The  shape  is  altered  by  the 
action  of  the  atmospheric  pressure  on  the  yielding  chest  wall  at  the  points 
of  least  resistance,  i.e.,  just  external  to  the  beads,  causing  a  lateral  flattening 
or  broad  shallow  concavity.  Deformity  is  increased  by  respiratory  obstruc- 
tion, giving  rise  to  pigeon-breast,  a  peculiarity  not  found  in  uncomplicated 
rickets.  The  pressure  of  the  arms  and  the  dorsal  decubitus  also  modify 
the  shape  of  the  softened  yielding  bones.  The  ordinary  rachitic  chest  is 
fiddle-shaped  in  transverse  section,  increased  antero-posteriorly  and 
narrowed  transversely  by  the  sinking  in  of  the  lateral  furrows.  The 
sternum  and  cartilages  are  convex  forward.  In  a  few  cases  the  sternum  is 
depressed  between  the  projecting  cartilages.  A  slight  depression  may  be 
seen  or  felt  anterior  to  the  rosary.  Extending  across  the  lower  part  of  the 
thorax  transversely  is  a  groove  or  depression,  called  the  "  rachitic  girdle," 
or  "Harrison's  sulcus  "  ;  it  is  most  marked  on  the  right  side  and  deeper 
on  inspiration.  Breathing  is  increased  in  frequency,  and  chiefly  diaphrag- 
matic if  the  thorax  is  much  affected,  and  the  area  of  cardiac  dulness  may 
be  enlarged. 

The  spine  shows  no  change  in  mild  cases.  In  severe  ones  it  projects 
as  a  gradual  kyphotic  curve  in  the  dorso-lumbar  region,  from  the  middle 
of  the  back  to  the  sacrum,  when  the  child  sits  up.  The  curve  is  due  to 
laxity  of  the  ligaments  and  generally,  but  not  invariably,  disappears  if  the 
child  is  suspended  or  laid  on  its  belly  with  the  legs  extended.  If  it  exists 
in  a  severe  degree  for  a  long  time  it  may  cause  permanent  deformity.  This 
type  of  rachitic  curve  is  not  infrequently  mistaken  for  commencing  spinal 
caries.  Lateral  curvature,  commonly  convex  to  the  right  in  the  dorsal 
region,  in  children  under  three  is  usually  rachitic,  and  occasionally 
associated  with  some  rotation  of  the  vertebrae. 

The  anterior  diameter  of  the  pelvis  is  often  diminished,  and  the  supra- 
pubic arch  narrowed.  The  iliac  crests  are  thickened,  and  occasionally  the 
pelvis  is  very  irregular  in  shape  or  "  crumpled."  These  changes  are  due 
to  the  weight  of  the  body  and  abdominal  viscera,  and  lead  to  subsequent 
difficulties  in  labour. 

The  clavicle  may  be  thickened  at  the  sternal  end,  prominent  about  the 
middle  from  green-stick  fracture,  or  project  upwards  and  forwards  at  the 
junction  of  the  middle  with  the  inner  third,  due  to  muscular  traction  and 
weight  of  the  arm.  The  infra-spinous  fossa  may  be  unduly  convex.  In  an 
infant,  who  crawls  on  the  hands  and  knees  or  supports  itself  on  its  hands, 
the  humerus  develops  a  forward  and  outward  curve  about  the  attachment 
of  the  deltoid.  The  epiphyses  are  enlarged,  the  lower  one  being  the  more 
easily  felt.  Much  epiphyseal  change  takes  place  in  the  radius  and  ulna, 
especially  at  the  lower  end,  and  in  crawlers  these  bones  develop  marked 
curves  and  are  very  liable  to  green-stick  fracture.  Pronation  of  the  hand 
results  from  a  spiral  bend  in  the  radius.  The  hands  are  not  characteristic. 
The  fingers  are  somewhat  hyperextended  and  may  seem  beaded,  from  the 


Rickets.  187 

joints  being  smaller  than  the  middle  of  the  phalanges.  Deformities 
of  the  metacarpals  and  phalanges  are  rare,  but  the  latter  may  appear 
thickened  and  spindle-shaped.  Neurath  states  that  periosteal  thicken- 
ing can  be  demonstrated  by  X-rays.  I  doubt  there  being  any  actual 
thickening. 

In  the  lower  extremity  deformity  is  more  common,  because  of  the 
weight  of  the  body  in  standing  and  walking.  The  femur  develops  a  forward 
and  outward  curve.  If  the  child  is  allowed  to  sit  cross-legged,  the  bone 
is  rotated  outwards  and  the  toes  are  much  turned  out  in  walking.  Coxa 
vara  is  due  to  the  weight  of  the  trunk.  Knock-knee  is  more  common  in 
females,  and  is  either  due  to  overgrowth  of  the  internal  condyle  or  weakness 
of  the  lateral  ligaments.  Bow-legs  in  slight  cases  are  apparent,  not  real, 
being  due  to  enlargement  of  the  epiphyses.  In  children  who  stand  or  walk, 
(here  is  actual  curvature  of  the  bone  outwards,  and  this  is  often  associated 
with  an  antero-posterior  curve,  usually  situated  and  perhaps  extreme 
at  the  junction  of  the  middle  and  lower  thirds  of  the  bones.  Bowing  is  not 
always  equal  in  the  two  legs.  Sometimes  it  is  unilateral  and  associated 
with  knock-knee  on  the  other  side.  In  rare  instances  it  is  due  to  sub- 
periosteal fracture.  Even  in  severe  cases  the  bones  of  the  foot  are  not 
appreciably  affected.  In  the  lower  limb  the  enlargement  of  the  distal  end 
of  the  tibia  may  be  the  only  indication  of  rickets. 

It  is  clear  that  slight  deformities  of  the  extremities  are  due  to  epiphyseal 
overgrowth,  and  that  the  more  severe  and  more  permanent  ones  are 
produced  by  bending  of  the  shafts  under  the  superincumbent  weight,  due 
to  crawling,  standing,  sitting  and  walking.  Growth  may  be  arrested, 
especially  in  the  lower  extremities. 

Laxity  and  elongation  of  the  ligaments  produce  weak  ankles,  flat-foot, 
over-extension  of  the  knee  (calf  knee,  genu  recurvatum),  knock-knee, 
spinal  deformities,  and  unnatural  mobility  of  joints  or  acrobatic  rickets. 
Possibly  this  type  is  entirely  due  to  hypotonicity  of  muscles.  The  muscles 
are  small,  flabby,  atonic  and  badly  developed.  The  motor  functions  are 
impaired,  delayed  or  lost.  Hence  arises  delay  in  the  child  learning  to  sit, 
stand  and  walk.  This  is  an  advantage  by  preventing  deformity.  Late 
walking  is  common,  and  the  child  may  not  even  attempt  to  walk  until  3  years 
of  age.  Sometimes  the  muscles  of  the  legs  are  so  weak  and  atrophied  that 
the  child  comes  under  treatment  for  supposed  paralysis.  The  weakness 
may  be  very  marked,  though  the  skeletal  changes  are  slight.  The  elec- 
trical reactions  are  normal  or  exaggerated. 

The  muscles  of  the  abdominal  wall  and  of  the  alimentary  canal  are 
weak  ;  the  contracted  chest  pushes  down  the  abdominal  organs  ;  and  the 
pelvis  is  flat.  Flatulent  distension  is  common  because  of  disordered  diges- 
tion. Hence  arises  a  condition  of  "  pot-belly"  or  "  frog-belly,"  in  which  the 
abdomen  is  uniformly  enlarged,  tense  and  tympanitic,  the  recti  often 
separated  (diastasis  of  the  recti),  and  an  umbilical  hernia  may  be  present. 


188  Chapter   XV. 

The  stomach  and  colon  are  much  distended  from  fermentation  of  their 
contents. 

Apparent  enlargement  of  the  liver,  which  is  normally  large  in  infants 
and  projects  into  the  abdominal  cavity  because  of  the  more  horizontal 
position  of  the  lower  ribs,  is  due  to  the  rachitic  deformity  of  the  chest 
and  laxity  of  the  ligaments,  downward  displacement  and  greater  exposure 
of  its  surface.  True  enlargement  may  occur,  and  the  liver  is  smooth  and 
firmer  than  normal.  It  is  due  to  a  portal  cirrhosis,  interlobular  in  type, 
set  up  by  toxaemia  resulting  from  the  gastro-intestinal  catarrh  so  often 
present.  Hogben  (1888)  described  a  hypertrophic  or  biliary  type,  mono- 
lobular  and  interlobular,  with  an  increase  in  the  number  of  small  bile  ducts. 
It  is  difficult  to  accept  this  explanation  for  jaundice  does  not  occur. 

The  spleen  can  often  be  felt,  for  it  is  displaced  downwards  and  more 
exposed  by  eversion  of  the  lower  ribs.  Possibly  a  simple  hyperplasia  occurs 
during  the  acute  stages,  and  fibroid  changes  later  on,  as  the  result  of 
associated  toxsemia  conditions. 

Course  and  Prognosis. — The  disease  is  very  chronic  and  lasts  for 
months,  or  even  more  than  2  years.  Its  course  is  modified  by  treatment. 
Sometimes  it  is  latent,  or  there  may  be  exacerbations.  Usually  the  active 
symptoms  cease  when  a  mixed  diet  is  given,  that  is  about  the  end  of  the 
first  year.  Different  parts  of  the  skeletal  system  are  progressively  involved, 
recovery  taking  place  in  one  while  another  becomes  affected.  Thus, 
in  the  first  6  months  craniotabes  and  beads  may  be  the  only  signs  ;  later 
on  the  thorax  is  affected  ;  then  kyphosis,  bony  deformities,  etc.,  arise. 
Signs  of  improvement  are  diminished  sweating  and  restlessness,  disappear- 
ance of  craniotabes,  increase  in  muscular  power  and  improved  general 
nutrition.  Deformities  slowly  but  steadily  improve,  except  in  the  worst 
cases,  in  which  they  may  persist  throughout  life  in  the  modified  form  of 
pigeon-breast,  Harrison's  sulcus,  eversion  of  the  costal  arch,  kyphosis, 
pelvic  deformities,  and  knock-knees  or  bow-legs.     Relapses  are  rare. 

It  is  never  fatal,  per  se,  but  is  the  cause  of  increased  mortality  from 
other  diseases,  especially  those  of  the  respiratory  and  alimentary  system. 
Laryngitis,  bronchitis  and  broncho-pneumonia  are  much  more  fatal  in  the 
rachitic,  because  of  the  weakness  of  the  respiratory  muscles  and  the 
thoracic  deformity.  Death  may  also  result  from  laryngospasm,  convul- 
sions, tetany  or  gastro-enteric  complications.  The  deformity  of  the  chest 
retards  growth  by  interfering  with  efficient  lung  expansion  and  oxidation. 
Apart  from  this  deformity  the  disease  has  no  permanent  influence  on  the 
general  health.  A  child  may  be  stunted  from  arrested  growth  at  the 
epiphyses.  The  mental  development  may  be  retarded  by  malnutrition 
or  on  account  of  the  physical  disabilities. 

Diagnosis. — Beading  of  the  ribs  and  enlarged  epiphyses  are  diagnostic. 
Restlessness,  head  sweating,  irregular  dentition,  craniotabes,  a  large  fon- 
tanels and   backward  development  may  be  due  to  other  causes,  but  in 


Rickets.  189 

conjunction  are  strongly  suggestive.  A  large  fontanelle  and  delayed  den- 
tition may  be  due  to  cretinism  ;  a  large  head,  to  hydrocephalus  ;  delayed 
walking,  to  backwardness;  and  muscular  weakness,  to  paralysis.  Curvature 
of  the  spine  may  simulate  caries.  If  the  bony  changes  are  slight  and  the 
muscular  weakness  great,  it  is  difficult  to  be  certain  that  all  are  due  to 
rickets  ;  even  if  the  bony  changes  are  well  marked,  the  extreme  weakness 
may  suggest  an  additional  affection.  The  presence  of  knee-jerks  and 
normal  electrical  reactions  distinguish  the  muscular  weakness  from  that  of 
infantile  palsy  ;  while  exaggerated  reflexes  and  rigidity  indicate  cerebral 
paralysis.  The  large  belly  may  simulate  tabes  mesenterica.  Achon- 
droplasia causes  stunting  and  false  beading.  Syphilitic  epiphysitis  is 
generally  monarticular  and  in  infants  under  6  months  of  age.  The  pain 
and  tenderness  of  scurvy  must  not  be  ascribed  to  rickets.  The  rachitic 
element  may  lead  to  errors  in  diagnosis,  if  present  in  other  diseases.  Many 
nervous  and  catarrhal  conditions  have  their  origin  in  this  disease.  Mentally 
deficient  children  are  often  rachitic,  but  the  backwardness  must  not  be 
ascribed  to  the  rickets. 

Recrudescenl  Rickets  sometimes  called  "Adolescent"  or  "Late" 
Rickets,  is  rare.  Charles  West  stated  he  had  never  seen  the  disease  begin 
later  than  3  years  of  age.  Sir  William  Jenner  referred  to  a  case  in  a  girl, 
aged  9  ;  and  since  then  at  least  30  cases,  some  of  them  doubtful,  have 
been  reported.  Two-thirds  of  the  cases  are  girls.  In  a  girl,  aged  11  years, 
who  came  under  my  care  in  1896,  the  disease  was  said  to  have  begun  at 
the  age  of  4  years  ;  she  was  anaemic,  wasted,  extremely  feeble,  and  had 
irregular  fever,  up  to  102-103°  F.  for  16  days.  Under  treatment  there  was 
very  great  diminution  in  the  size  of  the  beads  and  epiphyses.  The  disease 
appeared  never  to  have  subsided  since  its  onset,  but  to  have  remained 
quiescent.  We  can  divide  the  cases  into  three  types.  In  the  first  there 
is  a  recrudescence  or  relapse,  the  disease  never  having  been  completely  in 
abeyance  ;  in  the  second  type  there  has  been  a  true  recurrence  ;  and  in 
the  third  the  patients  are  said  to  have  been  unaffected  in  infancy.  The 
common  age  of  onset  is  12-18,  and  in  a  few  at  6-11  years  of  age.  Ossifica- 
tion is  not  complete  at  this  time  and  rapid  growth  takes  place  at  puberty. 
One  of  Clutton's  cases  showed  premature  sexual  development.  The 
affection  comes  on  with  stiffness  and  pain  in  the  joints  and  leg  muscles, 
and  the  gait  may  suggest  hip  disease.  This  is  followed  by  enlargement  of 
the  epiphyses  and  beading.  The  skull  is  unaffected.  The  deformities  in- 
clude flat-foot,  genu  valgum  and  varum,  various  femoral  and  tibial  curves, 
coxa  vara  and  scoliosis.  In  a  case  of  Little's  (1900),  a  boy,  aged  17,  with 
symptoms  since  the  age  of  5,  the  epiphyses  were  swollen  and  the  bones 
soft,  showing  irregular  ossification  and  islets  of  ossification  typical  of 
rickets.  It  may  be  more  or  less  unilateral,  but  the  diagnosis  in  cases  of 
limited  distribution  must  be  accepted  with  caution.  Possibly  some  of  the 
recorded  cases  are  instances  of  osteomalacia,  from  which  it  can  be  dis- 
tinguished by  the  disturbance  of  endochondral  ossification. 


190  Chapter   X  V. 

Intra-uterine  Rickets,  sometimes  called  " Festal"  or  "Congenital.'''' — 
it  is  doubtful  whether  true  intra-uterine  rickets  has  ever  occurred.  An 
open  fontanelle,  soft  bones,  costo-chondral  swellings  and  protuberant 
belly  occur  in  all  infants.  The  results  of  histological  examination  of  the 
bones  and  cartilages  are  not  accepted  by  some  observers  as  characteristic 
of  rickets.  Charrin  and  Le  Play  (1905)  ascribed  the  rosary,  craniotabes, 
enlarged  epiphyses,  etc.,  in  a  child  born  at  8  months,  of  a  mother  aged  47, 
who  had  been  subject  to  privations,  to  true  rickets.  They  based  their 
opinion  on  macroscopic  and  microscopic  examination  and  chemical 
analysis.  It  has  been  divided  into  two  classes,  the  joztal  form,  which 
develops  and  is  cured  during  intra-uterine  life,  and  a  congenital  form. 
Possibly  it  may  be  present  and  give  rise  to  no  definite  signs  until  some- 
time after  birth.  It  must  not  be  confounded  with  achondroplasia,  nor 
with  syphilitic  osteochondritis,  and  it  is  certainly  not  justifiable  to  accept 
beading  of  the  ribs  in  the  newborn  as  proof  of  rickets.  Fractures  in  utero 
are  commonly  due  to  osteogenesis  imperfecta. 

Treatment. — Prophylaxis  consists  in  care  of  the  mother  during 
pregnancy  and  lactation,  suitable  diet  for  the  child,  fresh  air,  sunlight,  a 
daily  bath,  and  exercise  or  massage.  The  value  of  drugs  is  difficult  to 
estimate,  for  active  symptoms  usually  cease  at  12-18  months  of  age,  and 
even  if  untreated  the  disease  subsides  when  the  child  obtains  a  mixed  diet. 
Mild  cases  recover  without  any  special  treatment.  If  the  child  is  not 
breast-fed,  the  diet  must  contain  a  liberal  proportion  of  fat  and  protein  in 
the  form  of  cream,  milk,  eggs,  red  meat,  butter,  bacon  fat,  and  suet,  if 
suitable  at  the  age  of  the  child.  It  is  generally  advisable  to  diminish 
the  amount  of  carbohydrates  and  allow  a  liberal  supply  of  salt.  There  is 
probably  enough  phosphoric  acid  in  the  tissues  to  seize  on  any  spare  sodium. 

Let  the  child  have  light  and  air  in  the  nursery,  and  be  out  in  the  open 
air  and  sun  as  much  as  possible.  Country  air  is  better  than  urban,  but 
there  is  no  special  virtue  in  the  seaside.  A  daily  salt  bath  (a  handful  of 
rock  salt  to  a  bucketful  of  water)  at  a  temperature  of  70-80°  F.,  followed 
by  drv  rubbing,  is  a  useful  stimulant  and  diminishes  the  liability  to  taking 
cold.  On  account  of  the  susceptibility  to  chills,  the  neck,  legs  and  arms 
should  be  covered,  and  at  night  the  child  should  wear  a  flannel  nightdress, 
tied  below  the  feet,  or  pyjamas  and  socks.  The  pillow  must  be  firm  and 
not  soft.  If  the  alimentary  track  is  out  of  order  and  fermentation  has 
induced  atony,  flatulent  distension  and  separation  of  the  recti,  the  diet 
must  be  reduced  and  a  mixture  given  of  ol.  ricini  m.  10-15,  tinct.  rhei  m. 
5-10,  tinct.  nucis  vomicae  m.  \-\,  and  sod.  sulphocarb.  gr.  3-5,  t.d.s. 

Cod-liver  oil  is  the  best  drug,  alone  or  in  combination  with  maltine 
and  syrup  ferri  phosph.  co.  Phosphate,  lacto-phosphate  and  hypophos- 
phites  of  lime  do  not  appear  to  have  much  value.  A  suitable  mixture  is 
that  of  calcium  and  sodium  hypophos.  aa.  gr.  J,  ol.  morrhuse  and  glycerin  aa. 
m.  20,  ol.  cassiae  m.   xjj,  and   tragacanth  mucilage  to   1  dr.      Phosphorus 


Rickets.  191 

has  boen  called  by  Kassowitz  "  the  iron  of  rickety  children."  It  is  given 
in  daily  doses  of  f-1  dr.  of  phosphorus  gr.  ■£-  in  3  oz.  of  cod-liver  oil,  to  which 
the  credit  should  be  given.  Suprarenal  extract  is  also  said  to  exert  a 
favourable  influence  on  the  craniotabes.  sweating,  nervous  manifestations, 
and  general  condition  of  the  child.  Arsenic  and  iron  are  useful  if  there  is 
much  anaemia. 

Respiratory  exercises  assist  in  the  proper  expansion  of  the  chest,  but 
are  distinctly  injurious  if  it  is  found  that  the  chest  wall  sinks  in  on  inspiration. 
A  firm  abdominal  bandage  is  of  some  assistance.  Adenoids  and  enlarged 
tonsils  must  be  removed.  For  lordosis  the  child  must  sleep  on  a  hard 
level  bed,  with  a  pillow  under  the  spine  if  the  curve  is  severe.  For  a  few 
minutes  daily  it  should  be  placed  on  the  belly  with  buttocks  elevated, 
while  pressure  is  applied  to  the  spine.  Massage  of  the  spinal  muscles  is 
useful,  and  a  spinal  support  is  permissible,  to  allow  the  child  to  sit  up  for 
short  periods  at  a  time.  Sitting  must  be  prohibited  if  the  disease  is  very 
active,  for  fear  of  pelvic  deformity.  Bowing  of  the  legs  is  best  treated  by 
massage.  The  best  splints  are  made  of  poroplastic  felt.  They  are  made 
to  extend  from  a  little  above  the  knee  to  the  ground,  and  fastened  by  a  strap 
round  the  ankle,  another  below  the  knee,  and  a  third  round  the  middle  of 
the  calf.  The  last  one  is  of  chief  importance.  It  is  fastened  round  a  square 
leather  pad  on  the  outer  side  of  the  calf  and  tightened  daily.  These  splints 
are  easily  put  on  and  off,  can  be  kept  clean,  and  do  not  interfere  with 
exercise.'  External  splints  are  permissible,  if  they  extend  2  or  3  ins.  below 
the  feet  and  are  of  uneven  length,  and  thus  keep  the  child  off  its  feet. 
They  must  be  worn  at  night,  if  the  limbs  are  curled  up  in  bad  positions. 
This  treatment  may  increase  the  pressure  on  the  upper  limbs,  for  the 
child  crawls  about  on  the  hands  and  knees.  It  is  most  suitable  when  the 
disease  is  stationary  in  the  upper  limbs  though  progressive  in  the  lower 
ones.  Slight  bowing,  which  does  not  increase,  requires  no  special  treatment. 
A  tracing  of  the  limbs  on  paper,  when  the  child  is  first  seen,  enables  one  to 
estimate  any  increase  in  curvature  on  a  subsequent  visit.  It  is  sometimes 
recommended  that  deformities  should  be  treated  by  osteotomy  after  the 
age  of  3  years,  on  the  ground  that  delay  only  perpetuates  the  condition  and 
the  changes  in  the  bony  surfaces  and  ligaments.  It  is  better  to  delay 
operative  treatment  until  the  seventh  year,  for  many  bad  cases  get  well, 
as  the  result  of  the  natural  tendency  of  bone  to  assume  the  normal  shape. 
Knock-knee  in  the  early  stages  is  treated  by  massage  and  an  external 
splint,  with  a  certain  amount  of  pressure  exerted  by  a  bandage  over  the  knee. 
In  late  stages  operation  is  necessary. 

The  essential  treatment  of  the  disease  is  preventive.  If  it  has  once 
commenced  proper  diet  and  management  prevent  disastrous  results.  A 
marked  case  of  rickets  in  private  practice  is  a  grave  reproach  to  the  regular 
medical  attendant. 


Chapter  XVI. 

DISORDERS    OF    BONE    FORMATION. 

Achondroplasia — Cleido- Cranial      Dysostosis     vel      Anosteoplasia — Osteo- 
genesis Imperfecta  vel  Periosteal   Aplasia. 

The  nomenclature  of  these  various  affections  has  caused  considerable 
confusion,  for  it  is  by  no  means  uncommon  to  find  different  diseases  described 
under  the  same  name. 

It  would  be  advisable  to  make  use  of  the  term  "  Osteogenesis  Imper- 
fecta "  as  a  generic  name  for  the  group  of  bone  affections  in  which  ossifica- 
tion is  defective.  To  simplify  the  nomenclature  we  might  speak  of  Achondro- 
plasia, an  affection  in  which  those  bones  developed  in  cartilage  are  chiefly 
at  fault ;  Anosteoplasia,  a  condition  the  antithesis  of  achondroplasia,  in 
that  the  defect  is  in  the  development  of  the  membrane  bones  ;  and  use 
the  name,  Periosteal  Aplasia,  for  those  cases  at  present  described  under  the 
title  of  Osteogenesis  Imperfecta,  for  in  this  the  developmental  defect  is 
apparently  in  the  periosteal  formation  of  bone,  that  is,  in  the  osteogenetic 
layers  of  the  periosteum.  I  have  adopted  this  nomenclature  in  the  titles 
of  these  diseases. 

Achondroplasia.  —  Syn  :  Chondrodystrophia  Fcetalis —  Congenital 
Pickets. — Parrot,  in  1878,  gave  the  name  of  achondroplasia  to  a  foetal 
systemic  bone  disease,  with  characteristic  clinical  features,  definite  patho- 
logical anatomy,  and  of  unknown  causation.  Since  Kaufmann's  mono- 
graph (1892)  it  has  been  known  as  chondrodystrophy  fcetalis,  but  it  has 
frequently  been  described  under  other  names.  It  affects  the  cartilage, 
but  not  the  membrane  bones,  and  has  nothing  in  common  with  rickets  or 
cretinism. 

Although  the  first  case  was  recorded  by  Siimmering,  in  1791,  it  is  a 
disease  of  great  antiquity  and  is  represented  by  the  Egyptian  gods,  Pthah 
and  Bes  ;  by  dwarfs,  in  pictures  by  Velasquez  ;  by  some  statues  of  Silenus  ; 
and  by  the  effigy  attached  to  the  tomb  of  Knoumhotpon,  chief  cook  of 
Pharaoh,  in  the  necropolis  of  the  School  of  Memphis.  The  disease  is  not 
uncommon  and  probably  occurs  in  calves,  sheep,  goats  and  pigs  ;  but 
some  of  these  so-called  cases  in  animals  are  monstrosities.  Frequently 
it  is  associated  with  hydramnios,  abnormal  presentations,  and  prematurity. 
Or  the  infants  are  stillborn,  or  only  survive  a  short  time.  Their  hold  on 
life  is  precarious  at  first.     Later  on  they  are  as  strong  as  ordinary  children. 


Disorders  of  Bone  Formation.  193 

The  characteristic  feature  is  stunting  of  the  upper  and  lower  limbs, 
the  vertebral  column  being  unaffected  or  even  abnormally  long.  At  birth 
the  head  is  large,  and  appears  still  more  so  on  account  of  the  shortness  of 
the  limbs.  Its  circumference  equals  or  even  exceeds  the  length  of  the  body. 
It  is  brachycephalic,  globular,  with  projecting  forehead  and  flattened  nasal 
bones.  The  arms  do  not  reach  the  waist,  and  the  shortness  of  the  lower 
limbs  causes  the  navel  to  be  lower  than  the  mid-point  between  crown  and 
sole,  its  position  in  normal  infants.  The  mid-point  may  be  as  high  as  the 
xiphoid  cartilage.  The  limbs  are  often  bent,  deformed,  and  occasionally 
fractured.  The  epiphyses  are  normal  or  appear  enlarged,  and  the  costo- 
chondral  articulations  are  thickened,  in  "  rosary  "  style.  As  a  whole  the 
infant  is  obese,  with  prominent  belly,  thickened  skin  and  subcutaneous 
tissues,  and  fine,  soft,  abundant  hair.  The  eyelids  are  thick  and  there 
may  be  epicanthus.  The  lips  and  tongue  are  thick,  and  the  tongue  protrudes. 
The  nose  is  retracted,  and  there  may  be  a  deep  depression  at  its  root  or 
marked  flattening  of  the  whole  nasal  region,  with  decided  prognathus. 
The  face  is  relatively  small.  Thus,  there  is  a  close  resemblance  to  the 
cretinoid  state,  and  less  so  to  rickets. 

Survivors  are  apt  to  be  mistaken  for  cretins  ;  but  can  easily  be  dis- 
tinguished therefrom.  They  are  quite  as  intelligent  as  other  children  of 
the  same  age,  except  that  they  may  be  a  little  backward  through  being- 
kept  away  from  school.  The  disease  is  over,  though  its  effects  remain. 
They  may  be  described  as  obese,  micro melic  dwarfs,  with  broad  heads, 
long  bodies  and  short  limbs,  who  attain  a  height  of  3-4  ft. 

They  are  often  bow-legged,  and  their  gait  waddling  or  quite  natural. 
The  fontanelle  is  large,  and  remains  so  for  a  long  time  ;  the  palate  rather 
unduly  arched,  but  dentition  is  normal.  Hydrocephalus  is  not  uncommon. 
The  shortening  especially  affects  the  femora  and  humeri.  The  pelvis  is 
small  and  contracted,  with  the  sacrum  projecting  strongly  forward  and  the 
spine  in  a  position  of  marked  lordosis.  The  fingers  are  stunted,  the  three 
middle  ones  of  equal  length,  divergent,  curved,  and  cannot  be  easily 
approximated  ;  the  toes  are  short.  The  child  may  be  quite  robust  and 
able  to  walk  at  an  early  age,  but  more  often  walking  is  delayed.  Obesity 
disappears  as  it  gets  older.     Inguinal  hernia  is  frequent. 

Instances  of  heredity  have  occurred.  Seligmann  has  pointed  out  that 
achondroplasic  Dexter-Kerry  cows  may  have  cretinous  calves.  Shattock 
regards  it  as  a  para-cretinous  condition  ;  but  the  thyroid  gland  is  normal. 
It  has  been  ascribed  to  inflammation  of  the  cartilages  or  an  anomalous 
form  of  osteomyelitis  in  the  first  months  of  foetal  life.  The  vascularity  of 
the  growing  cartilage  is  always  increased,  but  bone  is  imperfectly  formed 
and  ossification  arrested.  There  is  a  deficiency  or  absence  of  the  pro- 
liferating zone  of  cells  at  the  epiphyseal  line,  and  more  or  less  complete 
inhibition  of  the  normal  arrangement  of  the  cells  in  columns  preparatory 
to   ossification.      Bone   formation   is   periosteal  ;     and  the  bones   become 

o 


194  Chapter  XVI. 

very  dense,  compact  and  bossed.  The  beads  on  the  ribs  are  due  to  a 
bony  investing  ring  derived  from  the  periosteum.  The  cartilage  bones  at 
the  base  of  the  skull  are  stunted  in  consequence  of  premature  synostosis 
of  the  basi-sphenoid,  basi-occipital  and  prsesphenoid.  These  bones  form 
the  fundamental  bone  of  Hyrtl  or  the  os  tribasilare  of  Virchow,  which  may  be 
shortened  independently  of  premature  union,  and  is  not  shortened  in  every 
case.  To  this  shortening  are  ascribed  the  prognathus  and  depression  of  the 
nasal  bridge.  The  membranous  bones  of  the  skull  and  the  clavicles,  ossified 
very  early  in  foetal  life,  are  unaffected. 

Kaufmann  has  described  three  varieties,  all  of  which  may  be  found 
in  the  same  individual,  though  one  usually  predominates.  Rudimentary 
row  formation  is  present  in  all.  In  Chondrodystrophia  Fcetalis  hypoplastica 
the  epiphyseal  cartilages  are  diminished  in  consequence  of  deficient  pro- 
liferation of  cartilage  cells.  Miss  Mowler,  in  Dicken's  book,  "  David 
Copperfield,"  is  a  case  of  this  type.  In  C.F.  kyperplastica,  there  is  great 
proliferation  of  the  cells  and  enlargement  of  the  epiphyses.  In  C.F. 
malica  the  cartilages  are  much  softened,  and  the  epiphyses  more  or  less 
gelatinous.  Each  variety  shows  increased  vascularity  in  the  cartilage. 
Periosteal  bone  formation  and  the  deposition  of  calcium  salts  go  on 
normally.  A  periosteal  lamella  or  inclusion  has  been  described  in  the 
human  foetus  (Urtel),  and  in  the  calf  (Eberth).  This  is  a  layer  of  con- 
nective tissue,  starting  from  the  periosteum,  making  its  way  in  between 
the  epiphysis  and  diaphysis,  and  more  or  less  separating  them.  Its  extent 
varies  from  a  mere  trace  to  a  definite  partition  reaching  to  the  axis  of  the 
bone.  By  encroaching  upon  the  epiphyseal  line,  it  precludes  growth  in 
length  and  may  entirely  stop  the  growth  of  the  bone.  It  is  the  main  cause 
of  the  physical  peculiarities. 

It  is  of  the  utmost  importance  to  differentiate  this  affection  from 
cretinism  in  early  life.  The  main  differences  are  an  unimpaired  mental 
state,  a  normal  thyroid,  a  periosteal  lamella,  and  the  absence  of  myxcedema. 
Thyroid  treatment  is  of  no  benefit.  The  bones  of  cretins  show  nothing 
abnormal  beyond  exceedingly  slow  ossification. 

Anosteoplasia.  —  Syn.  :  Osteodijstrophy  Fcetalis  —  Cleido  -  Cranial 
Dysostosis. — Seeing  that  this  affection  is  the  antithesis  of  achondroplasia 
or  chondrodystrophy  fcetalis,  it  may  be  named  anosteoplasia  or  osteodys- 
trophy fcetalis,  rather  than  cleido-cranial  dysostosis  under  which  it  is 
generally  described.  Scheuthauer  (1871)  noted  the  connection  between 
the  deformity  of  the  cranium  and  the  clavicles,  but  the  first  full  description 
was  given  by  Marie  and  Sainton,  in  1897.  There  are  now  about  40  cases 
on  record. 

The  disease  is  hereditary,  and  may  affect  father  and  son,  or  mother 
and  daughter  ;  or  may  occur  as  an  isolated  peculiarity.  It  is  a  defect  in  the 
development  of  the  membrane  bones.  The  ossification  of  the  membrane 
bones  of  the  skull  is  much  retarded,  and  the  fontanelles  may  remain  open 


Disorders  of  Bone  Formation.  195 

till  a  late  age.  The  skull  is  globular,  brachycephalic,  with  frontal  or  parietal 
bosses.  The  face,  nasal  bones,  jaws  and  mastoids  are  small ;  the  palate 
high  and  deficient  ;  the  teeth  few,  irregular  and  delayed  ;  the  clavicles 
rudimentary,  atrophied  or  absent. 

The  clavicle  is  said  to  be  developed  in  membrane  (Bruch),  in  cartilage 
(Kolliker),  or  mixed  (Gegenbauer).  That  it  is  developed  in  two  parts  is 
shown  by  cases  in  which  the  outer  half  is  absent ;  others  in  which  there  is 
a  rudimentary  inner  or  outer  part,  or  two  contiguous  but  unjoined  halves, 
forming  a  kind  of  loose  joint.  The  bone  may  be  completely  absent;  form 
short,  floating  osseous  bands,  partly  rudimentary  and  attached  by  a 
fibrous  band  to  the  coracoid  ;  or  almost  absent  and  contain  no  bone. 
The  clavicular  defect  enables  the  shoulders  to  be  approximated  in  front. 

The  dystrophy  is  not  limited  to  the  membrane  bones.  It  may  affect 
the  general  growth  and  be  associated  with  dwarfism  and  infantilism. 
Intellectually  and  psychically  these  children  are  normal. 

Periosteal  Aplasia. — -Syn.  ;  Osteogenesis  Imperfecta — Fragilitas 
Ossium — Infantile  Osteomalacia — Brittle  Bones —  Osteopsathyrosis. — This 
affection  is  a  systemic  bone  disease,  which  commences  in  early  foetal  life 
and  is  usually  fatal  before  birth.  It  is  characterised  by  multiple  fractures 
and  extensive  craniotabes,  due  to  defective  ossification  of  the  diaphyses 
and  of  the  bones  of  the  cranial  vault.  The  epiphyses  and  basis  cranii  are 
normal. 

The  first  case  was  described  by  Berdenave  in  1763,  and  the  name  given 
by  Vrolik  in  1849.  Up  to  1906  about  130  cases  of  multiple  spontaneous 
fractures,  probably  due  to  this  cause,  had  been  recorded.  Most  of  the 
cases  are  those  of  premature  or  stillborn  children,  and  it  has  been  generally 
assumed  that  the  affection  is  incompatible  with  extra-uterine  life.  In 
some  instances  the  fractures  did  not  begin  until  a  few  months  (3-9)  after 
birth.  Other  cases  of  fragilitas  occur  later  in  life,  coming  on  about  puberty, 
and  rarely  earlier,  and  are  probably  of  different  pathology.  Fractures 
may  also  occur  in  scurvy  and  rickets  in  consequence  of  bone  atrophy. 
A  true  mollifies  ossium  or  osteomalacia  has  also  been  reported  as  early  as 
the  fifth  year  of  life  ;  and  a  rachitic  softening,  due  to  the  formation  of 
spongy  bone  containing  little  or  no  lime  salts,  in  the  "  limeless  bone  " 
variety  of  rickets. 

Nothing  definite  is  known  about  the  etiology,  except  that  it  is  not  due 
to  congenital  syphilis,  rickets  or  nervous  lesions.  Heredity  has  been  noted 
in  15  per  cent.  (Griffith,  1897).  It  has  been  transmitted  through  three 
generations  (Harmer)  ;  and  it  has  affected  9  out  of  10  children,  and  a  child 
■of  one  of  these. 

The  bones  are  delicate  and  fragile,  and  broken  with  extreme  ease. 
Sometimes  the  periosteal  shell  can  be  crushed  between  the  finger  and 
thumb.      On  section  they  are  found  very  porous,   with    thin  defective 


196  Chapter   X  VI. 

trabecule,  and  a  thin  outer  periosteal  layer  of  small  imperfectly  laminated 
bone  plates  or  trabecule,  and  large  marrow  spaces  instead  of  Haversian 
canals.  The  marrow  is  composed  of  cedematous  myxomatous  connective 
tissue.  Calcification  is  defective,  and  new  bone  is  formed  by  direct  con- 
version of  cartilage  cells,  and  not  by  the  deposition  of  bone  by  osteoblasts 
on  a  previous  cartilaginous  matrix.  The  disease  is  confined  to  the  bones 
of  the  cranial  vault  and  the  shafts  of  the  bones.  It  prevents  normal 
development  as  soon  as  the  stage  of  true  bone  formation  is  reached. 
Apparently  it  is  a  defect  in  periosteal  bone  formation. 

The  newborn  infant  is  usually  very  weak  and,  if  handled  with  great 
care,  may  escape  fracture  for  some  days  or  months.  More  often  fractures 
are  present  at  birth.  In  appearance  the  child  may  be  normal,  smaller  than 
normal,  or  look  obese  and  cedematous  from  thickening  of  the  skin  and  sub- 
cutaneous tissues.  In  this  respect  it  is  rather  like  achondroplasia,  but  the 
extremities  are  not  stunted,  except  as  a  result  of  fractures.  The  limbs 
may  be  bent  and  deformed,  and  the  bones  so  brittle  that  they  fracture  on  the 
least  provocation,  or  unduly  soft  and  bend  without  breaking.  As  many 
as  113  fractures  have  been  counted  in  a  newborn  child  (Chaussier).  They 
may  be  so  numerous  that  the  callus  thrown  out  makes  the  bone  nodular. 
In  the  ribs  this  may  give  rise  to  spurious  beading.  False  joints  are  rare. 
In  order  of  frequency  the  thigh,  leg,  upper  extremity,  clavicles  and  ribs  are 
affected;  rarely  the  hand  and  lower  jaw.  They  unite  readily  with  for- 
mation of  much  callus.  The  head  is  large,  sutures  widely  open  from 
deficient  ossification,  and  exhibits  craniotabes  or  is  even  completely  mem- 
branous. The  fractures  are  complete  and  rarely  preceded  by  pain,  though 
it  has  been  recorded,  and  there  is  little  pain  at  the  time  or  during  tire  process 
of  healing  ;  no  doubt  on  account  of  the  slight  shock  and  damage  to  the 
soft  parts.  Marked  deformity  results  from  malposition  and  bending, 
perhaps  inability  to  walk  or  stand,  and  scoliosis.  After  the  first  few  months 
of  life  the  general  health  is  unimpaired,  and  the  intelligence  normal ;  nearly 
all  learn  to  walk.  Irregular  fever  and  pain  on  movement,  before  fracture 
occurs,  have  been  reported  in  some  cases.  X-ray  examination  : — the 
medullary  cavity  appears  proportionately  large  ;  the  epiphyseal  line 
sharply  defined  ;   and  the  shadow  of  the  shaft  feeble  or  unduly  translucent. 

The  disease  persists  throughout  life  and  affects  the  whole  skeleton. 
Probably  the  active  process  subsides  during  intra-uterine  life  or  soon 
after,  and  the  fragility  is  simply  the  result.  Cases  vary  in  degree,  some  are 
mild,  while  in  others  the  liability  to  fracture  is  so  great  that  the  patient 
is  confined  permanently  to  bed  ;  crippling  is  common.  Many  die  from 
complications  within  two  years  of  birth,  and  others  have  lived  to  30  years. 
In  those  that  survive  the  skull  bones  become  ossified  and  the  liability  to 
fracture  gradually  becomes  less.  The  diagnosis  from  achondroplasia  is 
simple.     Craniotabes  with  false  beading  of  the  ribs  may  be  mistaken  for 


Disorders  oj  Bone  Formation.  197 

rickets,  but  in  this  the  epiphyses  are  enlarged.  Osteomalacia  begins  about 
or  after  puberty.  The  liability  to  fractures  in  congenital  syphilis  also 
begins  about  puberty,  and  more  violence  is  necessary.  Nothing  can  be  done 
for  these  patients  except  placing  them  in  a  position  to  avoid  fracture, 
protecting  the  limbs,  and  attending  to  the  general  health. 


Chapter  XVII. 

ANOMALIES    AND    DISORDERS    OF    GROWTH. 

Dwarfs  —  Symptomatic   Infantilism  — Ateleiosis  —  Precocity  —  Obesity  — 
Gigantism — Hemihypertrophy. 

A  normal  or  physiological  dwarf  is  an  undergrown  child  or  adult, 
not  deformed,  whose  development  has  proceeded  symmetrically  at  a  normal 
rate,  except  as  regards  extent  in  comparison  with  other  races,  families  of 
the  same  race,  or  members  of  the  same  family.  The  best  illustration  is 
the  race  of  pygmies  in  Central  Africa,  whose  height  is  about  4  feet.  It  is 
not  due  to  any  pathological  process.  Ossification,  epiphyseal  union  and 
sexual  development  take  place  at  the  usual  time. 

A  phocomelic  dwarf  is  one  in  whom  intermediate  parts  of  the  limbs 
are  absent.  In  micromelic  dwarfs  the  limbs  are  unduly  small,  e.g.,  achon- 
droplasia. True  dwarfs  or  Nanasomes  are  of  two  types  :  (1)  Primordial 
or  sexual  dwarfs,  in  other  words,  small  adults  ;  and  (2)  Infantile  or  asexual 
dwarfs,  i.e.,  permanent  children.  To  the  group  of  nanasomes  Hastings 
Gilford  has  given  the  name  of  Ateleiosis,  a  Greek  word  meaning  "  not 
arriving  at  perfection." 

Symptomatic  Infantilism  or  Dwarfism  is  a  term  used  for  dwarfism 
associated  with  delayed  ossification,  dentition  and  sexual  development. 
It  is  the  result  of  some  illness  or  general  nutritional  disorder,  which  interferes 
with  growth.  In  these  cases  the  development  of  the  body  is  delayed  or 
arrested.  It  remains  small,  weak  and  slender.  Usually  there  is  merely 
mental  and  physical  delay,  a  variation  within  the  limits  of  health.  The 
common  causes  are  general  dystrophies,  congenital  heart  disease,  mitral 
stenosis,  tuberculosis  and  congenital  syphilis.  It  may  be  due  to  cirrhosis 
of  the  liver,  "  Hepatic  Infantilism  "  ;  absence  or  deficiency  of  the  secretion 
of  the  pancreas,  the  "Pancreatic  Infantilism  "  of  Byrom  Bramwell  ;  to 
malaria  and  poisons,  e.g.,  alcohol,  nicotine  and  lead  ;  to  rickets,  micro- 
cephalus,  spinal  caries  or  lateral  curvature  ;  to  thyroid  insufficiency  and 
to  idiocy.  Herter  (1908)  has  described  a  "Toxcemic  Infantilism  "  of  intes- 
tinal origin.  The  abdomen  is  distended,  and  the  stools  contain  much  fat, 
soap,  fatty  acids  and  mucus.  It  is  apparently  identical  with  Bramwell's 
type,  but  Herter  ascribes  it  to  the  prevalence  of  B.  bifidus  and  B.  infantilis, 
which  replace  the  normal  intestinal  flora.  In  microcephalus  the  body 
remains  small  through  an  attempt  to  adapt  growth  to  the  size  of  the  brain. 


Anomalies  and  Disorders  of  Growth.  199 

In  congenital  syphilis  sexual  development  is  commonly,  but  not  always, 
arrested  for  a  time.  These  patients  ultimately  reach  maturity.  Mongols 
generally  remain  small. 

Thyroid  insufficiency  produces  various  types,  of  which  cretinism  is  the 
most  common.  Its  effect  may  be  limited  to  a  simple  delay  in  growth  or 
a  general  infantilism.  Thyroidectomy  in  young  animals  causes  dwarfism, 
sexual  atrophy  and  deficient  intelligence.  Brissaud  described  an  acquired 
myxoedematous  type,  sometimes  called  Myxcedematous  Infantilism,  in 
which  physical  development  is  arrested,  the  morphological  characters  of 
childhood  persist  after  puberty,  and  general  mental  deficiency  is  often 
present.  Another  type,  described  by  Loraine  as  due  to  congenital  non- 
development  of  the  arteries,  is  sometimes  combined  with  thyroid  insufficiency. 
Congenital  diminution  of  the  lumen  of  the  larger  arteries  (Anangioplasia) 
has  been  found  combined  with  lymphatism  in  the  idiopathic  epilepsy  of 
Oldmacher. 

Lymphatic  Infantilism  is  a  variety  described  in  children  of  large 
French  cities,  and  probably  occurs  elsewhere.  The  child  develops  rapidly 
and  is  precocious  until  the  tenth  or  eleventh  year,  and  then  stops.  He 
becomes  lethargic  and  ceases  to  grow.  The  development  of  the  testes  is 
arrested,  and  the  mammse  enlarge  and  sometimes  form  abscesses.  He  gets 
pale  and  fat,  and  is  like  a  bag  of  fat.  A  violent  shock  to  the  circulation, 
such  as  a  cold  bath  or  douche,  may  cause  sudden  death.  In  this  respect 
it  is  comparable  with  the  status  lymphaticus. 

Ateleiosis  is  divided  by  Gilford  into  two  groups  :  Asexual  and  Sexual. 
They  are  well-proportioned  dwarfs  with  childish  faces  and  intelligence, 
irregular  and  backward  teeth,  small  bones  and  muscles,  and  an  imperfect 
sexual  system.  It  is  of  unknown  causation.  In  the  asexual  type  the  whole 
body  is  affected,  but  the  sexual  organs  are  the  most  backward.  It  is  not 
hereditary  and  is  usually  only  seen  in  one  of  a  family.  It  may  commence 
before  birth,  in  infancy,  or  at  any  stage  of  development.  Hence  its 
characteristics  vary  with  the  time  of  onset.  Those  affected  are  not 
necessarily  dwarfs,  since  it  may  not  begin  until  an  average  height  has  been 
obtained.  The  affection  is  one  of  delay  rather  than  of  arrest,  for  growth 
and  development  may  proceed  very  slowly  for  many  years  after  these 
processes  normally  cease,  e.g.  up  to  30  years.  The  degree  of  delay  is  often 
irregular,  some  parts  being  more  backward  than  others.  In  a  case  of 
Gilford's  the  actual  age  of  the  boy  was  12  years,  but  the  generative  organs 
were  like  those  of  an  infant  at  birth,  the  head  and  face  like  those  of  a 
2-year  old  child,  the  bodily  development  that  of  a  3-year  old  child, 
the  epiphyseal  development  that  of  6  years,  and  the  teeth  only  1  year 
delayed.  The  thyroid  seemed  normal  and  there  were  no  signs  of  cretinism. 
The  general  appearance  of  the  patient  is  that  of  a  much  younger  child.  The 
body  proportions,  contour  and  intelligence  are  those  of  a  child,  and  the 
testes  are  commonly  undescended. 


200  Chapter   X  VII. 

In  sexual  ateleiosis  development  is  delayed  until  puberty.  The  epi- 
physes then  unite  and  the  sexual  organs  mature  normally  The  child 
resembles  a  miniature  adult,  but  retains  the  physiognomy,  proportions  and 
stature  of  a  child.  Occasionally  facial  hair  grows  in  the  male.  Although 
epiphyseal  union  takes  place  as  usual,  the  bones  do  not  grow  in  length 
and  thickness  at  puberty.  The  muscular  system  develops  well.  These 
patients  differ  from  normal  dwarfs  in  the  retention  of  many  childish 
•  characteristics.  They  tend  to  die  out.  The  affection  is  often  hereditary 
and  may  affect  more  than  one  child  in  a  family.  Some  of  them  have 
children  of  normal  size,  and  occasionally  have  a  child  of  the  asexual  type. 
Such  an  occurrence  suggests  that  there  is  a  close  connection  between  the 
two  varieties.  Many  of  the  notable  dwarfs  in  history  belong  to  one  or 
other  of  these  types  of  ateleiosis,  while  others  are  achondroplasic  dwarfs. 
Some  are  said  to  have  lived  to  extreme  old  age.  Gibson,  painter  to  Charles  I, 
lived  78  years  ;  Tom  Thumb,  46  years  ;  Boruwlaski,  a  Pole,  died  at 
Durham  in  1837  aged  98  ;  and  Richebourg,  a  little  over  2  feet  in  height, 
died  in  Paris  in  1858  aged  90.  Sexual  immaturity  delays  growth  and 
sexual  hypoplasia  precedes  the  skeletal  defects,  but  ateleiosis  must  not  be 
regarded  merely  as  sexual  infantilism.  In  this  there  is  no  special  type  of 
face,  mental  development  is  normal,  and  the  sex  organs  are  by  no  means 
infantile  though  delayed  in  development.  Premature  senile  changes 
occur  in  both  types  of  ateleiosis. 

Physical  and  Sexual  Precocity  develop  under  various  conditions  and 
take  different  forms,  viz. — 

Premature  sexual  development. 

Precocious  obesity,  with  or  without  premature  sexual  development ; 
in  both  sexes. 

Abnormal  strength  and  muscularity  ;    in  males  only. 

Hirsuties  ;  present  in  almost  all  cases  and  not  necessarily  associated 
with  other  signs  of  sexual  maturity. 

Gigantism  and  Acromegaly. 

In  some  cases  there  is  no  obvious  lesion  of  the  glandular  organs. 
Others  are  associated  with  hypertrophy  or  tumours  of  pineal  and  pituitary 
glands,  testes  and  ovaries.  Obesity  and  excessive  muscularity  occur  in 
hyperplasia  and  tumours  of  the  adrenal  cortex.  In  a  fourth  group  there  is 
arrested  mental  development.  On  the  other  hand  tumours  may  be  present 
in  these  various  regions  without  any  sign  of  precocity  or  obesity.  Probably 
the  thyroid  and  thymus  glands  are  also  related  in  some  way  with  physical 
and  sexual  development.  Precocity  is  possibly  dependent  on  hyper- 
secretion, while  defective  secretion  in  some  one  or  more  of  the  ductless  and 
accessory  glands  leads  to  sexual  infantilism,  dwarfism,  muscular  atrophy, 
myasthenia,  general  alopecia,  and  impotence  or  loss  of  sexual  function. 

Obesity  of  hereditary  origin  rarely  shows  itself  in  early  life.  Dietetic 
obesity   may   occur  in  infants,  even  the   breast-fed,  from   an  excess   of 


Anomalies  and  Disorders  of  Growth.  201 

carbohydrates  in  the  food,  and  is  exaggerated  by  imperfect  oxidation,  as  in 
anaemic  girls  at  puberty.  Excessive  diet  is  a  common  cause.  Yorke  Davies 
(1890)  reported  the  case  of  a  boy  weighing  117  lbs.  at  5  years  of  age  and 
height  4  feet.  He  ate  all  day  long  and  was  fairly  intelligent.  Giant 
foetuses  of  20-24J  lbs.  have  been  recorded,  generally  overdue,  stillborn, 
and  fatal  to  the  mother.  In  congenital  obesity  the  child  is  large  at  birth  ; 
steadily  fattens,  apart  from  excessive  appetite  or  sexual  abnormality,  and 
maintains  good  health.  Some  of  the  cases  of  obesity  associated  with 
imbecility  are  cretinoid,  and  improve  on  thyroid  treatment.  An  excessive 
deposit  of  fat  is  not  uncommon  in  idiots.  Obesity  is  a  stigma  of  degenera- 
tion, when  associated  with  early  menstruation  and  masculine  aspect ; 
with  large  mamma?,  deficient  hair  and  feminine  aspect  in  the  male  ;  or  with 
a  tendency  to  giantism.  Abnormal  obesity  occurs  with  both  infantilism 
and  precocity.  The  infantilism  may  remain  permanent  as  regards  stature, 
mental  and  sexual  development.  Possibly  these  cases  belong  to  the 
group  of  Myxcedematous  Infantilism. 

Guthrie  has  added  much  to  our  knowledge  of  this  subject.  He 
distinguished  precocious  obesity  from  the  other  forms  by  the  blotchy  state 
of  the  skin.  It  occurs  most  often  with  precocious  sexual  development, 
occasionally  without,  and  is  generally  due  to  hypernephromata,  less  often 
to  ovarian  tumours.  In  Guthrie's  female  patient  no  tumour  was  found. 
Curiously  in  both  sexes  the  hypernephroma  is  almost  always  on  the  left 
side.  The  muscular  type  is  seen  in  males,  the  child  being  of  the  "  John 
Bull  "  or  "  Miniature  Drayman  "  type.  Out  of  16  collected  cases,  7  were 
■examined  post  mortem  and  revealed  ;  hypernephroma  4,  pineal  tumour 
2,  testicular  tumour  1.  The  hirsuties  and  sexual  development  may  be  that 
of  an  adult.  Premature  sexual  development  accelerates  growth  and 
ossification.  Three  cases  in  one  family  were  reported  by  H.  B.  Kobinson 
(1902),  one  girl  and  two  boys  under  6  years  of  age. 

Premature  Senility,  called  by  Hastings  Gilford  "Progeria,''''  from  a 
Greek  word  meaning  "  prematurely  old,"  is  a  rare  condition.  One  case 
was  described  by  Hutchinson,  at  age  3|,  and  completed  by  Gilford.  He 
died  from  syncope  at  17  years  of  age.  Another  began  during  the  first 
dentition  and  died  from  angina  pectoris,  aged  18  years.  The  boys  were 
remarkably  alike  ;  of  small  stature  and  proportions,  and  with  imperfectly 
developed  clavicles,  lower  jaw  and  membrane  bones  of  the  skull.  The  face 
was  wizened  and  emaciated,  hair  scanty  and  white,  skin  shrivelled,  body 
devoid  of  subcutaneous  fat,  hands  knotted  and  with  conspicuous  veins  and 
tendons,  voice  piping,  and  gait  and  standing  posture  those  of  old  age. 
Anatomically  there  were  found  atheroma  and  calcification  of  the  arteries 
and  valves,  fibroid  kidneys,  shrivelled  adrenals  and  atrophied  intestines. 
Somewhat  similar  senile  changes  in  the  arteries  and  fibrosis  of  pancreas, 
thyroid,  pituitary  and  mesenteric  glands,  and  spleen,  Avere  found  by  Ean- 
som  in  a  woman,  aged  27,  who  died  from  diabetes.     The  sex  organs  were 


202  Chapter   XVII. 

entirely  undeveloped.  Premature  greyness  of  the  hair  has  also  been* 
reported  by  Caldwell  in  a  case  of  sexual  ateleiosis,  and  probably  Ransom' & 
patient  was  of  the  same  type. 

Gigantism. — Simple  overgrowth  is  an  exaggeration  of  normal  growth., 
and  to  a  certain  extent  characteristic  of  different  families.  If  excessive  it 
produces  giantism,  and  is  due  to  delayed  epiphyseal  union  in  long  bones. 
Apparently  giantism  is  acromegaly  in  the  course  of  growth  ;  acromegaly 
being  produced  without  giantism  if  the  epiphyses  have  united.  Acromegaly 
may  exhibit  a  tendency  to  myxoedema  in  early  stages  and  to  exophthalmic 
goitre  in  later  ones.  Giantism  seldom  begins  before  the  age  of  seven  years. 
Giantism  and  acromegaly  are  often  due  to  tumours  or  other  affection  of  the- 
pituitary  body.  Giants  are  weak  mentally  and  physically,  sexually 
undeveloped,  and  die  from  trivial  causes  under  the  age  of  30,  usually  under 
22.  These  cases  are  interesting  in  comparison  with  those  due  to  thyroid 
deficiency.  Congenital  absence  of  the  thyroid  and  sporadic  cretinism 
produce  dwarfing.  Disease  of  the  pituitary  gland  causes  giantism  if  the 
epiphyses  have  not  united,  and  acromegaly  if  they  have.  Enlargement  of 
the  pituitary  body  has  been  found  in  myxoedema  and  cretinism,  and 
fibrous  goitre  in  acromegaly.  Therefore,  the  evidence  favours  the  view  that 
loss  of  pituitary  function  leads  to  late  ossification,  and  loss  of  thyroid  func- 
tion leads  to  early  ossification,  while  possibly  the  two  factors  may  be 
sometimes  co-existent.  Tamburini  found  the  thymus  enlarged  in  8  out  of 
11  cases  of  acromegaly  with  pituitary  tumour.  Furthermore,  hypertrophy 
of  the  hypophysis  cerebri  follows  castration  and  extirpation  of  the  thyroid 
The  thyroid  was  enlarged  in  5  out  of  23  cases  of  acromegaly,  atrophied  in  5, 
normal  in  11  (Woods  Hutchinson). 

Hemihypertrophy,  a  condition  of  obscure  origin,  gives  the  child  the 
appearance  of  being  composed  of  two  halves,  one  much  larger  than  the 
other.  The  difference  in  size  may  extend  to  the  internal  organs  or  be 
limited  to  one  or  more  of  the  external  structures.  It  is  congenital  and 
non-progressive.  When  a  limb,  usually  the  leg,  is  affected,  the  bones  are 
generally  involved.  In  one  recorded  case,  limited  to  the  left  side  of  the 
head  and  face,  the  cause  was  a  multiple  neurofibromatosis.  Chronic  en- 
largement of  one  limb  may  depend  on  a  nsevoid  condition  or  lymphatic 
obstruction,  giving  rise  to  hypertrophy  of  the  cellular  tissues.  In 
McGregor's  case  the  right  leg  was  chiefly  affected  and  the  head  not  at 
all.  He  died  in  his  twelfth  year  after  amputation  of  the  limb  and  the- 
right  optic  thalamus  was  found  enlarged,  the  pituitary  body  normal. 


CHAPTER    XVIII. 

THE    THYROID    GLAND. 

Congenital     Goitre  —  Acute     Thyroiditis  —  Cretinism  —  Myxcedema  —  Ex- 
ophthalmic  Goitre — Parathyroids —  Thyroglossal   Fistula —  Hygroma. 

At  birth  the  thyroid  gland  weighs  1-2  drs.  and  contains  colloid 
material.  Iodine,  bromine  and  arsenic  have  been  found  in  it  by  different 
observers.  In  childhood  the  lateral  lobes  are  usually  equal ;  sometimes 
the  right  is  greater  than  the  left ;  and  in  rare  instances  one  lobe  may  be 
absent.  The  isthmus  may  be  absent  or  fused  with  one  or  other  lobe. 
The  pyramidal  process  is  present  in  about  half  the  cases  ;  it  is  attached  to 
the  hyoid  bone,  less  often  to  the  thyroid  cartilage,  to  the  isthmus  or  a  lateral 
lobe,  or  bifurcated  and  attached  to  both  lobes  ;  and  is  rarely  double.  In 
60  children  under  the  age  of  10  years,  C.  F.  Marshall  found  the  foramen 
caecum  absent  in  23,  represented  by  a  slight  pit  in  28,  and  as  a  ductus 
lingualis,  J  in.  long,  in  9. 

Festal  or  Congenital  Goitre  is  commonly  hereditary  and  occurs  in 
goitrous  districts.  Either  parent  may  be  affected,  but  in  many  instances 
neither  is  goitrous.  It  is  noteworthy  in  this  connection  that  Halsted 
extirpated  the  thyroid  of  pregnant  bitches,  and  found  that  in  the  full- 
time  puppies  the  thyroid  gland  was  enlarged.  Many  of  the  infants  are 
premature,  stillborn,  or  die  soon  after  birth  ;  males  predominate.  Several 
sporadic  cases  have  been  ascribed  to  the  action  of  chlorate  of  potash  given 
to  the  mother  during  pregnancy,  with  a  view  to  preventing  miscarriages. 
In  these  cases  the  mother  was  a  non-goitrous  multipara  and  had  had 
numerous  miscarriages,  but  had  never  before  borne  goitrous  children. 
Many  women  have  taken  this  drug  without  it  affecting  the  child.  A  similar 
goitre  has  followed  the  administration  of  iodide  of  potassium  to  a  syphilitic 
mother.  Generally  the  chlorate  was  taken  at  the  same  time.  Ballantyne 
found  evidence  of  thyroid  hypertrophy  in  the  fourth  month  of  foetal  life. 
Most  of  these  infants  with  congenital  goitres,  ascribed  to  chlorate  of 
potash,  have  died  within  a  few  hours.  In  a  case  of  Simpson's  (I860)  the 
tumour  gradually  shrank,  and  at  4  years  of  age  the  child  seemed  healthy. 
In  goitrous  districts,  e.g.,  Gilgit  and  Chitral,  endemic  goitre  is  only 
occasionally  congenital  and  rarely  a  cause  of  cretinism  (McCarrison,  1908). 
The  goitrous  enlargement  may  be  vascular,  parenchymatous  or  adenoma- 
tous.   The  vascular  type  is  most  common  ;   large  blood  vessels  and  sinuses 


204  Chapter   X  VIII. 

are  present,  the  acini  are  fcetal  in  character  and  contain  no  colloid,  and  no 
cysts  are  found.  The  adenomatous  tumour  is  encapsuled  in  the  substance  of 
the  gland,  contains  one  or  more  cysts,  and  even  cartilage  at  the  early 
age  of  2  months.  Occasionally  it  is  fibro-cystic.  The  parenchymatous  type 
is  the  same  as  in  adults. 

The  symptoms  are  those  of  a  tumour  in  the  neck  and  due  to  pressure. 
In  mild  cases  there  is  only  slight  dyspnoea  or  hoarseness.  Large  tumours 
cause  severe  dyspnoea,  asphyxia,  cyanosis  and  retraction  of  the  lower  ribs. 
They  have  to  be  diagnosed  from  congenital  cysts  in  the  neck  and  enlarge- 
ment of  the  thymus.  Mild  forms  recover  spontaneously  ;  large  tumours 
cause  death  from  pressure  on  the  trachea,  oesophagus,  blood  vessels  or 
nerves,  unless  relieved  by  surgical  measures. 

Acquired  Goitre  may  be  sporadic  or  endemic.  Its  characteristics  are 
the  same  as  in  adults.  It  often  dates  back  to  infancy  ;  is  more  common  in 
girls  and  on  the  right  side  ;  of  the  parenchymatous  type  ;  and  often  gets 
well  spontaneously.  The  treatment  consists  in  change  of  locality,  alkaline 
waters,  syr.  ferri  iodidi  and  other  iodides,  inunction  with  iodine  or  ung. 
pot.  iod.,  and  operation. 

Acute  Thyroiditis. — Acute  inflammation  of  the  thyroid  is  due  to 
injury  or  strangulation,  or  a  sequel  of  some  infection,  e.g.  vaccination, 
specific  fevers,  throat  affections  and  parotitis.  A  local  swelling  is  found, 
either  to  one  side  of,  or  over,  the  trachea.  It  moves  on  deglutition  and 
may  cause  pain,  hoarseness,  cough,  dysphagia  and  fever  ;  occasionally 
some  dyspnoea  and  cerebral  congestion.  The  pulse  rate  is  increased  out  of 
proportion  to  the  fever.  It  subsides  or  terminates  in  abscess.  Apply  cold 
and  incise  if  necessary  ;   tracheotomy  is  rarely  required. 

Cretinism. — Cretinism,  or  congenital  myxcedema,  and  myxoedema  are 
almost  identical  in  their  pathology,  but  clinically  present  points  of  differ- 
ence on  account  of  the  age-incidence  of  the  disease.  In  cretinism  thyroid 
function  has  not  developed,  while  in  myxoedema  it  is  lost ;  and  the  older 
the  child  at  the  onset  the  less  complete  are  the  signs.  Cretinism  may  be 
goitrous  or  non-goitrous,  endemic  or  sporadic.  The  endemic  type  is 
associated  with  endemic  goitre  and  deaf-mutism.  It  occurs  in  the  valleys  of 
mountainous  districts  and  is  due  to  some  cause  in  the  climate,  soil,  or  water. 

Endemic  Goitre  is  an  infective  disease,  and  is  present  in  the  mother 
in  almost  every  case  of  cretinism  in  goitrous  districts.  These  goitres  are 
deficient  in  thyroidin,  and  the  mothers  are  apt  to  have  tetany  during 
pregnancy.  The  cretinism  is  due  to  defective  maternal  thyroid  function 
and  a  toxic  effect  on  the  thyroid  of  the  infant.  Goitre  is  present  in  75  out 
of  100  endemic  cretins  over  10  years  of  age,  but  endemic  goitre  in  the  child 
is  rarely  the  cause  of  cretinism.  McCarrison  found  that  in  all  but  2  out  of 
88  cretins  the  goitre  appeared  subsequently  to  the  cretinoid  symptoms, 
and  that  only  17  per  cent,  under  10  years  of  age  had  goitre.  The  goitre  is 
generally  adenomatous  and  functionally  inactive. 


The  Thyroid  Gland.  205 

Sporadic  Cretinism  rarely  affects  more  than  one  in  a  family.  The 
thyroid  is  almost  universally  absent,  occasionally  small  or  cirrhotic,  and 
rarely  a  cystic  goitre.  Infantile  or  Juvenile  Myxoedema  may  follow  local 
injury,  thyroiditis  or  a  specific  fever.  A  post-natal  infection  in  early  life 
accounts  for  some  sporadic  cases.  In  the  juvenile  type  the  child  develops 
normally,  until  some  illness,  and  then  in  a  few  months  growth  stops  and 
signs  of  cretinism  appear.  Thus,  it  may  be  spoken  of  as  "  Acquired 
Cretinism.''''  Psychic  factors,  such  as  grief,  fright,  nervous  shocks,  injury, 
and  impairment  of  nutrition  from  any  cause,  are  exciting  rather  than 
.  causal  factors  in  sporadic  and  in  many  cases  of  acquired  cretinism  ;  the 
true  cause  being  latent  congenital  thyroid  defect. 

Symptoms. — There  is  no  doubt  that  cretinism  and  myxcedema  are  due 
to  deficiency  of  thyroid  secretion  or  Athyroidism.  In  its  mildest  form  it 
gives  rise  to  delayed  closure  of  the  fontanelle,  delayed  growth,  mental 
dulness  and  occasionally  enuresis.  Between  this  and  the  worst  type 
of  cretinism  are  many  grades.  Typical  cretins  are  abnormally  small,  and 
backward  in  physical  and  mental  development.  Infants  rarely  give  signs 
before  6  months  of  age,  or  not  until  weaned,  because  up  to  this  time  they 
obtain  some  thyroidin  in  the  milk.  An  infant  cretin  has  a  wrinkled  fore- 
head, puffy  expressionless  face,  broad  short  hands,  subnormal  tem- 
perature, and  is  undergrown.  The  characteristics  of  the  disease  are  numer- 
ous. The  skull  may  be  normal ;  dolichocephalic,  enlarged  posteriorly  ; 
or  brachycephalic.  The  fontanelle  is  widely  open.  The  hair  is  short,  coarse 
and  scanty  ;  it  may  be  fine,  silky  and  luxuriant  in  early  cases.  The  com- 
plexion is  muddy,  with  dusky  flush  on  the  cheeks  ;  features  doughy,  thick,, 
bloated  and  devoid  of  expression,  or  dull,  heavy,  sad  and  unchanging. 
The  lips  are  thick,  everted  and  mauve  in  colour  ;  the  tongue  large,  thick, 
and  often  kept  partly  out  of  a  large  half-opened  mouth  ;  dentition  late  and 
milk  teeth  long  retained.  The  nose  is  depressed  at  the  root,  short,  and 
spreads  out  enormously  towards  the  alse.  The  eyes  are  wide  apart,  squint 
common  and  nystagmus  rare;  the  eyelids  swollen  and  baggy.  The  skin 
is  dry,  rough,  and  of  a  parchment-like  tint ;  it  is  redundant,  causing 
puckering  of  the  forehead  and  puffy  folds  below  the  eyes.  The  abdomen  is 
protuberant  and  umbilical  hernia  frequent ;  sometimes  there  is  extreme- 
lordosis.  The  body  is  stunted  ;  the  limbs  stunted  and  often  crooked. 
The  hands  are  spade-like,  thick  and  podgy,  short  and  broad,  with  square 
finger  tips.  Both  hands  and  feet  are  blue  and  cold,  so  much  so  as  to  suggest 
congenital  heart  disease.  The  muscles  are  flabby  and  badly  developed  ; 
the  movements  deliberate  and  few.  Speech  is  delayed  and  words  are 
scanty  ;  voice  guttural  and  monotonous  in  later  life.  Masses  of  solid 
oedema,  forming  "  fatty  tumours  "  or  "  supra-clavicular  pads,"  develop. 
Constipation  is  present  from  the  earliest  life  ;  the  vital  powers  are  low  and 
the  temperature  subnormal ;  the  child  sensitive  to  cold.  The  mental 
condition  is  dull,  stolid,  lethargic  and  backward.  Sometimes  the  child  is 
unable  to  recognise  anyone.     Many  are  good-natured  ;    some  idiotic  and 


206  diaper   XVIII. 

unable  to  speak  ;  a  few  destructive  and  vicious.  They  are  heavy  sleepers  ; 
averse  to  bodily  exercise  or  too  weak  for  it.  The  sexual  functions  do  not 
develop  and  the  sexual  organs  remain  undeveloped  in  the  male,  but  not 
invariably  so  in  the  female.    Beard,  axillary  and  pubic  hair  are  absent. 

The  Diagnosis  of  the  condition  in  the  early  stages  of  life  is  of  the  utmost 
importance  for  it  is  very  amenable  to  treatment.  It  is  often  diagnosed  in 
error,  and  more  often  is  not  recognised  for  some  months  or  years.  In  the 
breast-fed  the  symptoms  are  delayed  and  rarely  obvious  until  6  months  of 
age.  Macroglossia,  apathy,  constipation  and  backwardness  are  suggestive 
signs. 

The  Prognosis  is  hopeless  if  no  treatment  is  adopted.  Many  die  young 
and  few  grow  up  ;  life  has  been  prolonged  to  40  or  60  years,  without  any 
improvement  in  the  mental  state  as  age  advances.  Death  is  commonly  due 
to  broncho-pneumonia,  tuberculosis,  infectious  disease  or  diarrhoea. 
The  effects  of  thyroid  treatment  depend  on  the  duration  of  life  before 
treatment.  It  is  more  effective  in  the  sporadic  than  in  the  endemic  type. 
The  longer  the  disease  is  untreated,  the  less  is  the  improvement.  If 
treatment  is  begun  during  the  first  year  of  life,  the  patient  may  grow  up 
a  normal  child.  Even  in  late  cases  remarkable  improvement  takes  place. 
The  physical  and  mental  conditions  are  usually  proportionate,  but  one 
may  be  more  backward  than  the  other.  Improvement  takes  place  more 
■quickly  in  the  physical  than  the  mental  state,  and  may  be  limited  to  it. 
When  the  mental  state  is  only  slightly  altered  and  treatment  begun  early, 
the  outlook  is  good.  One  of  the  first  indications  of  improvement,  evident 
in  3-5  weeks,  is  the  diminution  in  the  size  of  the  tongue.  Children  taking 
thyroid  extract  do  not  succumb  so  readily  to  infectious  disease.  The 
treatment  is  of  little  use  for  old  cretins,  except  to  improve  the  appearance 
and  epidermal  structures.  Female  cretins  sometimes  become  pregnant  and 
bear  marasmic  or  hydrocephalic  infants. 

Treatment. — Give  thyroid  in  small  doses  twice  or  thrice  a  day,  and 
increase  it  until  the  maximum  dose  for  the  child  is  reached.  Continue 
the  maximum  dose  for  some  time,  and  then  gradually  reduce  it  to  the 
minimum  dose.  The  treatment  must  never  be  wholly  omitted  for  long. 
The  early  signs  of  a  slightly  excessive  dose  are  nasal  catarrh  (L.  Williams), 
rapid  pulse  and  vomiting.  Over-dosage  produces  mental  excitement, 
irritability,  restlessness,  sleeplessness,  depression,  headache,  thirst,  vomiting, 
urgent  dyspnoea,  obscure  pains,  palpitations,  intolerance  of  heat,  rise  of 
temperature  and  loss  of  weight.  For  such  symptoms  keep  the  child  in  bed 
and  omit  the  drug  temporarily,  or  reduce  the  dose.  There  is  no  danger  to 
the  heart  from  overstrain,  as  in  adults,  although  the  cardiac  muscles  may 
atrophy,  for  the  child's  blood  pressure  is  low.  A  slight  rise  of  temperature 
indicates  the  proper  dose.  Give  liquor  thyroidei  m.  1-5,  thyroid  tabloids 
grs.  -|-5,  or  iodothyrine  grs.  10,  three  times  a  day,  or  from  ^-fth  part  of 
fresh  raw  sheep's  thyroid  twice  a  week.  One  sheep's  thyroid  is  equal  to 
100  minims  of  the  liquor.     A  suitable  dose  for  a  child  of  6  months  is  gr.  \-\, 


The  Thyroid  Gland,  207 

three  times  a  day.  The  signs  of  improvement  are  that  the  temperature 
rises  to  normal  and  remains  there ;  initial  loss  followed  by  gain  of  weight, 
improved  intelligence  and  growth  in  height.  The  skin  becomes  normal 
and  subcutaneous  swelling  disappears.  The  eyes  are  brighter  and  the 
face  more  intelligent,  with  a  natural  flush  on  the  cheeks.  The  tongue  is 
not  protruded,  the  voice  less  guttural,  and  snoring  ceases.  The  hair  falls  out, 
and  is  replaced  by  softer  and  more  natural  growth.  The  appetite  is  good, 
dentition  active,  bowels  not  constipated,  abdomen  smaller  and  hernia 
disappears.  There  is  a  marked  change  in  6  months.  The  child  may  grow 
an  inch  in  the  first  month,  and  from  6-8  ins.  in  a  year.  The  rapid  growth 
may  lead  to  the  legs  bending,  when  the  child  begins  to  stand  and  run. 
Lateral  curvature  is  often  present  in  cretins  after  the  age  of  childhood,  and 
is  increased  by  rapid  growth.  The  resulting  deformities  are  similar  to  those 
of  rickets  and  due  to  bone  softening.  If  the  treatment  is  stopped,  a  goitre 
may  develop,  for  the  gland  is  not  always  quite  atrophied.  Cretins  must 
be  kept  warm,  for  they  are  very  liable  to  catch  cold  ;  carefully  fed,  for  they 
are  apt  to  get  diarrhoea  ;  and  guarded  against  infection,  to  which  they  are 
particularly  susceptible. 

Exophthalmic  Goitre  is  very  rare  in  children.  Barret  (1902)  collected 
42  cases  under  15  years,  the  youngest  was  4  years  of  age.  Of  5  cases 
recorded  since,  :>ne  was  a  girl,  3  years  old,  in  whom  the  disease  followed 
whooping  cough  and  was  fatal  in  her  seventh  year  (Batchelor).  It  is  more 
common  in  girls.  The  symptoms  are  much  the  same  as  in  adults.  Tachy- 
cardia is  often  the  first  sign  ;  sometimes  tremor,  goitre  or  exophthalmos, 
the  latter  may  be  absent.  Tremor  is  uncommon  but  chorea  is  frequent. 
The  child  finds  it  impossible  to  keep  still.  Other  symptoms  include  great 
irritability  and  attacks  of  passion,  anaemia,  debility,  loss  of  flesh,  sweating, 
attacks  of  vomiting  and  diarrhoea,  headache  and  depression.  Retraction 
of  the  upper  lids  (Stellwag),  defective  convergence  (Mcebius),  and  delayed 
movement  of  the  upper  lid  on  looking  downwards  (von  Grsefe)  are  also 
noted.  The  goitre  is  generally  of  the  vascular  type,  and  present  for  a 
considerable  time  before  other  symptoms  appear.  Sometimes  cardiac 
symptoms  come  on  suddenly  or  in  the  course  of  a  few  days,  e.g.,  after 
whooping  cough  and  broncho-pneumonia.  Headache  and  fatigue  are  noted 
early.  On  the  whole  the  onset  is  more  acute  than  in  the  adult.  The 
frequency  of  the  pulse  is  a  fair  measure  of  the  progress  of  the  disease.  Some 
of  these  acute  cases  have  recovered  in  from  1-6  weeks.  Exceptionally  it 
lasts  from  2-4  years  and  ends  fatally  from  exhaustion,  vomiting  or  diarrhoea. 
The  duration  is  less  than  in  the  adult.  Death  is  rarely  due  directly  to  the 
disease.  Apparently  it  is  caused  by  hypersecretion  of  the  thyroid,  an 
excess  of  normal  secretion.  In  adults  the  parathyroids  have  been  found 
atrophied  and  the  thymus  persistent,  sometimes  enlarged.  Myxoedema 
is  a  rare  sequel.  These  cases  are  treated  by  rest  in  bed,  open  air,  over- 
feeding,   massage,    cold    compresses,    hydrotherapy,    faradic    baths    and 


208  Chapter   X  VIII. 

faradisation  of  the  goitre.  X-rays  may  be  useful  at  the  onset,  rendering  the 
gland  smaller  and  harder,  and  reducing  the  pulse,  tremors  and  nervous- 
ness. They  should  only  be  used  on  one  side  as  they  may  cause  complete 
sclerosis  of  the  gland  and  myxcedema.  Surgical  treatment  consists  in 
partial  thyroidectomy,  ligature  of  thyroid  arteries,  or  division  of  the 
cervical  sympathetic  between  the  middle  and  upper  ganglia.  Most  adults 
get  well  without  surgical  intervention.  The  chief  drugs  given  are  cod-liver 
oil,  arsenic,  iodine,  bromide,  belladonna,  iron,  phosphoric  acid  and  phos- 
phates ;  and  the  serum  prepared  from  sheep  or  goats  after  thyroidectomy. 
Iodipin  or  red  oxide  of  mercury  ointment  (1  in  4)  can  be  rubbed  in  locally. 

Parathyroids. — These  glands,  1-4  in  number,  are  situated  in  pairs 
attached  to  the  posterior  surface  of  the  lateral  lobes,  towards  the  lower  and 
median  border,  close  to  the  oesophagus  and  trachea.  They  are  yellowish  or 
brownish  red,  round  or  flattened,  like  lymph  glands,  often  imbedded  in 
fat  and  difficult  to  identify.  In  structure  they  consist  of  large  cells  with 
deeply  staining  nuclei,  arranged  in  columns  in  a  stroma  of  connective 
tissue  and  a  fibrous  capsule.  They  are  very  liable  to  haemorrhage,  especially 
at  or  after  birth,  and  may  form  cysts  which  slowly  disappear.  Operations 
have  shown  that  extirpation  in  animals  and  man  is  followed  by  tetany  ; 
but  if  some  parathyroid  tissue  is  left,  the  tetany  is  mild  and  of  short  dura- 
tion. Haemorrhages  and  hyperplasia  of  the  gland  have  been  found  in  tetany. 
The  gland  is  essential  to  life  ;  no  animal  has  been  kept  alive  after  complete 
removal  of  it.  It  regulates  the  motor  nerve  function.  Apparently  they  are 
not  embryonal  thyroids.  But  extirpation  of  the  thyroid  in  man,  monkeys 
and  dogs  causes  acute  myxcedema.  In  rabbits  this  does  not  happen  for  the 
parathyroids  escape  removal.  This  implies  that  the  functions  of  the  two 
glands  are  identical. 

Thyroglossal  Fistula  and  Cysts. — The  thyroglossal  duct  or  tract  runs 
from  the  foramen  caecum  at  the  base  of  the  tongue  downwards  in  the  middle 
line  of  the  pharynx.  As  the  hyoid  bone  develops  it  cuts  the  duct  into  an 
upper  and  lower  part.  The  upper  part  forms  the  lingual  duct  and  becomes 
obliterated,  except  the  foramen  caecum.  It  is  rarely  so  patent  that  a  probe 
can  be  passed  downwards  from  the  foramen.  If  unobliterated  it  may 
become  distended  with  secretion,  often  sebaceous,  forming  a  cyst  which  is 
variously  named  lingual  dermoid,  lingual  hygroma  ox  hyomandibular  cyst. 
This  projects  under  the  tongue  like  a  ranula,  or  submentally  in  the  median 
line  ;  it  is  lined  by  squamous  epithelium.  If  it  bursts  or  is  opened,  it  leaves 
a  fistula  with  an  orifice,  usually  in  the  median  line  just  below  the  symphysis, 
through  which  a  fine  probe  can  be  passed  up  to  the  base  of  the  tongue.  It 
must  be  excised  from  the  neck. 

From  the  lower  part  of  the  thyroglossal  duct  the  isthmus  of  the  thyroid 
gland  is  developed.  The  cysts  arising  from  this  portion  are  named  thyroid 
dermoids  :  thyro-hyoid,  if  associated  with  the  second  cleft ;  crico-thyroid, 
if   associated  with  the  third  cleft.    The   cyst  may  reach  as  low  as  the 


The  Thyroid  Gland.  209 

manubrium.  It  is  lined  by  compound  epithelium,  sometimes  ciliated,  and 
may  contain  thyroid  tissue.  Cysts  or  fistulse  of  this  nature  usually  have  a 
pedicle  passing  through  the  thyro-hyoid  or  crico-thyroid  membrane.  They 
are  firmly  attached  to  the  hyoid  bone,  and  resection  may  be  necessary  for 
perfect  cure. 

Lateral  Cysts  may  be  of  the  same  type,  may  start  in  lateral  diverticula 
of  the  different  clefts,  or  be  of  lymphatic  origin.  They  are  sometimes  called 
Cystic  Hygromata  of  the  neck,  and  may  be  dermoids,  adenomata,  etc. 
Sometimes  the  cyst  increases  in  size  on  expiratory  effort.  Congenital  cystic 
hygromata,  unilocular  or  multilocular,  may  be  situated  in  other  places,  such 
as  the  axilla. 

Branchial  Fistulce  open  in  front  of  the  sterno-mastoid,  above  the  left 
sterno-clavicular  joint  or  bilaterally  at  the  level  of  the  crico-thyroid  space. 
They  terminate  on  the  outer  surface  of  the  pharynx  near  the  posterior 
faucial  pillar. 


Chapter  XIX, 

THE    ADRENAL    GLANDS. 

The  Adrenal  Glands  are  rarely  absent.  Probably  in  such  cases  accessory 
ones  have  been  overlooked.  The  weight  is  i  that  of  the  kidney 
in  the  newborn ;  -^g-  in  the  adult.  The  cortex  is  closely  related 
developmentally  to  the  genital  glands.  It  is  derived  from  the  pronephros  ; 
from  a  part  of  the  mesodermic  epithelium  covering  the  Wolffian  body. 
The  medulla  is  connected  genetically  with  the  sympathetic  system,  being 
derived  from  the  same  blastema.  Its  cells  are  chromophil  ones,  staining 
intensely  yellow  or  brown  with  chromic  acid  and  its  salts.  Chromatin  or 
chromophil  cells  are  widely  distributed  through  the  body  in  the  newborn. 
These  glands  receive  their  blood  supply  from  the  aorta,  the  renal  artery, 
and  the  arteries  of  the  diaphragm. 

Functions. — Death  is  stated  by  Biedl  to  follow  experimental  removal  of 
the  cortex.  As  it  is  impossible  to  separate  it  from  the  medulla  the  experi- 
ment is  of  little  value.  In  some  way  the  gland  is  connected  with  the  growth 
and  development  of  the  sexual  organs,  and  apparently  the  sexual  function 
depends  on  the  cortex.  Excessive  development  of  the  clitoris  has  been 
found  in  conjunction  with  adrenal  hyperplasia.  Excessive  development 
of  the  sexual  organs,  pubic  hair  and  fat,  has  been  found  in  association  with 
hypernephroma  ;  but  may  occur  without  hypernephroma.  In  cases  of 
retarded  sex  development,  osteogenesis  imperfecta  and  some  develop- 
mental errors  in  the  nervous  system,  hypoplasia  has  been  found.  Possibly 
the  cortex  secretes  some  substance  which  neutralizes  the  toxic  products  of 
metabolism.  It  contains  no  pressor  substance,  though  it  may  possess  an 
internal  secretion  which  assists  in  the  elaboration  of  the  pressor  substance, 
adrenalin,  secreted  by  the  medulla.  Adrenalin  causes  constriction  of  the 
arterioles  by  direct  action  ;  and  increases  the  rate  and  energy  of  the  heart- 
beat by  its  effect  on  the  central  nervous  system.  This  pressor  substance 
is  probably  formed  also  in  the  chromophil  cells,  called  ZuckerkandV s 
parasympathetic  bodies,  in  connection  with  the  sympathetic  and  in  the 
pituitary  body,  possibly  Luschka's  gland,  and  the  intercarotid  gland. 
The  anterior  lobe  of  the  pituitary  body  and  the  adrenal  cortex  have  several 
points  of  resemblance.  The  pituitary  yields  a  pressor  substance  and 
hyperplasia  is  associated  with  acromegaly. 

Apparently  the  most  important  function  of  the  adrenal  glands  is  to 
maintain  blood  pressure.     The  diphtheria  toxin  seems  to  have  a  profound 


The   Adrenal  Glands.  211 

influence  on  these  glands,  so  that  they  are  unable  to  maintain  blood 
pressure  sufficiently,  and  death  may  result.  The  internal  secretion  may  be 
absent  in  Addison's  disease  and  asthenia  from  prolonged  wasting.  Possibly 
it  is  diminished,  causing  partial  inadequacy,  in  tuberculosis,  neurasthenia 
and  cyclic  albuminuria.  Acute  insufficiency  has  been  described  in  adults, 
almost  always  associated  with  adrenal  haemorrhage.  Conditions  in  which 
it  is  increased  and  altered  in  quality  require  investigation. 

Affections  of  the  Adrenal  Glands. — On  account  of  its  liberal  and 
peculiar  blood  supply  it  is  liable  to  hyperaemia  and  haemorrhage, 
especially  under  high  blood  pressure,  e.g.  in  fits.  Infarcts  are  [not  un- 
common. Suprarenal  apoplexy  in  the  newborn  has  been  already  discussed 
(p.  130). 

Adrenal  Tumours  may  be  simple  ;  may  be  associated  with  metastases 
of  the  skull  (Hutchison's  type) ;  with  simultaneous  sarcoma  of  the  liver  ; 
with  precocious  puberty. 

Hutchison's  type  occurs  in  infants  and  young  children.  It  starts  with 
ecchymosis  of  the  eyelids  and  exophthalmos,  either  spontaneously  or  after 
trauma.  Anaemia  and  debility  may  be  noted  for  some  weeks  previously. 
A  growth  appears  in  the  adjacent  temporal  region,  and  enlarged  lymph  nodes 
in  front  of  the  ear  and  at  the  angle  of  the  jaw.  Pain  in  the  head  is  frequent. 
Total  blindness  is  rare,  but  optic  neuritis  may  occur.  Vomiting  is  rare  in 
spite  of  extension  towards  the  brain  ;  fever  is  usually  absent  and  anaemia 
secondary.  The  size  of  the  abdomen  depends  on  that  of  the  growth  ;  there 
is  no  ascites.  The  growth  is  unilateral,  occasionally  bilateral ;  varies 
in  size  from  a  walnut  to  a  child's  head  ;  and  has  little  tendency  to  invade 
neighbouring  organs.  On  section  it  is  smooth,  greyish  white  or  yellow,  and 
mottled  with  haemorrhages.    Death  is  due  to  anaemia  and  cachexia. 

Out  of  15  collected  cases  all  but  2  were  under  3  years  of  age.  Nine  out 
of  13  were  males.  Structurally  they  are  described  as  sarcomata  :  of  small 
round  cells,  4  ;  round  and  oval  cells,  3  ;  lymphosarcoma,  2  ;  medullary,  1  ; 
melanotic,  1  ;  and  sarcoma,  1  ;  and  hypernephroma,  2.  In  6  the  cranial 
bones  and  lymph  nodes  were  alone  involved.  Metastases  have  been  reported 
in  the  calvarium  in  all  cases,  ribs  4,  spine  1,  sternum  1,  tibia  1,  bone  marrow 
and  periosteum  of  several  long  bones  1,  and  once  in  the  ovaries  and  parietal 
pleura,  also  in  the  liver  and  kidneys.  Primary  adrenal  tumours  without 
metastases  in  the  skull  rarely,  if  ever,  involve  other  bones.  In  the  early 
stages  the  swelling  may  be  mistaken  for  a  sarcoma  of  the  orbit,  but  in 
this  affection  the  pre-auricular  glands  are  rarely  enlarged. 

Simultaneous  sarcoma  of  the  adrenal  and  liver  has  been  found  in  the 
first  weeks  of  life.  There  is  a  diffuse  infiltration  with  small  round  cells. 
The  liver  is  enormously  enlarged,  without  ascites  and  usually  without 
jaundice.    Other  varieties  of  tumour  are  very  rare. 

Precocious  Puberty. — The  relationship  of  tumours  to  precocious  puberty 
is  considered  on  page  200.    It  is  most  commonly  of  the  obese  type,  in  girls 


212  Chapter   XIX. 

of  1-8  years  with  large  genitals,  hirsuties,  brunette  type  of  skin,  sullen 
disposition  and  dull  intellect.  Thirst,  increased  appetite  and  vomiting 
may  occur,  and  sometimes  haematuria.  The  tumours  are  hypernephromata 
and  show  adrenal  structure.  Probably  there  is  an  excess  of  adrenal 
secretion. 

Addison's  Disease. — Monti  states  that  11  out  of  290  cases  occurred  in 
children.  The  main  symptoms  are  emaciation,  pallor,  asthenia  out  of  all 
proportion  to  the  amount  of  wasting,  and  pigmentation  of  the  skin.  This 
pigmentation  may  be  an  early  sign  or  appear  quite  late.  It  may  be  limited 
to  the  palate  or  distributed  in  the  usual  situations.  Other  symptoms  are 
dyspepsia,  intractable  vomiting,  profuse  diarrhoea,  apathy,  headache, 
vertigo,  convulsions ;  subnormal  temperature,  occasionally  febrile 
paroxysms.  It  lasts  for  months,  sometimes  for  years.  It  may  be  fatal  in  a 
few  days  with  symptoms  like  those  of  peritonitis.  Diagnosis  is  almost 
impossible  in  early  stages.  Grunbaum  states  that  adrenalin  by  mouth 
raises  blood  pressure  in  this  disease,  but  not  otherwise.  The  autopsy  may 
reveal  tuberculosis,  total  or  partial,  of  one  or  both  glands  ;  conversion  of 
the  glands  into  scar  tissue  ;  tumours  or  hyperplasia.  The  glands  some- 
times appear  healthy.  The  disease  is  caused  by  affections  of  the  glands,  or 
the  coeliac  ganglion  and  sympathetic  nerves  which  control  their  secretion. 
Treatment  so  far  has  proved  unavailing. 

Acute  Insufficiency  of  the  adrenals  sometimes  occurs.  E.S.  Lavenson 
(1909)  classifies  cases  according  to  the  clinical  symptoms  into  groups  ; 
(1)  Sudden  onset  with  epigastric  pain  and  tenderness,  followed  by 
abdominal  distension  and  death  in  a  few  days.  (2)  Profound  asthenia 
and  death  within  a  few  days.  (3)  Convulsions,  coma  and  delirium  or 
a  typhoid  state.  (4)  Sudden  death,  usually  due  to  haemorrhage. 
(5)  Purpuric  rash  or  hemorrhage  into  abdominal  viscera.  Some  cases 
present  symptoms  of  more  than  one  group. 


Chapter  XX. 

THE    MOUTH    AND    JAWS. 

Structural     Defects — The     Tongue — Stomatitis — Uvula — The     Teeth    and 
Dentition — The  Salivary  Glands. 

Apart  from  deformities,  disorders  of  trie  mouth,  are  commonly  due  to 
microbial  infection  to  which  it  is  unduly  liable,  because  of  the  delicacy 
of  the  mucous  membrane  and  the  absence  of  saliva  in  the  early  months  of 
life.  At  all  ages  organisms  are  found  which  become  virulent  under  suitable 
conditions.  Thus,  the  micrococcus  of  sputum  septicaemia,  staphylococci, 
diplococcus  pneumoniae  and  the  diphtheria  bacillus  may  be  present  in  the 
saliva  of  children  apparently  healthy.  The  oral  secretions  are  not  bac- 
tericidal nor  is  the  cavity  sterile,  but  the  harmless  microbes  present 
crowd  out  the  pathogenic  ones. 

Care  of  the  Mouth. — It  is  frequently  recommended  that  the  infant's 
mouth  should  be  wiped  out  gently  after  each  feed,  with  a  soft  rag  dipped  in 
clean  water  or  weak  boric  acid  solution.  This  is  quite  imnecessary  and  a 
common  source  of  injury  to  the  mucous  membrane.  The  teeth  should  be 
cleaned  twice  a  day.  During  illness  the  lips  are  apt  to  be  dry,  cracked  and 
covered  with  sordes  ;  and  the  tongue  parched,  furred  and  cracked. 
Benzoated  lard  or  cold  cream  should  be  applied  to  the  lips.  For  cleansing  the 
mouth  and  removing  fur  from  the  tongue,  swab  hourly  in  bad  cases  with 
lemon  juice,  glycerine  and  water,  glyc.  ac.  borici.,  boroglyceride  1  in  40,  or 
a  solution  of  boric  acid  or  Listerine.  Another  useful  mixture  is  sod.  bicarb, 
grs.  10,  sod.  bibor.  grs.  10,  glycerin,  dr.  1,  tinct.  myrrhae  m.  1-10,  water 
to  1  oz.  As  antiseptics  salicylic  acid  and  benzoic  acid  solutions,  1  in  200, 
are  the  best.  Eucalyptol  and  thymol  are  mere  deodorants.  Bicarbonate 
and  biborate  of  soda  are  used  to  dissolve  mucus  ;  weak  sulphurous  acid 
for  the  destruction  of  moulds  ;  liquor  sodse  chlorinatae  or  chlorine  water 
for  fcetor  and  ulcers.  As  disinfectants  and  deodorants  use,  for  douching, 
permanganate  of  zinc  gr.  yo  in  5  oz.  of  water ;  peroxide  of  hydrogen, 
2  per  cent.  ;  lysoform,  0-5  per  cent.  For  more  constant  action  formamint 
tablets  can  be  sucked  frequently;  each  contains  formic  aldehyde  gr.  £: 
or  lozenges  made  of  thymol  0-20,  alcohol  2-00,  sugar  200  gms., 
flavoured  with  essence  of  peppermint  and  divided  into  200  parts.  Para- 
sitic growths  and  ulcers  are  best  treated  by  painting  with  solution  of  silver 


214  Chapter   XX. 

nitrate,  2  per  cent.,  pure  carbolic,  copper  sulphate  grs.  2  to  1  oz.,  zinc  chloride 
grs.  20  to  1  oz.,  tincture  of  iodine,  or  boric  acid  10  per  cent,  solution. 

Deformity  of  the  Jaws  in  relation  to  Suckling. — The  tongue  is  large  and 
muscular,  and  the  cheeks  contain  pads  of  fat  immediately  over  the  bucci- 
nator, bulging  inwards  and  known  as  "  sucking  pads."  The  under  surface 
of  the  upper  lip  is  somewhat  papillated  and  the  levator  labii  superioris 
well  developed.  These  structures  are  utilised  in  the  act  of  suckling,  in 
which  the  movements  are  analogous  to  those  adopted  in  milking  cows 
and  involve  compression  rather  than  sucking.  The  baby  takes  into  its 
mouth  the  nipple  and  a  portion  of  the  areola,  a  cone-shaped  mass,  the  base 
of  which  it  squeezes  between  the  palate  and  the  lower  jaw  by  elevation  of 
the  lower  jaw,  thus  forcing  out  the  milk  from  the  distended  ampullae.  The 
tongue  is  partially  protruded  over  the  lower  gums,  but  the  cheeks  remain 
passive  and  are  not  drawn  in  as  in  suction.  In  ordinary  bottle  feeding, 
especially  when  the  teat  is  small  and  like  the  so-called  dummy-teat  or 
"  comforter,"  the  process  is  almost  entirely  one  of  suction.  This  is  said  to 
produce  evil  mechanical  effects  on  the  jaws  and  teeth. 

To  this  have  been  ascribed  irregularity  of  the  teeth,  deformities  of 
the  hard  palate  and  dental  arches,  mouth  breathing,  nasal  obstruction  and 
deviations  of  the  septum.  The  child  constantly  has  its  mouth  partially 
open.  Though  the  jaws  are  closed,  the  upper  and  lower  incisors  do  not 
meet  and  leave  a  gap  big  enough  to  admit  the  tip  of  the  little  finger  ;  and 
the  upper  incisors  overlap  the  lower.  The  palate  is  high,  narrow  and 
arched,  and  causes  contraction  of  the  nose  and  nasal  fossae.  The  arch 
of  the  lower  jaw  may  be  narrowed  ;  the  teeth  are  crowded.  These  children 
often  suffer  from  adenoids  and  large  tonsils.  It  is  a  moot  point  whether 
the  deformities  are  primary  or  a  secondary  result  from  continued  sucking, 
the  constant  pressure  by  a  hard  teat  and  atmospheric  pressure  ;  or  whether 
they  are  due  to  the  adenoid  and  tonsillar  hypertrophy.  They  have 
increased  in  frequency  during  recent  years,  coincidently  with  the  increase 
in  bottle-feeding  and  use  of  comforters.  In  races  where  breast-feeding  is 
the  rule,  these  deformities  and  the  occurrence  of  adenoids  are  distinctly 
rare.  It  is  more  probable  that  the  deformities  are  due  to  adenoids,  for 
they  are  frequent  in  the  breast-fed.  If  they  were  due  to  bottle-feeding 
they  should  be  much  more  prominent  in  infants,  whereas  they  are  rare 
before  the  age  of  6  years.  Moreover,  all  these  deformities  may  occur 
independently  of  each  other.  It  is  important  that  a  proper  cone-shaped 
nipple  should  be  used  in  bottle-feeding  and  comforters  forbidden,  for 
undoubtedly  the  act  of  sucking  may  help  to  produce  deformity  in  infants 
predisposed  to  it  by  the  presence  of  adenoids.  The  relationship  of  these 
deformities  to  nasal  obstruction  is  considered  more  fully  in  a  subsequent 
chapter. 

Hare-lip  and  Cleft  Palate. — A  hare-lip,  whether  median  or  lateral, 
should  be  operated  on  about  the  end  of  the  first  month  of  life.    The  sooner 


The  Mouth    and  Jaws.  215 

it  is  done,  the  better  is  the  subsequent  development  of  the  mouth  and 
nose,  and  the  closer  is  the  approximation  of  the  edges  of  the  cleft  in  the 
alveolus,  if  present.  The  voice  will  develop  normally,  if  there  is  no  defect 
in  the  alveolus,  but  even  a  small  notch  in  this  may  cause  lisping. 

The  operative  treatment  of  cleft  palate  depends  partly  on  the  extent 
of  the  cleft.  If  it  is  limited  to  the  soft  palate  and  there  is  no  other  defect, 
articulation  will  become  perfect,  provided  the  cleft  is  cured  before  the 
child  acquires  bad  habits.  It  should  be  closed  about  the  end  of  the  second 
or  beginning  of  the  third  year  of  life.  In  early  infancy  the  parts  are  so 
small  and  the  tissues  so  friable  that  the  operation  is  difficult,  immediate 
results  may  be  bad,  and  the  new  soft  palate  small  and  imperfect. 

If  the  cleft  is  in  the  hard  palate,  articulation  will  never  be  quite  perfect, 
no  matter  how  early  the  closure  is  effected,  for  there  is  associated  defect 
in  the  nasal  chambers.  Articulation  does  not  depend  entirely  on  perfection 
of  the  velum.  The  voice  is  somewhat  the  same  as  that  of  a  child  with  a 
high  palate  encroaching  on  the  nasal  chambers.  Such  a  voice  may  be 
independent  of  palatal  defect  and  be  due  to  defective  co-ordination  of 
palatal  muscles.  On  physiological  grounds  the  cleft  should  be  closed  as  soon 
as  possible.  Arbuthnot  Lane  recommends  the  fifth  week  as  the  best  age, 
while  other  surgeons  prefer  to  postpone  operation  until  the  third  to  the 
sixth  year.  It  should  be  done  in  the  fourth  year  by  preference,  or  in  the 
third  year  if  the  child  is  strong  and  healthy.  Bad  habits  of  speech  are 
rarely  learnt  earlier.  If  done  early,  the  naso-pharynx  is  exposed  sooner 
to  the  mechanical  factors  on  which  its  proper  development  depends,  and 
the  voice  is  said  not  to  become  nasal ;  the  child  is  healthy  ;  the  operation 
is  easier  because  of  the  absence  of  teeth  and  the  possibility  of  obtaining  a 
greater  flap,  and  the  tissues  repair  well.  The  child  is  more  tractable,  and 
the  general  health  is  improved  because  food  can  be  taken  better.  Against 
the  early  operation,  it  may  be  urged  that  the  results  are  as  good  or  better 
at  a  later  age  ;  that  a  nasal  voice  will  occur  in  any  case  if  the  cleft  is  in  the 
hard  palate  ;  that  the  risk  of  death  from  shock  and  the  risk  of  sepsis  are 
greater,  unless  the  teeth  are  carious ;  that  the  tissues  are  more  lacerable  and 
liable  to  slough  ;  that  the  late  operation  is  easier  because  there  is  more 
room  and  more  tissue  to  deal  with  ;  and  that  older  children  are  kept  quiet 
more  easily  after  the  operation.  Certainly  the  operation  on  the  soft  palate 
at  a  very  early  age  is  often  unsatisfactory,  being  followed  by  much  fibrosis 
and  subsequent  contraction.  Undoubtedly  the  risks  are  less  in  the  later 
operation  and  the  results  as  good,  if  it  is  done  before  the  fifth  year.  It  is 
always  important  to  train  the  voice  afterwards,  especially  in  saying  "  S  " 
and  "  TH." 

If  the  cleft  is  very  large  it  may  be  better  to  operate  early,  and  to 
adopt  Brophy's  method  of  forcibly  approximating  the  maxillary  and 
palate  bones  by  wire  sutures.  By  this  means  the  halves  of  the  velum  are 
brought  close  together  and  can  be  adjusted  without  tension.      It  should 


216  Chapter  XX. 

be  done  10  days  to  3  months  after  birth  ;  after  that  the  bones  are  too 
fully  ossified  to  be  displaced  by  a  safe  degree  of  violence.  The  hard  palate 
should  be  closed  before  the  soft,  and  the  hare-lip  operated  on  subsequently. 
It  is  a  severe  operation. 

Cleft  palate  interferes  'with  suckling.  A  teat  with  a  flange  on  each  side 
to  fill  up  the  cleft,  may  enable  the  child  to  take  the  bottle.  If  not,  it  must 
be  fed  by  a  spoon  or  nasal  tube. 

Alveolar  Defects. — Total  necrosis  of  the  inferior  maxilla  has  followed 
on  alveolar  abscess  and  noma.  Partial  necrosis  of  the  alveolar  border  of 
both  upper  and  lower  jaw  may  occur  from  inflammatory  and  septic  infec- 
tions of  the  mouth.  In  one  child  an  attack  of  measles  was  followed  by  this 
type  of  necrosis  on  the  left  side,  with  separation  of  the  bone  and  the  exposure 
of  the  permanent  teeth,  which  subsequently  dropped  out.  Cicatricial 
bands  may  be  caused  by  ulcerative  stomatitis  or  cancrum  oris  and  produce 
closure  of  the  jaws. 

Micrognathia,  or  smallness  of  the  lower  jaw,  produces  a  bird-like 
facial  aspect.  The  prominence  of  the  chin  is  lost  and  the  upper  incisors 
project.  In  unilateral  cases  the  hyoid  bone  and  the  larynx  may  be  dis- 
placed to  one  side.  Opening  the  mouth,  mastication  and  speech  are 
interfered  with,  especially  if  anchylosis  exists.  Congenital  cases  are  rare, 
and  generally  associated  with  developmental  defects  incompatible  with 
life.  The  condition  is  due  to  premature  ossification  of  the  lower  jaw  on  one 
or  both  sides,  or  to  anchylosis  from  excessive  development  and  altered 
direction  of  growth  of  the  coronoid  process  and  great  wing  of  the  sphenoid. 
The  acquired  variety  is  caused  by  interference  with  the  growth  of  the 
epiphyses,  or  irregular  nutrition  of  one  or  both  halves  of  the  jaw.  Hence, 
it  may  result  from  injury  at  birth  or  subsequently,  and  from  secondary 
necrosis  due  to  periostitis  or  osteomyelitis,  cancrum  oris  and  abscess  in 
front  of  the  ear.  Surgical  treatment  is  of  little  value  as  regards  appear- 
ance. Resection  of  the  coronoid  process  cures  anchylosis  and  osteoplastic 
resection  of  the  lower  jaw  offers  some  hope  of  improvement. 

The  mouth  may  be  abnormally  large,  Macrostoma  ;  abnormally  small, 
Microstoma ;  and  rarely  there  is  unusual  hypertrophy  of  one  or  both  lips, 
Macrochilia,  commonly  noevoid  or  due  to  lymphangiectasis. 

The  Tongue. — Dryness  of  the  tongue  may  be  due  to  absence  or 
deficiency  of  saliva  from  defective  secretion  or  blockage  of  the  parotid 
ducts.  It  may  result  temporarily  from  fear  or  it  may  be  due  to  mouth 
breathing.  The  fur  on  the  tongue  is  formed  by  proliferation  of  the  epithe- 
lium and  is  increased  by  fever.  Its  appearance  is  modified  by  the  lack  of 
attrition  and  cleaning  of  the  tongue  by  food.  A  tongue  always  becomes 
furred  when  the  child  is  fed  on  liquid  diet,  partly  because  of  the  diet,  partly 
because  of  the  illness  which  renders  such  a  diet  necessary.  In  addition  the 
tongue  is  modified  by  congestion  and  inflammation.      Glossitis  is  usually 


The  Mouth    and  Jaws.  217 

part  of  a  general  stomatitis.  It  may  be  caused  by  mechanical  injury, 
sharp  teeth,  and  irritants. 

The  tongue  may  be  dotted  or  stippled ;  heavily  coated  or  plastered 
with  a  thick  paint-like  coat;  strawberry-like,  due  to  prominent  red 
papillre  on  a  white  background ;  furred  or  shaggy ;  dry,  brown,  and 
encrusted ;  red,  smooth  and  dry,  denuded  of  epithelium  ( Raspberry 
Tongue)  ;   or  cleaning,  beginning  at  the  tip  and  sides. 

The  Geographical  Tongue  (Annulus  Migrans,  Glossitis  Areata  Exfola- 
tiva)  is  greyish  white  from  hyperplasia  and  red  from  denudation  of  epithe- 
lium. It  is  generally  seen  at  one  to  four  years  of  age  and  is  possibly  a  sign 
of  the  exudative  diathesis.  A  greyish  white  spot  appears  on  the  edge  of  the 
tongue  and  extends  on  to  the  dorsum.  It  spreads  by  irregular  concentric 
rings  and  becomes  reddish  in  the  centre.  There  is  no  ulceration.  The  rest 
of  the  tongue  may  be  coated.  Sometimes  the  patches  are  multiple  and 
coalesce.  The  course  is  chronic,  the  results  negative,  and  treatment  un- 
necessary. It  can  be  painted  with  strong  chromic  acid  and  then  Avashed 
with  alum  lotion. 

Tongue-tie  is  unimportant  but,  if  the  fraenum  extends  right  to  the 
tip,  it  may  interfere  with  suckling  and  affect  speech  subsequently.  It  can 
be  snipped  with  a  pair  of  scissors,  taking  care  to  keep  close  to  the  tongue 
and  do  too  little  rather  than  too  much.  In  rare  instances  the  tongue 
is  adherent  to  the  floor  of  the  mouth  by  easily  separable  adhesions. 
Lip-tie  is  a  similar  condition,  due  to  an  abnormally  short  frsenum  of  the 
upper  or  lower  lip.  Sublingual  Ulcer,  at  the  junction  of  the  freenum  with 
the  floor  of  the  tongue,  is  generally  due  to  whooping  cough  or  other 
spasmodic  cough,  and  occasionally  to  the  friction  of  the  lower  incisor  teeth 
in  infants.  Earely  a  Sublingual  Fibroma  grows  from  the  freenum  in  infants 
and  may  ulcerate.  It  is  probably  due  to  irritation  by  the  incisor  teeth. 
Macroglossia  is  due  to  hyperplasia,  mainly  interstitial.  It  interferes  with 
or  prevents  swallowing.  The  tongue  is  unduly  large,  protrudes  from  the 
mouth,  and  may  become  eroded  and  fissured.  It  is  seen  in  cretins  and  less 
often  in  mongols.  Muscular  macroglossia,  lymphangioma,  naevus,  tumours, 
and  gummata  are  rare.  A  few  cases  of  macroglossia,  due  to  neuro-fibro- 
matosis,  are  on  record. 

The  Mouth. — Erythematous  Stomatitis  in  the  newborn  is  the  name  given 
to  the  bright  red  appearance  of  the  mucous  membrane  of  the  mouth  and 
tongue  present  at  birth.  Aphthce  in  the  Newborn,  or  Bednar's  Aphtha? 
{Ulcera  Pterygoidea),  were  described  by  Bednar,  in  1850,  as  only  seen  in 
babes  from  2  days  to  6  weeks  of  age,  on  the  hard  and  soft  palate.  They 
are  usually  bilateral  and  symmetrical,  one  on  each  side  of  the  median  line  or 
united  by  a  bridge  and  butterfly  shaped.  At  first  there  is  injection  of  the 
mucous  membrane  ;  next  a  superficial  epithelial  necrosis,  forming  a  greyish 
or  yellowish  white  adherent  secretion,  which  is  soon  exfoliated  and  leaves 
a  superficial  ulcer.     These  yellowish  white  patches  are  oval  in  shape  and 


218  Chapter  XX. 

surrounded  by  a  red  areola.  They  are  due  to  rubbing  and  mechanical 
cleansing  of  the  mouth  after  birth,  and  even  before  feeding,  for  they  may  be 
found  before  the  child  is  put  to  the  breast.  If  infected  with  pyogenic 
organisms,  they  may  give  rise  to  sepsis.  Epithelial  Pearls,  milia  of  the 
mouth,  are  masses  of  epithelium  on  the  gums  and  hard  palate,  minute, 
and  milky- white  or  yellowish  in  colour.  They  undergo  absorption,  but  may 
ulcerate.  Retention  cysts  of  mucous  glands  may  also  ulcerate.  Both 
these  conditions  may  be  mistaken  for  Bednar's  aphthse.  Treatment  consists 
in  painting  with  2  per  cent,  silver  nitrate  solution. 

Thrush  or  Parasitic  or  Aphthous  Stomatitis  is  due  to  the  o'idium  albicans, 
mycoderma  vini  or  the  saccharomyces  albicans.  The  fungus  can  easily  be 
found  by  microscopic  examination.  It  is  rare  in  the  breast-fed,  most  com- 
mon in  the  first  few  months  of  life,  in  the  bottle-fed,  and  under  bad 
hygienic  surroundings.  Prolonged  illness  and  malnutrition  are  important 
predisposing  causes.  The  growth  of  the  organism  is  favoured  by  dryness 
of  the  mouth,  and  its  acid  reaction  and  undue  cleaning.  The  infection  is 
usually  derived  from  milk,  and  is  spread  by  infected  teats,  comforters  and 
spoons.  Associated  with  more  or  less  catarrhal  stomatitis,  small  whitish 
patches  of  fibrinous  exudation  are  seen  on  the  tongue,  lips,  cheeks  and  gums. 
At  first  they  are  discrete,  more  or  less  circular,  and  look  like  flakes  of  curdled 
milk.  They  are  apt  to  coalesce  into  larger  patches,  sufficiently  extensive 
to  cover  the  whole  buccal  cavity  and  fauces,  and  extend  to  the  naso- 
pharynx and  oesophagus,  occasionally  to  the  larynx  and  stomach.  Pene- 
tration of  the  epithelium  by  the  fungus  makes  them  adhere  to  the  mucous 
membrane,  and  leave  raw  bleeding  surfaces  if  forcibly  detached.  Partial 
exfoliation  results  from  epithelial  proliferation.  After  a  day  or  two  they 
become  drier,  yellowish  and  less  adherent ;  and  finally  brownish  and  drop 
off,  leaving  normal  mucous  membrane.  They  often  appear  and  recur  in 
the  debilitated,  and  are  a  sign  of  cachexia.  Thrush  gives  rise  to  malaise, 
fever,  enlargement  of  the  submaxillary  lymph  glands,  anorexia,  wasting, 
and  intestinal  catarrh.  Irritating  intestinal  discharges  produce  soreness 
and  ulceration  of  the  buttocks,  and  have  given  rise  to  the  saying  that  "the 
thrush  has  gone  through  the  child."  In  rare  instances  it  causes  general 
infection,  with  metastases  in  the  form  of  embolic  abscesses,  perhaps  due  to 
mixed  infection.  The  quickest  cure  is  to  paint  the  patches  with  2  per  cent, 
nitrate  of  silver  solution.  Boric  acid,  10  per  cent.,  is  also  efficacious.  The 
child  may  suck  a  formamint  tablet,  crushed  and  put  in  a  stout  muslin  bag, 
at  frequent  intervals. 

Perleche  (pour  lecher)  is  so-called  because  of  the  tendency  to  lick  the 
red  and  rough  affected  angles  of  the  mouth.  Later  on,  radiating  cracks 
appear  and  fissures,  which  are  covered  with  exudate,  are  painful  and  bleed 
readily.  They  usually  heal  without  forming  scars.  The  disease  chiefly 
occurs  in  school  children,  and  is  probably  due  to  infection  spread  by  pencil 
sucking.    It  may  simulate  mucous  plaques,  but  it  does  not  affect  the  inner 


The  Mouth    and  Jaws.  219 

surface  of  the  cheeks  or  cause  deep  ulceration,  and  is  localised.  It  is  treated 
by  Friar's  balsam,  silver  nitrate,  tincture  of  iodine  or  antiseptic  drying 
powder.  Eczema  of  the  lips  and  herpes  labialis  are  simple  and  common 
affections. 

Catarrhal  Stomatitis  occurs  at  any  age,  but  is  most  frequent  in  the 
first  year  of  life.  It  is  usually  secondary  to  dentition  or  local  conditions  and 
general  disease.  The  mouth  is  hot  and  patches  of  intense  redness  are 
scattered  over  the  swollen  mucous  membrane,  especially  on  the  tongue  and 
gums.  The  child  is  fretful  and  restless,  suffers  pain  on  eating,  and  there 
is  much  salivation.  The  tongue  is  usually  furred  on  the  dorsum.  After 
a  time  the  epithelium  necroses  and  forms  yellowish  patches,  passing  into 
the  type  of  true  aphthous  stomatitis.  Most  inflammations  of  the  mouth 
are  preceded  by  the  catarrhal  form  of  stomatitis.  In  its  mildest  type  simple 
desquamation  occurs,  and  the  tongue  and  gums  especially  remain  intensely 
red. 

True  Aphthous  or  Maculofibrinous  Stomatitis  is  most  common  at  the 
crawling  age.  Small,  discrete,  yellowish  white  spots,  subepithelial,  with  a 
reddish  inflammatory  areola,  develop  as  a  further  stage  of  catarrhal 
stomatitis.  The  epithelium  is  rubbed  off,  and  the  fibrinous  deposit  rubbed 
off  or  absorbed,  leaving  a  shallow  ulcer  with  a  red  zone  which  soon  heals. 
It  usually  comes  on  suddenly  with  fever  and  causes  anorexia,  burning  pain, 
irritability,  sleeplessness,  and  occasionally  diarrhoea  and  submaxillary 
adenitis. 

Herpetic  Stomatitis  may  result  from  digestive  disturbance  and  is  not 
uncommon  in  the  course  of  marasmus.  Typical  outbreaks,  affecting  the 
anterior  end  and  the  sides  of  the  tongue,  and  the  inner  surfaces  of  the  lips, 
occurred  in  a  child  aged  26  months,  who  had  been  ill  for  18  months  with 
recurrent  ileo-colitis  and  marasmus. 

Membranous  Stomatitis  is  due  to  various  organisms  such  as  the 
diphtheria  bacillus,  pneumococcus,  staphylococcus  aureus  and,  rarely, 
the  streptococcus  pyogenes.  Occasionally  a  whitish  adherent  membrane 
forms  on  the  mucosa  in  debilitated  children  recovering  from  measles  or 
whooping  cough.  The  membrane  is  very  like  diphtheritic  membrane. 
The  tongue  is  rarely  attacked.  Impetigo  of  the  face  is  almost  always  present, 
and  the  staphylococcus  aureus  can  generally  be  found.  The  pneumococcal 
variety,  also  liable  to  be  mistaken  for  diphtheria,  affects  the  lips,  gums, 
cheeks,  throat  and  tonsils.  Gonococcal  infections  occasionally  occur,  even 
in  the  newborn. 

Ulcerative  Stomatitis  is  a  molecular  spreading  necrosis,  with  small  cell 
infiltration  at  the  onset.  A  spirillum  and  the  bacillus  fusiformis  are  often 
present.  It  occurs  at  4-14  years  of  age,  especially  at  the  period  of  the 
second  dentition.  The  chief  causes  are  carious  teeth  ;  infectious  disease, 
notably  measles  ;  insanitary  surroundings  ;  overcrowding  and  bad  diet. 
It  may  be  endemic  in  institutions.    A  similar  state  of  the  gums  may  occur 


220  Chapter   XX. 

in  mercuriatism,  scurvy,  purpura  and  leuksemia.  It  depends  on  the 
presence  of  teeth,  and  almost  always  begins  on  the  gums  of  the  lower  jaw, 
especially  round  the  lower  incisor  or  canine  teeth.  The  outer  surface  is 
more  affected  than  the  inner.  Swelling  and  redness  are  followed  by  necrosis 
of  the  mucous  membrane,  bleeding  and  purulent  exudation,  with  foetid 
odour  and  salivation.  The  teeth  may  be  buried  in  the  gums  or  the  roots 
denuded,  and  become  loose  and  drop  out.  The  tongue  is  thickly  furred, 
swollen  and  indented  by  the  teeth  ;  the  lips  and  cheeks  also  may  be 
swollen.  The  ulceration  is  liable  to  extend  to  the  side  of  the  tongue,  lips, 
cheeks,  and  occasionally  the  tonsils  and  soft  palate,  and  may  progress  on  to 
necrosis  of  the  alveolus  and  even  the  entire  jaw.  The  constitutional  symp- 
toms are  pallor,  fever,  irritability,  depression,  severe  mouth  pain,  anorexia, 
inability  to  take  food  and  toxsemia.  Most  cases  recover  in  7-10  days.  The 
chief  complications  are  adenitis,  abscess  in  the  glands  and  rarely  in  the 
tongue,  Angina  Ludoviei,  necrosis  of  alveolus  or  entire  jaw,  general  sepsis 
and  noma. 

The  general  treatment  of  these  mouth  affections  is  on  the  lines  men- 
tioned under  "  Care  of  the  Mouth,"  with  the  administration  of  chlorate  of 
potash  internally  and  diet  of  a  liberal  type.  The  mouth  in  ulcerative  affec- 
tions must  be  washed  out  frequently  with  Condy,  permanganate  of  potash 
or  permanganate  of  zinc  lotion,  and  the  ulcerated  parts  painted  with  tinc- 
ture of  myrrh  1  part,  glycer.  boracis  2  parts. 

Cancrum  Oris,  Noma  or  Gangrene  of  the  Mouth,  is  a  specific  necrotic 
process  peculiar  to  children.  It  is  never  primary,  but  generally  follows 
measles  (50  per  cent.),  scarlet  fever,  typhoid  fever,  and  occasionally  other 
fevers.  It  may  follow  diphtheria  and  ulcerative  stomatitis,  and  I  have  seen 
it,  in  a  girl  of  three,  as  a  sequel  of  acute  gastritis.  I  am  inclined  to  think  that 
the  administration  of  mercury  predisposes  to  the  infection.  To  a  certain 
extent  it  is  infectious  or  mildly  contagious,  and  may  break  out  in 
epidemic  violence  in  institutions  as  a  sequel  of  epidemic  measles. 

It  may  be  defined  as  a  mycosis  developing  on  a  specially  acquired 
predisposition.  The  filaments  spread  deeply  into  healthy  tissue  and 
give  rise  to  coagulation  necrosis,  analogous  to  hospital  gangrene  but 
without  the  production  of  gas.  Primarily  it  is  a  simple  infection, 
though  in  its  later  stage  it  is  a  mixed  one.  Decayed  teeth  predispose, 
through  setting  up  gum  conditions  favourable  to  the  growth  of  the  specific 
organisms. 

Bacteriology. — A  long  and  thread-like  leptothrix  is  often  found. 
Walsh  (1901)  thinks  two  organisms  are  necessary,  one  to  cause  primary 
necrosis  ;  and  the  other  a  saprophyte,  to  produce  putrefaction.  He  found 
diphtheria  bacilli  in  8  cases,  once  in  pure  culture  ;  4  after  measles  and  4 
after  ulcerative  stomatitis.  Herrman  (1905)  ascribes  it  to  two  different 
organisms  ;    one  the  "  fusiform  bacillus,"  commonly  found  in  Vincent's 


The  Mouth    and  Jaws.  221 

angina,  identical  with  the  spirillum  sputigenum  of  Miller  and  corresponding 
to  the  streptothrix  of  Seiffert- Perthes  ;  and  the  other  the  spirochete  den- 
tium  of  Miller.  These  organisms  are  believed  by  Herrman  to  be  different 
stages  of  the  same,  and  he  has  named  it  the  Spirochete  of  Necrosis.  Both 
are  motile  ;  normally  present  in  the  mouth,  except  in  toothless  infants  ; 
much  increased  in  number  by  hyperaemia  of  the  gums,  in  gingivitis,  in  ulcera- 
tive and  gangrenous  stomatitis,  different  stages  of  the  same  process,  and  in 
noma  of  other  parts.  The  organism  is  not  a  bacillus  and  cannot  be  grown 
or  stained  in  the  usual  way.  It  is  best  stained  by  dilute  carbol  fuchsin, 
and  is  decolourised  by  Gram.  It  requires  very  favourable  conditions  for  its 
development,  and  consequently  noma  is  only  slightly  contagious.  The 
arguments  in  favour  of  this  organism  being  a  causative  agent,  are  that  it  is 
present  in  very  large  numbers  or  in  nearly  pure  culture  ;  that  it  gradually 
disappears  during  healing  ;  that  very  few  other  organisms  are  present ; 
and  that  it  penetrates  into  apparently  healthy  tissue  beneath  the  necrotic 
layer.  On  the  other  hand  it  has  a  very  wide  distribution,  cases  are 
relatively  few,  and  it  is  possible  that  necrotic  tissues  afford  a  suitable  soil 
for  its  development.  Though  it  may  be  the  rnmmon  oiganism,  it  is  probable 
that  other  organisms  may  be  important  agents  in  some  cases. 

The  primary  lesion  is  an  inflammation  of  the  gums,  and  the  presence  of 
teeth  appears  to  be  essential.  The  tongue,  cheeks  and  tonsils  are  generally 
affected  secondarily.  In  rare  instances  it  begins  on  the  surface  of  the 
cheek  and  extends  inward,  on  the  ala  nasi  or  at  an  angle  of  the  mouth. 
It  may  affect  the  ear  or  vulva.  It  is  generally,  not  invariably,  unilateral. 
Frequently  it  begins  as  a  bleb  or  a  black  spot  on  the  inner  side  of  the  cheek, 
but  the  bleb  is  not  often  seen  as  the  cheek  rarely  attracts  attention  at  this 
stage.  Sometimes  slight  ulceration  of  the  mucous  membrane  is  found  first 
with  a  surrounding  of  intense  hardness.  The  cheek  is  swollen,  shiny  and 
of  a  waxy  pallor,  not  very  tender  or  painful,  and  feels  indurated.  This 
stage  is  followed  by  rapid  ulceration  and  extensive  gangrene  from  within 
outwards.  The  skin  of  the  cheeks  becomes  very  tense,  red  and  shiny,  then 
livid  and  black.  An  external  bleb  often  forms  ;  the  black  patch  becomes  a 
slough  and  perforation  ensues.  As  it  breaks  down  it  becomes  very  offensive 
and  the  fcetor  is  intense.  The  necrosis  extends  in  various  directions  and  a 
huge  excavation  is  formed.  Occasionally  the  parts  become  emphysematous. 
Haemorrhage  is  rare  for  the  vessels  may  be  penetrated  by  the  filaments 
and  are  plugged  with  clot.  These  cases  terminate  in  80-90  per  cent, 
fatally  from  sepsis,  secondary  infection  or  septic  pneumonia.  In  a  few 
the  process  is  arrested,  sloughing  ceases  and  rapid  healing  ensues,  but 
more  or  less  deformity  from  cicatricial  contraction  remains.  Teeth 
drop  out  and  there  may  be  necrosis  of  an  alveolus,  or  of  the  superior  or 
the  inferior  maxilla. 

Treatment  must  be  stimulating  ;  plenty  of  nutritious  food  ;  carbonate 
of  ammonia,  strychnia  and  cinchona,  and  brandy.    If  it  is  not  too  extensive, 


222  Chapter   XX. 

excision  and  free  cauterisation  with  Paquelin's  cautery  is  the  best  treat- 
ment. In  other  cases,  dry  with  lint  and  rub  nitric  acid  or  pure  carbolic 
with  sticks  into  the  edges  of  the  slough  after  cutting  away  the  sloughs  and 
sequestra.  During  the  process  protect  the  sound  skin,  applying  nitric 
acid  several  times  and  drying  after  each  application,  and  finally  dust  with 
iodoform  or  some  such  antiseptic,  and  smear  the  surface  well  with  carbolic 
oil.  Milder  measures  of  treatment  are  painting  with  tincture  of  iodine  or 
10  per  cent,  silver  nitrate  solution,  and  douching  frequently  with  2  per  cent, 
hydrogen  peroxide. 

Uvula.  —  The  uvula  may  be  bifid,  unduly  small  or  hypertrophied. 
If  very  large,  it  is  liable  to  cause  troublesome  spasmodic  cough,  gagging, 
and  even  attacks  of  dyspnoea.  A  portion  may  be  cut  off.  It  is  frequently 
swollen  and  cedematous  in  inflammatory  affections  of  the  mouth  and 
throat,  and  rarely  as  a  limited  disease.  Diphtheritic  patches  may  be 
seen  on  the  surface,  but  membrane  in  this  situation  is  not  necessarily 
diphtheritic.  Superficial  ulceration  is  not  uncommon.  A  rare  case  of 
calculus  has  been  reported  in  a  baby  of  2  months  old  (Goodall,  1898)  in  the 
form  of  a  white  globular  mass  on  the  anterior  surface  ;  it  produced  dyspnoea 
from  nasal  obstruction  on  lying  down.  In  structure  it  was  probably  a 
degenerated  mucous  gland.  A  few  similar  cases  of  calculus  of  the  soft 
palate  have  been  recorded  in  adults. 

The  Teeth  and  Dentition. — In  rare  instances  the  child  is  born  with  one 
or  more  teeth  already  cut,  a  condition  called  Bentitio  prcecox.  It  may  be 
a  family  peculiarity.  The  teeth  cut  are  generally  the  lower  central  incisors, 
occasionally  the  upper  ones,  and  rarely  the  molars.  As  many  as  nine 
were  present  in  one  case.  They  are  usually  loose,  fall  out  or  are  pulled  out, 
and  are  not  replaced  until  the  second  dentition.  Sometimes  they  are 
supernumerary  teeth  and  replaced  by  milk  teeth ;  occasionally  they 
remain  fixed.  They  are  generally  small,  ill-developed,  with  thin  and 
imperfect  enamel  and  perhaps  no  fang.  Premature  dentition  is  due  to  the 
premature  occurrence  of  the  process  leading  to  teething  ;  to  excessive 
development  of  the  teeth  or  an  atrophic  condition  of  the  gums  ;  possibly 
to  inflammation  in  the  dental  follicles  or  intra-uterine  stomatitis  ;  and 
may  be  associated  with  other  malformations  and  anomalies,  such  as  cleft 
palate.  They  are  not  an  indication  of  intelligence,  although  they  have 
been  recorded  in  the  past  in  Julius  Csesar,  Kichard  III,  Louis  XIV,  Mirabeau 
and  Mazarin.  If  they  are  loose  or  giving  rise  to  trouble,  they  must  be 
removed.  They  may  interfere  with  suckling,  injure  the  nipples,  or  cause 
ulceration  of  the  under  surface  of  the  tongue. 

Milk  Teeth. — The  20  temporary  milk  teeth  are  cut  in  the  following 
order  : — lower  central  incisors  at  5-9  months  ;  upper  central  and  lateral 
incisors,  at  8-10  months;  upper  molars,  lower  lateral  incisors  and  lower 
molars  at  12-14  months  ;  canines  at  16-22  months  ;  and  the  second  molars 
at  20-30  months.    Or  a  more  simple  table  may  be  given  as  follows  : — 


The  Mouth    and  Jaws. 


223 


Average. 

Date  of  Eruption  of  Milk  Teetli. 

Range. 

6  months 

Lower  Central  Incisors 

6-  9  months. 

9        „ 

Upper  Central  Incisors,   and 

Upper  Lateral  Incisors  . . 

8-12 

12         „ 

Upper         Molars,        Lower 
Lateral     Incisors        and 

Lower  Molars 

12-15        „ 

18         „ 

Canines 

15-24        „ 

24         „ 

Second  Molars 

20-36 

The  first  tooth  is  a  lower  median  incisor  in  85  per  cent.,  and  an  upper 
median  incisor  in  15  per  cent.  Spanton  (1907)  gives  the  average  date  of 
eruption  of  the  first  tooth  as  237  days  ;  males  252,  and  females  221.  The 
milk  teeth  drop  out  in  the  same  order  by  absorption  of  the  roots.  Teething 
is  due  to  absorption  or  atrophy  of  the  superjacent  gums,  and  is  not  helped 
by  lancing.  Sometimes  teeth  are  cut  unduly  early  for  no  apparent  reason 
or  from  congenital  syphilis.  In  the  mouth  at  birth  there  are  also  24 
permanent  teeth  ;  28  at  3  months,  and  32  at  3  years.  Breast-fed  children 
generally  cut  their  teeth  earlier  than  the  bottle-fed,  probably  because  the 
salts  in  human  milk  are  more  readily  assimilated  than  those  in  the  cooked 
milk  of  other  animals.  This  is  not  invariably  the  case,  for  bottle-fed  infants 
may  begin  teething  in  the  fourth  month  of  life.  Delayed  and  irregular 
dentition  are  due  to  cretinism,  rickets,  and  maldevelopment  from  numerous 
causes  (  Dentitio  tarda). 

Abnormalities  include  complete  absence  of  teeth  throughout  life,  an 
excessive  or  deficient  number,  displacement,  malformation,  irregular 
eruption  and  imperfect  development.  Supernumerary  teeth  are  usually 
small,  distinct,  and  in  the  upper  jaw.  In  prognathism  the  lower  teeth 
project  in  front  of  the  upper.  Thumb  sucking  forces  the  upper  teeth  out- 
wards and  the  lower  teeth  inwards.  Lip  sucking  forces  the  teeth  inwards. 
Structural  defects  in  the  milk  teeth  are  due  to  causes  acting  in  utero. 
J.  G.  Turner  (1907)  has  drawn  attention  to  malformation  of  enamel  trans- 
mitted through  five  generations  bv  those  affected,  but  not  by  the  unaffected. 
The  teeth  were  stunted  and  the  enamel  absent  or  defective.  It  especially 
involved  the  earlier  teeth,  and  the  third  molars  were  normal.  Hypoplasia, 
•or  imperfect  development  due  to  malnutrition,  affects  both  sets  of  teeth, 
but  especially  the  permanent  ones.  Of  the  milk  set  the  canines  and  molars 
are  most  damaged,  implying  an  early  post-natal  cause.  Of  the  permanent 
set  the  central  incisors,  the  parts  developed  during  the  first  two  years 
of  life,  are  most  imperfect.  If  the  defects  are  limited,  the  cause  may  be  a 
local  one.  Hutchinson's  teeth  are  defective  permanent  ones.  The  upper 
central  incisors  are  dwarfed,  laterally  and  vertically,  and  along  the  biting 
•edge  are  crescentically  notched.     The  lateral  incisors  are  peg-like,  and  the 


224  Chapter   XX. 

first  molars  "  dome-topped."     He  ascribed  the  malformation  to  syphilis  ; 
Henoch,  to  rickets. 

Dental  Caries. — The  predisposing  causes  include  heredity,  giving 
rise  to  irregularity  in  shape  and  size,  crowding,  pits  and  fissures,  and 
imperfect  chemical  structure  ;  severe  or  long  illness,  exanthemata,  chronic 
tuberculosis  and  toxic  conditions  in  early  life,  causing  flaws  in  the  enamel. 
The  portion  of  tooth  formed  at  this  time  is  discoloured,  pitted  and  grooved  ; 
and  there  is  abrupt  transition  to  normal  along  a  horizontal  line.  Diet  may 
influence  the  growth  of  the  tooth  before  the  age  of  six  years,  for  calcification 
begins  about  the  end  of  the  first  year.  Therefore  deficiency  of  lime  in  the 
food  is  a  factor.  Diet  also  affects  the  external  surfaces,  e.g.,  acids  and  a 
lack  of  hard  substances  which  clean  the  teeth.  Early  decay  of  the  milk 
teeth  is  due  to  acid  fermentation  of  food  in  the  mouth,  destroying  the 
enamel  and  permitting  penetration  of  the  dentinal  tubules  by  microbes, 
that  is,  it  progresses  from  without  inwards.  Circular  caries  at  the  base  is 
not  uncommon  and  may  lead  to  the  tooth  being  broken  off.  It  is  not 
eventually  basal  if  the  tooth  is  only  partly  cut.  The  upper  incisors  and 
molars  are  most  liable.  According  to  Miller's  Theory  of  Decay  the  first 
stage  is  decalcification  or  softening  of  the  inorganic  enamel,  and  secondarily 
dissolution  of  the  softened  residue.  The  decalcifying  agent  is  lactic  acid 
due  to  the  fermentation  of  particles  of  carbohydrate  lodged  between  the 
teeth.  It,  therefore,  depends  on  the  regularity  of  the  teeth  and  the  nature 
of  the  food,  neglect  of  cleanliness,  and  lack  of  cellulose  which  in  mastication 
acts  as  a  cleanser.  There  is  always  solution  of  continuity  of  the  enamel 
before  the  organic  material  of  the  dentine  is  attacked.  Thus,  caries  is 
essentially  microbic  in  origin.  Starchy  foods  are  particularly  apt  to  stick 
in  crevices,  whereas  sugars  are  soluble  and  quickly  washed  away. 

Disorders  of  Dentition. — Although  dentition  is  a  physiological  process 
and  normally  gives  rise  to  no  trouble  or  inconvenience,  like  most  vital 
processes  it  may  be  disturbed.  Its  influence  has  been  enormously  exagger- 
ated and  many  ailments,  general,  local  and  reflex,  have  been  ascribed  to  it, 
although  they  are  merely  coincident.  Rickets  is  the  true  cause  in  many 
instances,  by  virtue  of  its  nervous  instability  and  liability  to  catarrh. 
The  gums  may  be  hot,  tender  and  swollen,  and  the  child  feverish,  e.g., 
T.  105°  F.  It  is  probable  that  dentition  does  not  cause  fever,  unless  there 
is  oral  sepsis  or  pain  induced  by  inflamed  gums.  Traumatism,  due  to  biting 
teething  rings,  is  a  great  cause  of  gum  injury  and  gingivitis,  in  which  the 
gums  are  dry,  hot  and  covered  with  sticky  mucus.  Salivation  is  suppressed  ; 
stomatitis  and  adenitis  may  ensue.  On  account  of  the  itching  and  pain 
in  the  gums  the  child  is  irritable,  restless,  refuses  food,  keeps  putting  its 
fingers  in  its  mouth,  wakes  and  screams  with  pain  or  anger,  pulls  and  rubs 
the  ears  or  back  of  the  head,  and  is  generally  out  of  sorts.  The  tem- 
perature is  very  irregular  and  often  raised  for  several  days,  only  a  few  hours 
at  a  time.     While  feverish  the  child  is  liable  to  catarrh  of  the  respiratory 


The  Mouth    and   Jaws.  225 

passages  and  alimentary  tract.  Many  children  are  said  to  "  cut  their 
teeth  with  bronchitis  "  or  "  with  diarrhoea."  Among  the  poor  diarrhoea 
is  almost  synonymous  with  teething  and  is  rashly  neglected  in  consequence. 
The  digestive  disturbance  is  commonly  due  to  the  continuance  of  a  diet  as 
liberal  as  during  the  pre-febrile  stage.  Nervous  irritability  is  frequent 
in  the  rachitic  and  the  neurotic.  Nervous  symptoms,  such  as  laryngospasm, 
spasmodic  cough,  muscular  twitchings,  tetany  and  convulsions,  are  often 
ascribed  to  teething.  Fits  are  far  more  common  before  than  during  the 
teething  age.  They  are,  in  my  experience,  most  liable  to  coincide  with  the 
eruption  of  the  canines,  the  age  when  the  influence  of  rickets  is  often  well 
marked.  Otitis  media  and  earache  may  be  due  to  extension  of  inflammation, 
or  more  probably  to  adenoids  than  produced  by  teething.  In  all  cases  of 
disease  during  dentition  the  true  cause  of  the  illness  may  be  overlooked. 
I  have  known  acute  cerebrospinal  and  post-basal  meningitis,  pneumonia, 
the  onset  of  specific  fevers,  and  many  other  serious  and  mild  ailments 
wrongly  put  down  to  teething.  Almost  every  variety  of  rash,  especially 
those  due  to  intestinal  toxsemia,  has  been  called  a  "  gum  rash  "  or  "  teething 
rash.'"  We  may  sum  up  the  effects  of  dentition  as  follows.  It  is  painful  if 
the  gums  are  unhealthy.  Fever  is  due  to  local  inflammation  or  other  causes. 
Secondary  catarrh  of  the  mouth  may  extend  to  the  ears,  lungs  and  alimen- 
tary tract.  Bronchial  catarrh  may  arise  in  this  way  or  is  secondary  to 
catching  cold  while  feverish.  Diarrhoea  and  vomiting  may  result  from 
inability  to  digest  food  in  consequence  of  the  fever.  Irritability,  fretfulness, 
restlessness  and  insomnia  arise  from  local  irritation,  gingivitis,  stomatitis, 
and  gastro-intestinal  disturbance.  Convulsions  are  indirectly  produced  by 
teething,  in  consequence  of  imperfect  digestion  of  food,  colic,  and  the 
absorption  of  toxins  from  the  intestines  during  fever.  Thus,  the  disorders 
are  due  to  local  conditions,  fever,  and  secondary  reflex  irritation  acting  on 
an  unstable  nervous  system.  Retraction  of  the  head  is  sometimes  due  to 
the  eruption  of  molar  teeth.  Reflex  symptoms  are  most  likely  to  occur 
in  nervous  children.  In  a  boy,  aged  7,  local  pain  in  the  cheek  was  definitely 
due  to  caries  of  the  lower  molar.  Facial  eczema  is  sometimes  worse  during 
the  eruption  of  a  tooth. 

Permanent  Teeth. — The  first  molars  are  cut  at  6,  central  incisors  at  7, 
lateral  incisors  at  8,  and  the  bicuspids  at  10  and  11  years  of  age.  The 
canines  appear  between  12  and  13,  the  secondary  molars  between  12  and  15, 
and  the  third  molars  or  wisdom  teeth  after  the  age  of  17  years.  Sometimes 
wisdom  teeth  are  never  cut.  The  disorders  of  dentition  at  this  period  are 
those  of  local  discomfort  and  inflammation.  Ulcerative  stomatitis  and 
other  mouth  affections  may  be  set  up  by  irritation  of  the  fangs  of  partially 
extruded  milk  teeth.  Such  symptoms  as  fever,  restlessness,  insomnia, 
salivation,  reflex  cough,  earache  and  fits  depend  upon  local  secondary 
inflammation  or  are  of  intestinal  origin,  set  up  by  bolting  food  on  account 
of    pain    involved  in  mastication.     Nervous  symptoms   already  present 

Q 


226  Chapter   XX. 

may  be  exaggerated.  Fits  may  occur  in  the  predisposed.  Adenitis  is  not 
uncommon,  but  cancrum  oris  and  necrosis  of  the  jaw  are  rare  complications. 
Caries  is  dependent  upon  local  causes  and  constitutional  debility.  The 
early  appearance  of  the  first  molars  leads  to  them  being  mistaken  for 
temporary  teeth,  and  to  caries  being  neglected.  They  begin  to  calcify  in 
the  twenty-fifth  week  of  foetal  life.  They  should  be  carefully  watched,  and 
may  require  removal,  if  the  mouth  is  small,  for  crowding  of  the  teeth  is  a 
great  cause  of  decay. 

The  Teeth  and  Nutrition. — Good  health  and  digestion  depend  on  good 
mastication  and  for  this  good  teeth  are  necessary.  Up  to  the  age  of  10 
years  mastication  depends  on  the  temporary  teeth,  reinforced  at  6  years 
by  the  first  molars.  During  this  period  of  life  growth  is  very  active,  and 
it  is  important  that  the  milk  teeth  should  be  maintained  in  as  perfect  a 
state  as  possible  and  not  allowed  to  decay.  Caries  of  the  teeth  causes, 
imperfect  mastication  and  bolting  or  refusal  of  food  on  account  of  pain. 
It  may  set  up  periostitis,  alveolar  abscess,  necrosis  of  the  alveolus,  antral 
suppuration,  oral  sepsis,  ulcerative  stomatitis,  cervical  adenitis  and 
susceptibility  to  tuberculous  infection.  Constitutional  effects  arise  from  the 
absorption  of  toxins  from  the  mouth,  or  the  swallowing  of  decomposing  and 
septic  material  from  decaying  dentine  and  food  retained  in  the  cavities  of 
the  teeth.  Thus  are  produced  ansemia,  stomach  troubles  and  mal- 
nutrition, possibly  headache  and  fits.  The  malnutrition  and  reflex  irrita- 
tion predispose  to  pavor,  habit  spasm,  tremor  and  chorea.  Caries  is  pro- 
gressive and  spreads  from  one  tooth  to  another,  and  even  from  a  milk 
tooth  to  a  permanent  one.  An  alveolar  abscess  round  a  temporary  molar 
may  loosen  a  permanent  one  by  destroying  the  developing  roots. 

Serious  illness  and  disorders  of  nutrition  during  the  first  two  years 
of  life  affect  the  incisors,  canines  and  first  molars,  in  which  calcification  is 
proceeding.  Calcification  begins  in  the  other  teeth  in  the  third  year  of  life, 
and  may  be  affected  by  illness  then  or  subsequently,  up  to  the  time  it  is 
completed.  Fevers,  especially  measles,  do  much  harm.  The  enamel  is 
thinned,  pitted,  grooved  or  honey-combed.  Often  a  discoloured  transverse 
furrow  separates  the  affected  from  the  healthy  part  of  the  tooth.  Early 
caries  is  a  common  sequel.  Rickets  affects  the  permanent  teeth  by  mal- 
nutrition of  the  dental  germs,  often  due  to  local  mouth  affections  ;  and 
crowding,  from  imperfect  growth  of  the  jaw.  It  is  doubtful  whether 
mercury,  given  in  infancy,  affects  the  permanent  teeth,  though  it  is  said 
to  damage  the  enamel  of  the  first  molars,  incisors  and  canines.  More 
probably  the  dental  defect  is  due  to  malnutrition  or  local  affections  of  the 
mouth. 

Management  of  Dentition. — Teething  rings  do  more  harm  than  good. 
Keep  the  mouth  clean  and  allow  no  dirty  articles  to  be  put  in.  Use  a 
badger-hair  gum  brush  twice  a  day.  If  there  is  diarrhoea,  give  castor  oil, 
tincture  of  rhubarb  and  salol,  with  glycerine,  tragacanth,  and  peppermint 


The  Mouth    and  Jaws.  227 

water  three  or  four  times  a  day.  Bromides  and  tincture  of  opium  can  be 
added  if  necessary.  An  initial  dose  of  Dover's  powder,  gr.  |-1,  and  grey 
powder  grs.  1-2,  will  cut  short  the  attack.  For  nervous  irritability  and 
restlessness,  especially  if  there  is  the  least  indication  of  muscular  twitching, 
give  bromide  grs.  3-5,  orphenazone  grs.  1-2,  three  times  a  day.  Opiates  and 
teething  powders  are  unsuitable,  especially  the  latter,  because  of  the  uncer- 
tainty of  their  composition  ;  they  usually  contain  calomel  and  occasionally 
morphia.  Brush  tender  gums  with  chlorate  of  potash  grs.  10,  glyc.  boracis 
to  1  oz.  If  they  are  ulcerated  add  resorcin  grs.  10-20.  Local  sedatives  of 
laudanum,  cocaine,  etc.,  are  better  avoided.  The  use  of  the  lancet  is 
unnecessary,  for  there  is  no  tension  of  the  overlying  gum,  and  there  is  no 
evidence  that  lancing  assists  eruption.  The  subsequent  scar,  if  directly  over 
the  gum,  might  make  teething  more  difficult.  Local  bleeding  by  scarification 
affords  local  relief  and  reduces  the  tendency  to  convulsions. 

Care,  of  the  Teeth.. — Clean  teeth  do  not  decay.  The  greatest  care 
possible  should  be  taken  of  them  from  the  time  of  eruption.  They  should 
be  cleaned  twice  a  day,  with  a  soft  rag  at  first,  and  later  on  a  soft  tooth- 
brush and  a  mild  dentrifice,  such  as  prepared  chalk  or  soap  and  warm 
water  ;  a  few  crystals  of  permanganate  of  potash  and  a  few  drops  of 
tincture  of  myrrh  in  a  tumbler  of  water  ;  or  thymol  grs.  2,  ac.  benzoic, 
grs.  45,  tine,  eucalypt.  \  oz.,  ol.  gaulther.  m.  20,  sp.  vin.  rect.  ad.  1  oz.,  using 
a  few  drops  in  water.  Milk  teeth  should  be  periodically  inspected  and 
the  cavities  filled  up.  In  the  early  stages  of  caries  it  is  not  a  painful  process. 
By  this  means  the  teeth  are  preserved  as  long  as  possible  and  the  second 
dentition  will  be  more  satisfactory.  Useless  decayed  teeth  must  be 
removed,  though  the  extraction  of  temporary  molars  may  cause  irregu- 
larity of  the  permanent  teeth.  Still  greater  care  should  be  taken  of  the 
permanent  set.  Cracking  nuts,  biting  thread,  etc.,  are  liable  to  injure  the 
enamel.    The  teeth  should  be  brushed  after  each  meal. 

Toothache  or  Odontalgia. — An  examination  by  the  British  Dental 
Association  showed  that  there  were  37,000  decayed  teeth  in  10,500  children 
of  an  average  age  of  12  years  in  Poor  Law  Schools  ;  86  per  cent,  had  caries. 
In  560  Public  School  boys  of  the  same  age  3.521  carious  teeth  were  present, 
and  87  per  cent,  had  caries.  The  only  sign  may  be  neuralgia.  Frequently, 
the  local  disease  is  indicated  by  irritation  of  the  pulp  without  exposure, 
and  the  tooth  is  very  sensitive  to  heat  or  cold.  If  the  pulp  is  exposed, 
heat  or  cold  gives  rise  to  more  violent  pain,  often  widely  distributed,  referred, 
and  neuralgic.  Other  local  effects  are  suppuration  of  the  pulp  under  a 
stopping,  periostitis,  alveolar  abscess  or  fistula,  and  necrosis  of  the  root. 
Ansemia  and  submaxillary  adenitis  are  common. 

The  pain  is  relieved  by  a  hot  solution  of  bicarbonate  of  soda  ;  tannic  ac. 
1,  sp.  vin.  rect.  5  parts,  painted  on  the  gums  and  round  the  teeth  ;  a  plug 
of  cotton  wool  dipped  in  oil  of  cloves,  camphor,  creosote,  laudanum,  or 
chloroform  ;    and  Gregory  powder  or  phenacetin  internally. 


228  Chapter   XX. 

The  Salivary  Glands. — The  salivary  glands  are  rarely  affected  in  the 
newborn.  From  pyogenic  infection  both  the  submaxillary  and  the  sub- 
lingual glands  may  become  acutely  inflamed  and  suppurate,  discharging 
pus  through  the  ducts  or  forming  abscesses  (Sialo-  Adenitis).  Congenital 
and  progressive  Hypertrophy  of  the  sublingual  glands  has  been  reported. 
It  gave  rise  to  difficulty  in  nursing  and  a  bilateral  tumour  at  the  base 
of  the  tongue,  which  was  at  first  thought  to  be  a  double  ranula.  The 
tongue  became  enlarged,  dysphagia  increased,  and  the  child  wasted.  On 
operation  it  was  found  to  be  due  to  congenital  hypertrophy  or  chronic 
inflammation.  A  Ranula  is  a  congenital  or  acquired  retention  cyst  of  this 
gland,  usually  bilateral.  It  forms  a  reddish,  shining  swelling  under  the 
tongue.  Congenital  cysts  may  arise  in  other  glands,  due  to  atresia  of  the 
ducts.  Two  cases  of  bilateral  Swelling  of  the  Parotid  in  the  newborn  have 
been  reported.  The  swellings  were  soft,  elastic,  painless,  and  the  duct 
apparently  free ;  saliva  was  present.  They  gradually  subsided  in 
4  weeks.  Similar  swelling  might  be  due  to  occlusion  of  Steno's  duct. 
Angeioma,  adenoma,  sarcoma  and  tuberculosis  are  very  rare.  Acute 
Parotitis  is  due  to  iodism  or  mumps  (q.v.). 

Secondary  Parotitis  is  due  to  infection  from  the  mouth,  via  the  duct, 
and  occasionally  from  the  middle  ear,  via  the  Glaserian  fissure.  Pre- 
disposing factors  are  lack  of  care  in  cleaning  the  mouth  in  infants  after  food 
and  vomiting,  damage  done  to  the  mucous  membrane  in  this  process,  and 
mouth  breathing.  The  common  causes  are  enteric  fever,  scarlet  fever, 
pneumonia,  peritonitis,  stomatitis,  malnutrition,  and  operation  or  diseases 
in  which  feeding  by  mouth  is  temporarily  stopped.  It  is  non-contagious, 
usually  unilateral,  and  is  liable  to  suppurate,  except  in  the  mild  form 
often  seen  in  marasmic  infants.  In  marasmus  the  swelling  may  be  the 
only  indication.  More  often  it  is  ushered  in  by  local  pain  and  tenderness, 
and  pain  on  movement  of  the  jaw.  The  glands  are  swollen,  firm  and 
tender,  chiefly  in  front  of  the  ear.  Swelling  spreads  to  the  overlying  tissues, 
and  the  cheeks  become  brawny,  the  eyelids  puffy  and  the  lids  swollen. 
It  gives  rise  to  general  malaise,  dryness  of  the  mouth,  anorexia,  thirst, 
fever,  headache  and  depression  ;  sometimes  giddiness  and  tinnitus.  In 
4  or  5  days  the  inflammation  reaches  its  maximum.  It  then  subsides 
gradually  in  about  another  fortnight  or  suppurates.  Pus  may  be  deep- 
seated  and  cause  no  superficial  signs,  or  give  rise  to  increasing  brawniness, 
oedema,  redness  and  heat  of  the  skin,  and  a  softened  area  about  the  centre 
of  the  gland.  The  patient  is  more  ill,  with  irregular  fever,  perhaps  chilliness, 
and  shooting  pains.  As  the  abscess  increases  in  size,  it  burrows  into  the 
surrounding  tissues,  discharges  through  the  parotid  duct  or  bursts  into  the 
mouth,  external  auditory  meatus  or  through  the  cheek.  The  resulting 
fistula  heals  with  difficulty.  If  an  early  incision  is  made,  the  pus  is  dis- 
charged and  the  wound  heals  in  a  few  days.  Death  may  result  from 
septicaemia  or  from  the  primary  disease.     Necrosis  of  the  jaw,  destruction 


The  Mouth    and  Jaws.  229 

of  the  temporo-maxillary  articulation,  and  haemorrhage  or  thrombosis  of 
the  facial  artery  or  the  internal  jugular  vein  are  complications.  Facial 
palsy  is  the  most  common  sequel. 

Preventive  treatment  consists  in  oral  antisepsis,  sucking  a  rubber  teat, 
and  sialagogues.  At  the  onset  give  a  purge,  and  use  dilute  Condy  as  a 
mouth-wash.  Apply  cold  compresses  or  paint  with  glyc.  belladonnae. 
If  there  is  a  suspicion  of  pus,  surgical  measures  are  necessary.  An  incision 
should  be  made  on  the  fourth  to  sixth  day,  if  the  swelling  increases  and 
becomes  cedematous  or  if  the  temperature  is  high  and  intermittent.  Do  not 
wait  for  fluctuation.    Incise  the  parotid  fascia  freely. 

Salivation  is  due  to  local  causes  and  in  rare  instances  is  idiopathic, 
even  as  early  as  the  third  year.  It  is  produced  by  inflammatory  infections 
in  or  about  the  mouth  and  its  glandular  appendages  ;  by  reflex  causes,  such 
as  nausea,  vomiting,  gastralgia,  gastro-intestinal  derangements ;  hysteria, 
epilepsy,  hydrophobia  and  mania,  some  of  which  may  act  on  the  central 
nervous  system  ;  and  drugs,  such  as  jaborandi,  pilocarpin,  mercury,  lead 
and  antimony.  Idiopathic  salivation  may  set  in  early  during  dentition, 
perhaps  suddenly,  and  continue  indefinitely.  It  resembles  a  neurosis  in  its 
intermittent  character  and  its  tendency  to  be  affected  by  psychic 
influences  and  diminished  by  emotion.  Sometimes  it  only  occurs  during  the 
erect  posture  and  diminishes  or  ceases  during  sleep.  In  other  cases  there 
is  a  continual  dribbling,  night  and  day,  and  the  clothes  become  saturated. 
It  is  either  due  to  increased  secretion  or  to  failure  to  acquire  the  habit 
of  automatically  swallowing  the  saliva.  In  Jordan's  cases  (1897)  both 
children  bad  fed  largely  on  porridge.  The  duration  is  a  matter  of  uncer- 
tainty. It  tends  to  abate  with  the  development  of  the  body  and  to  yield 
to  drugs.  Iron  is  beneficial,  though  the  affection  is  not  due  to  the  anaemia 
which  may  be  present. 


Chapter  XXI 

THE    THROAT,    PHARNYX,    AND    (ESOPHAGUS. 

Tonsillar  Affections — Pharyngitis —  Adenoids — Retro-pharyngeal  and  Retro- 
esophageal Abscess — The  (Esophagus. 

Lymphoid  or  adenoid  tissue  surrounds  the  posterior  nares  and  fauces 
forming  Waldeyer's  Lymphatic  Ring.  It  is  aggregated  into  masses,  viz., 
(1)  The  Faucial  Tonsils  ;  (2)  The  Lingual  Tonsils,  two  small  masses  at  the 
base  of  the  tongue  between  the  V  of  the  calciform  papillae  and  the  glosso- 
epiglottidean  fossae,  tending  to  disappear  at  puberty ;  (3)  Luschka's 
or  the  Pharyngeal  Tonsil  ;  (4)  scattered  patches,  on  the  lateral  the  posterior 
walls  of  the  pharynx,  which  give  rise  to  chronic  follicular  or  granular 
pharyngitis.  The  lymphoid  tissue  in  the  membranous  part  of  the  Eus- 
tachian tube  is  called  the  tonsil  of  Gerlach. 

The  lymph  vessels  from  the  tonsils  run  to  the  submaxillary  glands, 
especially  those  at  the  angles  of  the  jaw,  and  thence  to  the  cervical  glands. 
Those  from  the  naso-pharynx  run  to  the  lateral  pharyngeal  glands  in  the 
bucco-pharyngeal  fascia  behind  the  tonsils,  or  into  the  small  retro-pharyn- 
geal glands,  and  thence  to  the  deep  cervical  glands.  Swelling  of  the  deep 
cervical  glands  alone  is  a  sign  of  naso-pharyngeal,  not  of  tonsillar  disease. 

The  Tonsils. —  Etiology  of  Throat  Affections. — Hereditary  predisposi- 
tion is  often  present.  The  rheumatic  diathesis  is  a  predisposing  cause  and 
an  attempt  has  been  made  to  differentiate  a  specific  rheumatic  sore  throat. 
Children  are  very  liable  to  catarrhal  affections  from  lowered  vitality,  cold 
winds,  chills  and  dusty  streets,  especially  the  irritating  dust  from  wood 
pavements  in  hot  weather.  Many  cases  are  due  to  various  infective  organ- 
isms, and  may  occur  in  specific  fevers.  The  decomposition  of  retained 
secretions  in  pitted  tonsils  is  a  constant  source  of  infection. 

Simple  Tonsillitis  is  a  catarrhal  inflammation.  In  its  mildest  form 
it  is  spoken  of  as  a  "  relaxed  sore  throat."  The  onset  of  a  severe  attack  is 
like  that  of  an  infectious  disease.  The  tongue  is  furred,  breath  offensive, 
vomiting  and  diarrhoea  common.  In  infants  there  may  be  convulsions. 
The  voice  is  thick,  mouth  open,  and  breathing  difficult.  Pain  varies  with  the 
severity,  so  too  the  constitutional  disturbance  and  fever  which  is  rarely 
above  104°  F.  Older  children  may  complain  of  dysphagia.  A  deep  red 
and  somewhat  glistening  erythema  of  the  tonsils  is  visible,  and  it  often 


The   Throat,   Pharynx,  and  (Esophagus.  231 

spreads  to  the  palate,  fauces  and  pharynx.  The  submaxillary  lymph 
nodes  are  enlarged  and  painful.    Kecovery  is  rapid. 

Follicular  or  Lacunar  Tonsillitis  is  common  in  children,  especially 
those  with  enlarged  tonsils,  and  infrequent  in  infants.  It  is  primarily  a 
microbial  inflammation  of  the  crypts  or  follicles,  and  the  glandular  tissues 
are  involved  secondarily.  The  follicular  variety  is  supposed  to  be  a  primary 
inflammation  of  the  lymph  follicles,  and  the  lacunar  variety  is  a  more 
severe  form,  either  general  or  limited  to  the  crypts.  The  distinction  is 
unnecessary,  for  it  is  doubtful  that  the  lymph  follicles  are  ever  primarily 
involved.  The  use  of  the  word  "  follicle  "  for  "  crypt,"  as  well  as  for  a 
collection  of  lymph  cells,  is  confusing. 

The  onset  is  acute  and  may  suggest  possibilities  of  a  specific  fever  or 
pneumonia.  Sometimes  the  child  seems  little  ill  and  has  no  local  dis- 
comfort. More  often  there  are  found  general  malaise,  headache,  muscular 
pains  and  a  temperature  of  101-105°  F.  Anorexia,  furred  tongue,  nausea, 
vomiting,  dysphagia  and  constipation  may  all  be  present.  Except  at  the 
onset  the  affection  is  almost  invariably  bilateral,  and  often  associated  with 
catarrh  of  the  fauces  and  pharynx.  The  tonsils  are  enlarged,  bright  red, 
and  covered  with  dots  of  whitish  or  yellowish- white  secretion,  projecting 
through  the  mouths  of  the  ducts  and  composed  of  cheesy  material,  in- 
spissated secretion,  mucus  or  muco-pus,  epithelial  cells,  debris  of  food,  and 
micro-organisms.  The  secretion  can  be  pressed  out  of  the  crypts  or  easily 
wiped  away  from  the  surface  with  a  swab,  leaving  no  ulcer  and  no  bleeding 
surface.  It  may  be  aggregated  by  coalescence  into  a  coherent  membrane 
with  no  definite  edge.  The  patches  quickly  re-appear  after  removal. 
The  submaxillary  lymph  nodes  are  generally  enlarged  and  tender.  Even 
severe  symptoms  subside  in  24  hours.  Fever  and  malaise  rarely  last  more 
than  2  or  3  days  and  the  exudation  disappears  in  another  clay  or  two,  the 
swelling  of  the  tonsil  subsiding  rather  more  slowly.  Occasionally  chronic 
follicular  tonsillitis  is  present  without  any  symptoms.  The  tonsils  are 
more  or  less  enlarged  and  the  crypts  invariably  blocked  with  secretion. 

The  younger  the  child  the  more  likely  are  the  throat  symptoms  to  be 
inconspicuous  or  absent,  and  the  affection  to  be  overlooked.  Pain  is  often 
absent.  Older  children  may  complain  of  soreness,  pain  on  swallowing  and 
pain  about  the  angle  of  the  jaw.  It  is  not  always  possible  to  exclude  scarlet 
fever  until  sufficient  time  has  elapsed  to  permit  the  appearance  of  a  rash. 
A  blotchy  erythema  is  not  uncommon,  but  differs  in  characters  and  dis- 
tribution from  the  scarlatinal  rash.  The  appearances  of  the  fauces  are 
sometimes  suggestive  of  diphtheria.  Cases  may  be  wrongly  diagnosed 
because  the  throat  is  not  examined. 

Septic  or  Ulcerative  Tonsillitis  differs  from  the  previous  variety  in 
being  more  virulent  and  not  limited  to  the  tonsil.  It  is  usually  unilateral 
at  the  onset  and  often  extends  to  the  soft  palate  and  uvula,  but  rarely 
beyond.     The  tonsil  is  deep  red  or  almost  purple  in  colour.     Patches  of 


232  Chapter   XXI. 

whitish,  dirty  yellow,  or  greyish  mucoid  secretion  are  visible,  and  on  their 
removal  superficial  bleeding  ulcers  are  exposed.  The  onset  is  sudden,  but 
without  vomiting.  The  degree  of  fever  and  pulse  rate  are  variable. 
Erythematous  rashes  are  not  uncommon.  The  tongue  is  foul,  the  local 
pain  of  definite  severity,  and  the  ordinary  symptoms  of  a  severe  throat 
affection  are  present.  The  throat  resembles  the  condition  seen  in  scarlatina. 
More  or  less  adenitis  is  present ;  temporary  and  slight,  or  severe  and  pro- 
longed and  ending  in  abscess.  The  course  of  the  illness  is  slow  and  there 
is  much  disturbance  in  health.    It  may  end  in  quinsy. 

The  Erysipelatous  Inflammation  of  the  fauces  sometimes  seen  in  adults 
has  never  come  under  my  notice  in  children.  Local  ulceration  may  start 
in  a  crypt.  If  the  mouth  of  a  cypt  is  blocked,  a  Tonsillar  Cyst  is  formed  and 
projects  above  the  surface  as  a  yellowish-white  globular  swelling  of  the  size 
of  a  pea.  It  leaves  a  superficial  ulcer  on  bursting.  Tuberculous  and  syphilitic 
ulcers  are  occasionally  seen. 

Pneumococcal  Angina. — The  pneumococcus  is  found  in  a  type  of  mem- 
branous sore  throat  very  like  that  of  diphtheria  ;  and  also  in  an  acute 
erythematous  type  which  only  differs  from  erysipelatous  inflammation  by 
its  slight  degree  of  oedema.  Both  these  forms  are  rarely  fatal  but  gangrene 
of  the  fauces  has  occurred.  As  the  pneumococcus  is  found  in  normal 
throats  it  cannot  be  accepted  as  the  undoubted  cause.  Friedlander's 
Bacillus  has  been  found  by  Mayer  (1900)  in  acute  and  chronic  membranous 
angina. 

In  streptococcal  cases  the  membrane  is  thinner,  looser,  and  less 
adherent  than  in  diphtheria  or  pneumonia  ;  the  temperature  more  per- 
sistent and  sloughing  more  prominent. 

Vincent's  Angina  is  occasionally  seen  in  children,  after  7  years  of  age, 
with  defective  teeth,  bad  health  and  unhealthy  surroundings.  Vincent 
described  a  mild  type,  in  which  he  found  fusiform  bacilli  with  staphy- 
lococci or  streptococci.  It  is  unilateral,  superficial  and  localised.  The 
onset  is  insidious.  There  may  be  glandular  enlargement,  offensive  breath, 
slight  dysphagia  and  little  fever,  occasionally  up  to  103°  F.  A  white, 
chalky  or  greyish,  soft,  false  membrane  is  found  on  some  part  of  the  tonsil, 
the  base  of  the  uvula  and  edge  of  the  soft  palate.  It  separates  slowly 
by  necrosis  leaving  a  shallow  ulcer  which  heals  in  7-14  days  ;  the  fever  only 
lasts  a  few  days.  In  a  more  severe  ulcero-membranous  type  a  fusiform 
bacillus  and  a  spirillum  or  spirochsete  are  found.  There  is  greater  destruc- 
tion of  tissue,  perhaps  of  the  whole  tonsil  and  uvula,  with  fever  and 
constitutional  symptoms,  such  as  scarlatiniform  rash,  purpura,  rheumatic 
pains,  anorexia  and  constipation  ;  and  occasionally  albuminuria,  myo- 
carditis and  endocarditis.  Some  of  these  are  due  to  secondary  streptococcal 
infection.  The  local  affection  gives  rise  to  foetid  breath,  salivation, 
dysphagia,  otalgia  and  submaxillary  adenitis.  It  is  usually  unilateral, 
but  may  attack  both  tonsils  and  spread  to  the  soft  palate,  tongue,  gums  and 


The   Throat,   Pharynx,  and  (Esophagus.  233 

lips.  It  lasts  from  1-3  weeks.  The  glands  rarely  suppurate.  A  certain 
amount  of  contraction  may  follow  severe  necrosis.  Occasionally  it  is  fatal 
from  broncho-pneumonia  or  toxaemia.  The  mild  cases,  in  which  the  necrosed 
epithelium  looks  like  membrane  and  hides  the  ulceration,  are  liable  to  be 
mistaken  for  diphtheria.  But  the  constitutional  symptoms  are  generally 
slight.     True  diphtheria  may  be  a  complication  or  sequel. 

False  Membrane  on  Tonsillotomy  Wounds  develops  in  24  hours.  It 
is  dirty  grey,  2  mm.  thick,  limited  to  the  surface  of  the  wound,  and  lasts 
for  5  or  6  days.  It  consists  of  leucocytes,  fibrin,  streptococci,  and  perhaps 
staphylococci  and  pseudo-diphtheria  bacilli. 

Quinsy  is  sometimes  an  acute  suppurative  inflammation  of  the  tonsil, 
but  almost  invariably  starts  in  the  areolar  tissue  between  the  tonsil  and  the 
pharyngeal  aponeurosis  and  terminates  in  resolution  or  in  abscess.  Hence, 
it  is  variously  described  as  acute  parenchymatous  or  phlegmonous  tonsillitis, 
or  as  tonsillar,  peritonsillar  or  palatal  abscess.  It  is  comparatively  rare  in 
early  life.  It  may  be  due  to  infection  via  the  tonsil,  or  secondary  to  septic 
or  follicular  tonsillitis  with  which  it  is  often  associated.  It  is  a  unilateral 
affection,  spreading  to  the  soft  palate  and  pillars  of  the  fauces,  and  some- 
times causes  a  plegmonous  inflammation  of  the  pharynx. 

The  onset  is  less  acute  and  the  local  symptoms  more  severe  than  in 
follicular  tonsillitis.  It  is  a  more  local  affection  with  less  fever,  malaise  and 
muscular  pains.  There  may  be  a  little  stiffness,  or  pain  in  the  throat  so 
severe  as  to  render  swallowing  impossible.  The  pain  is  felt  in  the  neck 
and,  being  due  to  inflammation  in  the  deeper  tissues,  it  may  be  severe 
although  there  is  little  to  be  seen  in  the  throat.  It  may  be  difficult  to  open 
the  mouth.  The  inflammation  spreads  to  the  mucosa,  and  the  tonsils, 
fauces,  uvula  and  soft  palate  are  intensely  red  and  swollen,  and  often 
acutely  oedematous.  The  tonsils  may  be  so  large  as  to  meet  in  the  middle 
line,  and  give  evidence  of  follicular  tonsillitis.  In  a  day  or  two  one  tonsil 
and  the  anterior  pillar  of  the  fauces  are  pushed  forward  and  upward  by 
the  swelling,  or  the  swelling  may  appear  on  the  soft  palate  in  front  of 
the  tonsil.  The  unilateral  swelling  bulges  the  palate  forward  and 
depresses  it,  displaces  the  uvula  to  one  side,  and  reduces  the  size  of  the 
faucial  channel.  The  tonsil,  though  enlarged,  may  be  hidden  from  view. 
Cervical  pain  may  cause  torticollis. 

The  swelling  is  more  easily  recognised  by  palpation  than  inspection, 
and  a  soft  spot,  indicating  suppuration,  more  easily  localised.  In  tonsillar 
abscess  the  general  bulging  of  the  palate  is  absent,  and  a  yellow  area 
shows  that  pus  is  nearing  the  surface.  In  peritonsillar  inflammation  the 
swelling  subsides  in  3-5  days,  if  no  pus  is  formed.  Frequently  pus  may  be 
present  in  2-3  days  and  the  abscess  bursts  spontaneously,  through  the 
supratonsillar  fossa,  above  and  external  to  the  tonsil  and  between  the 
faucial  pillars,  or  through  the  soft  palate.  If  it  bursts  during  sleep  the  pus 
may  run  into  the  larynx  and  cause  death. 


234  Chapter   XXL 

Gangrene  may  be  primary  or  secondary  to  diphtheria,  scarlet  fever, 
cancrum  oris  and  ulcerative  affections  of  the  mouth.  A  purple  spot 
appears  and  becomes  darker  in  colour.  An  ulcer  forms  and  necrosis  is 
rapid,  with  terrible  fcetor,  somewhat  faecal  in  odour.  It  does  not  always 
start  in  the  tonsil  or  remain  limited  to  it.    Death  results  from  sepsis. 

General  Diagnosis  of  Throat  Affections. — The  white  specks  of  thrush 
on  the  tonsil  simulate  those  of  follicular  tonsillitis,  but  there  are  other 
patches  on  the  buccal  mucosa,  tongue,  etc.  The  tonsils  are  of  normal 
colour,  the  patches  dead  white  and  asymmetrical,  and  there  is  neither  pain 
nor  adenitis.  In  measles  there  is  a  symmetrical  red  blush,  with  tiny  red 
papules,  chiefly  affecting  the  palate.  Pain  is  slight  or  absent,  and  buccal 
spots  are  often  present.  In  scarlet  fever  there  is  a  symmetrical,  vivid 
red  erythema  of  the  fauces,  uvula  and  tonsils,  sometimes  extending  to  the 
roof  of  the  mouth  and  pharynx.  The  buccal  mucosa  is  unaffected  and 
there  is  no  early  adenitis.  Pain  may  be  considerable  and  a  strawberry 
tongue  present.  Later  on  there  may  be  yellowish-white  or  dirty  white 
deposit,  soft  and  easily  broken  up,  with  ulceration.  In  diphtheria  the 
child  is  peculiarly  placid  in  aspect.  The  tonsil  is  a  little  reddened,  and 
there  is  a  unilateral,  tough,  adherent  deposit  or  membrane  with  definite 
edges,  not  limited  to  the  tonsil,  and  definite  odour.  Early  adenitis,  little 
or  no  pain,  and  laryngitis  are  often  present. 

Treatment  of  Throat  Affections. — The  general  measures  consist  in 
bed  and  a  liberal  diet  of  soft  and  nutritious  food.  An  initial  purge  is 
necessary  in  acute  attacks.  Quinine,  salol  or  salicylates  may  abort 
attacks,  if  given  freely,  but  salicylates  are  of  no  use  in  diphtheria  and 
scarlet  fever.  Phenacetin  and  phenazone  relieve  headache  and  restless- 
ness. Febrifuges  are  useful ;  alcohol,  if  there  is  cardiac  weakness  ;  iron, 
nux  vomica  and  strychnia,  as  tonics.  It  may  be  necessary  to  paint  with 
cocaine  1-5  per  cent.,  to  relieve  pain  and  permit  deglutition.  Local 
measures  include  hot  gargles,  fomentations  and  poultices  ;  ice  to  suck 
and  an  ice-bag  externally  ;  and  rarely  leeches.  Douching,  irrigation  and 
gargling  are  rarely  suitable  for  children.  Such  solutions  as  sanitas  1  per 
cent.,  liq.  calc.  chlorinatse  0-5  per  cent.,  liq.  sod.  chlorinatae,  chlorine 
water  and  very  weak  sulphurous  acid  can  be  used  ;  or  various  combina- 
tions of  the  chloride,  bicarbonate,  biborate,  salicylate  and  sulphate  of 
soda  and  boric  acid  p. a.,  1-3  drs.,  with  2  drs.  of  cherry  laurel  water,  to  the 
pint  of  water  may  be  used.  A  syphon  douche  should  consist  of  a  vulcanite 
end-piece  attached  to  a  long  rubber  tube,  and  be  inserted  between  the 
back  teeth.  The  child  must  be  firmly  wrapped  up  in  a  sheet,  the  arms 
confined,  in  a  sitting  posture  and  head  bent  forward,  with  the  nurse's 
left  arm  round  the  head  and  pressing  it  to  her  side.  Sprays  of  sublamin, 
a  non-toxic  mercurial,  1  in  1,000,  izal  or  cyllin  1  in  1,000,  perchloride  or 
biniodide  of  mercury  1  in  2,000,  glycothymolin  1  in  4,  or  liq.  sod.  chlorinatse 
1  in  8,  can  be  used.    On  the  whole,  if  local  applications  are  necessary,  it  is 


The   Throat,   Pharynx,  and  GEsophagus.  235 

best  to  paint  or  swab  with  pure  glycothymolin,  glycer.  ac.  tannici,  ichthyol 
and  water  p. a.  ;  tr.  benzoin,  co.  and  glyc.  p. a.  ;  liq.  sod.  chlor.  ;  resorcin 
grs.  10  to  1  oz.  ;  or  liq.  hyd.  perchlor.  and  glyc.  p. a.  Formamint  lozenges 
should  be  sucked  frequently.  The  insufflation  of  powders  is  unsatisfactory. 
In  young  children  the  struggling  and  distress  involved  in  local  treatment 
may  be  more  injurious  to  the  strength  of  the  child  than  is  compensated 
for  by  the  benefit  derived  from  it. 

Surgical  measures  are  required  in  quinsy,  if  there  is  much  swelling, 
oedema  or  any  sign  of  laryngeal  obstruction.  Even  if  pus  is  not  found, 
local  bleeding  does  good.  No  ansesthetic  is  permissible  for  there  may  be 
glottic  oedema.  Cleanse  the  throat  and  apply  a  5  per  cent,  cocaine  spray. 
With  the  child  in  a  sitting  posture,  the  head  steadied  and  the  throat  well 
illuminated,  push  a  pair  of  Lister's  sinus  forceps  into  the  soft  or  boggy  spot, 
backwards  and  a  trifle  outwards,  and  open  them  as  they  are  taken  out. 
The  soft  spot  is  generally  situated  in  the  soft  palate,  just  external  to  the 
supratonsillar  fossa,  at  the  point  where  a  vertical  line  corresponding  to  the 
anterior  faucial  pillar  crosses  a  line  drawn  horizontally  across  the  base  of 
the  uvula.  If  a  scalpel  is  used,  it  must  be  protected  by  sticking  plaster  up 
to  the  last  Jin.  It  is  inserted  in  the  same  situation  and  a  cut  made  upwards 
and  inwards. 

Enlarged  Tonsils. — Enlargement  of  the  tonsils  is  etiologically  due  to 
the  same  causes  as  adenoids.  It  takes  place  in  a  vertical,  antero-posterior 
or  horizontal  direction.  The  surface  is  normal,  rough  and  irregular,  patchy 
or  honey-combed  with  irregular  holes,  and  occasionally  papillated.  There 
are  two  types,  the  hard  and  the  soft,  depending  upon  the  relative  amount 
of  lymphoid  and  fibrous  tissue.  The  crypts  are  dilated  and  filled  with  cheesy 
matter  in  the  soft  variety,  or  obliterated  by  the  contraction  of  the  excessive 
fibrosis  in  the  hard  variety.  Usually  the  two  conditions  are  more  or  less 
combined. 

Chronic  parenchymatous  tonsillitis  is  common  in  children  and  often 
associated  with  adenoids.  The  tonsil  is  hard,  round  and  smooth.  Chronic 
lacunar  or  follicular  tonsillitis  is  liable  to  cause  toxsemia  and  fever  from 
absorption  of  decomposing  matter  in  the  crypts.  The  tonsil  is  large,  soft, 
and  irregularly  pitted. 

The  symptoms  ascribed  to  enlarged  tonsils  are  commonly  due  to 
adenoids,  so  tonsillotomy  alone  may  prove  a  failure.  Enlargement  causes 
difficulty  in  swallowing  ;  interference  with  mouth  breathing,  a  serious 
trouble  if  nasal  respiration  is  obstructed  by  adenoids  ;  a  thick,  indistinct 
voice  ;  deafness  from  upward  pressure  of  the  soft  palate  and  imperfect 
middle  ear  aeration  ;  and  maldevelopment.  The  lungs  are  imperfectly 
expanded,  the  ribs  sink  in  and  the  child  may  become  pigeon-breasted.  The 
blood  is  imperfectly  aerated  and  general  health  impaired.  Enuresis  and 
foetal  incontinence  occasionally  occur.  The  local  conditions  and  the  open 
mouth  lead  to  congestion,  the  entrance  and  growth  of  microbes,  attacks  of 


236  Chapter  XXI. 

tonsillitis,  and  enlargement  of  the  upper  set  of  the  deep  cervical  glands. 
which  may  suppurate.  Reflex  cough  is  produced.  It  is  dry  or  hacking 
and  almost  constant,  or  may  be  paroxysmal  and  spasmodic.  The  local 
irritation  causes  discomfort  in  the  throat  and  perhaps  pain  shooting  to  the 
ears.    Toxaemia,  and  adenitis  are  the  most  important  complications. 

If  the  tonsils  are  small,  hard  and  round,  and  contain  no  open  crypts, 
local  treatment  may  be  sufficient  and  spontaneous  atrophy  may  occur 
at  puberty.  The  soft  tonsils  may  diminish  in  size  after  acute  inflammation, 
or  remain  stationary  after  attaining  a  certain  size,  until  they  decrease  at 
puberty.  As  a  rule  they  improve  little  during  childhood  and  they  increase 
the  liability  of  the  child  to  acute  inflammation,  septic  infection,  scarlet 
fever,  diphtheria,  etc.  They  exaggerate  the  gravity  of  these  diseases  when 
they  occur  and  increase  the  liability  to  ear  disease. 

Local  treatment  consists  in  the  application  of  astringents  for  the  soft 
variety,  and  compound  tincture  of  iodine  in  either  type.  Cod-liver  oil, 
iodide  of  iron,  sea  air  and  a  high  dry  climate  are  beneficial.  Provided 
hypertrophy  is  not  due  to  recent  tonsillitis,  operation  should  be  done  if  there 
are  distinct  mechanical  obstruction,  recurrent  attacks  of  catarrh,  reflex 
cough,  ear  trouble  or  adenitis,  and  if  the  crypts  remain  blocked  with 
caseous  matter  or  discharge  foetid,  purulent  or  muco-purulent  secretion. 
The  operation  should  depend  upon  the  symptoms  and  not  on  the  age  or  the 
size,  unless  they  are  very  large.  It  is  not  urgent  in  mild  cases  at  about 
puberty,  unless  singing  is  taught. 

Tonsillotomy. — An  anaesthetic  is  required  for  a  nervous  child  or  if 
adenoids  are  removed  as  well.  A  recumbent  position  and  a  gag  are  then 
necessary.  In  other  cases  5-10  per  cent,  solution  of  eucaine  is  painted  on, 
and  the  tonsils  are  removed  by  a  spade-shaped  guillotine  with  the  child 
in  a  sitting  posture.  The  instrument  should  be  warmed,  and  care  taken 
to  first  encircle  the  lower  edge  of  the  tonsil  and  to  press  firmly  outwards. 
Adhesions  of  the  pillars  of  the  fauces,  if  present,  must  be  separated  first. 
The  operation  is  often  imperfectly  done,  a  small  slice  only  being  cut  off. 
The  portions  left  are  liable  to  recurrent  inflammation.  The  small  pad  left 
is  said  to  protect  the  carotid  artery,  and  to  prevent  an  excavation  in  which 
food  may  collect  and  decompose.  The  dangers  of  the  operation  are  slight. 
With  ordinary  care  the  carotid  cannot  be  wounded  by  the  guillotine  or  a 
blunt  pointed  bistoury.  An  abnormal  vessel  may  be  opened.  Usually 
the  patient  hardly  suffers  and  bleeding  stops  in  a  few  minutes,  especially 
if  the  patient  stands  up  after  the  operation.  Enucleation  is  a  more  com- 
plete cure  and  must  be  done  under  anaesthesia.  The  tip  of  the  finger 
is  inserted  into  the  supratonsillar  fossa  and  the  gland  separated  from 
above  downwards.  It  is  then  seized  with  tenaculum  forceps,  pulled 
inwards  and  rotated,  thus  twisting  and  tearing  the  vessels,  and  twisted 
or  cut  off.  There  is  Httle  bleeding,  no  late  haemorrhage,  and  no  possibility 
of   recurrent-       It  is  easy  in  the  fibrous  form,  but  in  the  soft  variety  is 


The   Throat,   Pharynx,  and  (Esophagus.  237 

more  difficult.  The  raw  surface  soou  heals.  Discomfort  and  pain  may 
last  two  days. 

Immediate  haemorrhage  after  tonsillotomy  is  rarely  serious,  but 
recurrent  haemorrhage  is  dangerous  and  liable  to  be  overlooked  for  the  blood 
is  swallowed.  For  general  oozing  give  ice  to  suck,  paint  the  surface  with 
adrenalin  solution,  or  apply  digital  pressure,  styptic  cotton,  or  a  mixture 
of  tannic  acid  3  parts  and  gallic  acid  1  part,  in  sufficient  water  to  make  a 
hard  mass,  rubbing  it  in  freely  and  applying  external  pressure  at  the 
same  time  (Hovell).  If  there  is  a  single  bleeding  point,  the  severed  tonsillar 
artery,  the  vessel  should  be  clamped  with  a  pair  of  Spencer- Wells  forceps 
left  in  situ.  Ligature  of  the  carotid  is  probably  never  required.  Bleeding  is 
venous  or  capillary,  and  ceases  as  soon  as  faintness  supervenes.  It  may  be 
kept  up  by  measures  adopted  for  its  prevention.  Another  method  is  to 
apply  gauze  and  stitch  the  pillars  together  for  24  hours.  Secondary 
haemorrhage  may  result,  from  the  separation  of  a  slough  opening  up  a  small 
vessel,  as  late  as  the  sixth  day.  Sepsis  and  septic  pneumonia  are  possible 
sequels  and  septic  throat  affections  sometimes  ensue.  Caries  of  the  teeth 
should  be  attended  to  before  operation,  and  antiseptic  precautions  adopted. 
Although  many  cases  are  operated  on  in  hospital  out-patient  departments 
with  impunity,  it  is  preferable  that  the  operation  should  be  performed  at 
home  or  in  hospital,  and  the  child  put  straight  to  bed  in  a  warm  room 
and  kept  there  for  2  or  3  days.  Exposure  to  cold  may  set  up  inflammation, 
and  exercise  may  bring  on  recurrent  haemorrhage.  The  child  should  be 
fed  on  boiled  milk,  cold  or  lukewarm,  and  then  soft  food  until  able  to 
swallow  comfortably.  After  food  the  throat  should  be  washed  out  or 
sprayed  with  an  alkaline  antiseptic  lotion.  The  wound  looks  grey  on  the 
day  after  operation  (p.  233).  Sepsis  is  indicated  by  an  ashy  grey  slough, 
furred  tongue,  offensive  breath,  adenitis,  painful  deglutition  and  fever. 
It  is  treated  by  calomel,  quinine,  perchloride  of  iron,  and  chlorine  spray 
or  gargle. 

Tuberculosis. — Both  the  faucial  and  pharyngeal  tonsils  may  be  infected 
by  food,  inhalation,  through  the  blood  stream,  or  by  coughed  up  sputum. 
Probably  the  infection  is  mainly  by  the  blood  stream.  Possibly  the 
bacillus  can  pass  into  the  lymphatics  and  infect  the  glands  without  causing 
a  primary  lesion  of  the  tonsils.  If  the  tonsils  are  tuberculous,  the  follicular 
glands  at  the  base  of  the  tongue  and  the  cervical  glands  are  likely  to  be 
infected.  Before  asserting  that  the  tonsillar  affection  is  primary  the  relative 
age  of  other  tuberculous  foci,  if  present,  must  be  considered. 

Fried  mann  found  evidence  of  tubercle  in  17  out  of  145  tonsils  removed 
at  operation  or  after  death.  Latham,  by  inoculation  experiments,  demon- 
strated the  presence  of  the  bacillus  in  7  out  of  45  similar  cases,  the  youngest 
being  3  months  of  age.  Sukchito  Ito  (1903)  only  found  6  cases  of  infection 
in  104  children  under  13  years  of  age  ;  none  primarily  tuberculous.  He 
examined  8,000  sections. 


238  Chapter   XXI. 

Considering  the  frequent  exposure  of  the  pharynx  to  infection,  primary 
tuberculosis  of  the  pharyngeal  tonsil  is  very  rare.  It  may  lead  to  cervical 
adenitis.  A  few  cases  have  been  described  in  children.  Inoculation 
experiments  are  unreliable  for  surface  contaminations  cannot  be  excluded, 
and  tubercle  bacilli  are  sometimes  found  in  the  healthy. 

Pharyngeal  Affections. — Periodical  attacks  of  congestion  in  the 
pharynx  are  associated  with  nasal  catarrh  or  may  start  in  the  naso- 
pharynx. They  are  described  under  the  name  of  Acute  Catarrhal  Pharyn- 
gitis, Pharyngitis  Superior,  Adenoiditis,  Pharyngeal  or  Retro-nasal  Angina, 
and  Post-nasal  Catarrh.  The  symptoms  are  fever,  slight  nasal  irritation 
and  snuffles,  nasal  voice,  muco-purulent  discharge,  earache,  deafness; 
cough,  especially  during  sleep  ;  paroxysms  of  dyspnoea,  occasionally  at 
night  ;  and  interference  "with  swallowing.  Tenacious  mucus  is  visible  on 
the  reddened  and  swollen  posterior  pharyngeal  wall.  The  attack  lasts 
from  a  few  days  to  a  week  or  more,  and  may  end  in  secondary  bronchitis. 
It  produces  adenoids  or  chronic  hyperplasia.  The  local  treatment  is  that 
suitable  for  adenoids. 

Follicular  or  lacunar  pharyngitis  causes  fever  and  general  malaise. 
It  is  often  overlooked,  for  it  may  be  only  diagnosable  by  posterior  rhinos- 
copy. The  pharyngeal  tonsil  is  covered  with  patches  of  follicular  secretion, 
similar  to  those  seen  in  follicular  tonsillitis.  The  follicles  may  open  into  a 
small  recess  in  the  middle  line  with  a  single  orifice.  The  exudation  may  be 
excessive  and  coherent  into  a  membranous  structure  simulating  diphtheria. 
It  may  extend  to  the  Eustachian  tube  and  cause  earache,  otitis  media  and 
even  meningitis.  Occasional  complications  are  parenchymatous  tonsillitis, 
quinsy,  adenitis,  erythematous  rashes,  and  laryngeal  or  respiratory  catarrh. 
It  may  simulate  typhoid  fever  because  of  fever,  gastric  symptoms  and 
enlarged  spleen  ;  or  meningitis,  if  the  nervous  symptoms  are  pronounced. 
The  treatment  consists  in  local  applications  to  the  pharynx,  by  a  large 
suitably  curved  brush,  and  nasal  douching. 

Pneumococcal  Pharyngitis  is  generally  associated  with  tonsillar  inflam- 
mation. Elliott,  of  Chester  (1909),  has  drawn  attention  to  cases  of  this  type 
in  children  and  adults.  They  were  characterised  by  pharyngitis,  a  tempera- 
ture up  to  102-103°  F.,  sudden  onset,  and  rapid  cervical  adenitis  of  the 
submaxillary,  deep  cervical  glands,  and  those  below  the  lobule  of  the 
ear.  The  duration  was  only  a  few  days,  and  there  was  no  ulceration.  In 
some  respects  this  is  like  glandular  fever  (q.v.). 

Pharyngeal  or  Post-adenoid  Abscess  is  due  to  secondary  infection,  via 
adenoids,  and  is  situated  in  the  connective  tissue  between  the  pharyngeal 
tonsil  and  aponeurosis.  The  symptoms  are  those  of  adenoids,  combined 
with  recent  sore  throat  and  rapid  increase  of  nasal  obstruction.  There  is 
no  difficulty  in  swallowing  unless  the  pharyngeal  catarrh  is  general.  A 
cystic  swelling,  usually  median  and  perhaps  extending  to  the  roof  of  the 
naso-pharynx,  is  felt,  on  digital  examination,  covered  by  adenoids.     It  is 


The   Throat,   Pharynx,  and  (Esophagus.  239 

evacuated  by  the  knife  or  by  pushing  sinus  forceps  into  the  centre  of  the 
swelling. 

Adenoids. — Syn.  ;  Post-nasal  growths  or  adenoids —  Adenoid  growths — 
Adenoid  vegetations  in  the  naso-pharynx. — The  name  of  adenoids  should  be 
limited  to  hypertrophy  of  Luschka's  gland,  a  circumscribed  mass  of  lym- 
phoid tissue  in  the  upper  part  of  the  posterior  wall  of  the  naso-pharynx  in 
the  middle  line,  oval  in  shape  with  the  long  axis  vertical.  It  is  roughly 
divided  into  two  lobes  by  a  median  longitudinal  groove  and  is  covered 
by  columnar  ciliated  epithelium.  This  gland  is  present  at  birth,  varies  in 
size,  at  its  maximum  between  4-6  years  of  age,  and  then  slowly  atrophies. 
It  is  impossible  to  draw  a  sharp  line  of  demarcation  between  a  physiological 
and  pathological  hypersemia  and  hyperplasia  of  the  gland.  Its  removal  may 
be  insufficient  for  cure,  because  the  rest  of  the  adenoid  tissue  of  Waldeyer's 
ring  may  be  hypertrophied,  perhaps  to  even  a  greater  extent.  Large 
masses  may  be  situated  round  the  posterior  choanae  and  Eustachian  tubes. 
This  is  flatly  contradicted  by  some  surgeons  who  state  that  this  region  may 
be  safely  left  alone. 

Etiology  and  Pathology. — Heredity  is  a  potent  factor  for  a  tendency 
to  lymphatic  hypertrophy  or  hyperplasia  is  present  in  many  children  of 
the  same  family.  Adenoids  are  constantly  associated  with  enlarged  tonsils. 
Important  factors  are  tuberculosis,  infective  fevers,  liability  to  catarrh  of 
the  respiratory  passages,  bad  hygienic  surroundings,  climatic  conditions, 
and  neglected  colds.  Some  of  these  tend  to  produce  lymphatic  hyperplasia 
and  others  to  cause  catarrhal  affections.  Interference  with  normal  breathing 
through  the  nose  may  be  a  result  and  not  a  cause.  Nearly  all  infants  with 
adenoids  are  rachitic,  but  rachitic  children  are  constantly  free  from 
adenoids.  A  highly  arched  palate  is  liable  to  occur  in  rickets,  catarrhal 
affections  are  common,  and  the  small  posterior  nares  are  easily  blocked  by 
the  swollen  lymphoid  tissue.  The  increase  in  size  from  a  small  patch  to  a 
mass  filling  the  naso-pharynx  is  due  to  inflammation  or  hypertrophy,  and 
the  growth  is  soft  or  hard  according  to  the  degree  of  fibrosis.  It  may  be 
quite  hard  and  fibrous.  Occasionally  cheesy  nodules  can  be  squeezed  out. 
The  central  recess  may  be  partly  converted  by  adhesions  into  a  cavity 
(  Tornwaldfs  Bursa).  The  adenoid  tissue  may  give  rise  to  trouble  from  the 
moment  of  birth,  such  as  difficulty  in  breathing,  stridor  and  inability  to 
suckle.     Operative  treatment  is  not  often  necessary  before  4  years  of  age. 

The  Symptoms  are  local  and  constitutional ;  nasal,  respiratory  and 
affecting  deglutition ;  obstructive,  catarrhal  and  reflex.  The  local 
symptoms  indicate  the  degree  of  obstruction.  The  child  is  a  mouth- 
breather  and  has  a  stupid  appearance  because  of  the  half-opened  mouth. 
Hence  arise  dryness  of  the  mouth  and  throat,  difficulty  in  swallowing, 
inability  to  suck  freely  without  stopping  to  take  breath,  noisy  breathing 
and  snoring  during  sleep,  perhaps  amounting  to  a  congenital  stridor  in 
infants    or    attacks   like   laryngospasm,    early   decay   of   the   teeth,    and 


240  Chapter   XXI. 

imperfect  oxygenation  of  the  blood.  To  the  indirect  effects  of  imperfect 
respiration  and  mouth-breathing  are  ascribed  the  narrow,  highly  arched 
palate,  long  and  narrow  face,  narrow  nasal  fossse,  deformities  of  the  upper 
jaw  and  of  the  chest.  Recession  of  the  lower  ribs  is  common  in  infants. 
Head  sweating  and  "  snatchy  "  sleep  are  due  to  deficient  oxygenation.  The 
voice  is  stuffy  and  dead.  There  is  difficulty  in  pronouncing  certain  conso- 
nants, M  and  N  pronounced  as  EB  and  ED,  backwardness  in  learning 
to  articulate  clearly  and  perhaps  stammering.  Speech  is  most  likely 
to  be  defective  in  the  congenital  cases.  The  nasal  signs  include  lateral 
compression  of  the  anterior  nares,  snuffling,  recurrent  or  chronic  mucoid, 
muco-purulent  or  purulent  discharge,  periodical  "  colds,"  sometimes 
epistaxis,  and  occasionally  paroxysmal  sneezing  attacks  like  those  of 
hay-fever.  Respiratory  catarrh,  hoarseness  and  asthmatical  symptoms  may 
occur.  Cough  is  variable,  short,  dry,  hacking,  barking  or  choking  in 
character  ;  the  most  typical  type  is  a  paroxysmal  cough  which  may 
simulate  whooping  cough.  It  may  be  constant  while  awake  ;  occur  chiefly 
on  lying  down  ;  wake  the  child  up  during  sleep,  or  be  worst  in  the  early 
morning.  Its  persistence  may  render  operation  necessary,  and  its  severity 
may  cause  vomiting  or  even  involuntary  defaecation.  Ear  troubles  are 
very  important.  At  first  there  may  be  slight  attacks  of  earache,  and  then 
recurrent  and  more  severe  ones  ;  a  gradually  increasing  or  recurrent  deaf- 
ness ;  and  finally  attacks  of  otitis  media  and  otorrhoea.  The  tympanic 
membrane  is  depressed.  The  cervical  glands  are  often  enlarged  and 
liable  to  septic  infection  or  to  become  tuberculous.  The  vacant,  semi- 
idiotic  facial  aspect,  due  to  the  half-open  mouth,  gives  the  impression  of 
mental  dulness  or  hebetude,  which  is  more  apt  to  be  due  to  deficient 
aeration.  The  child  may  be  backward,  but  the  intellect  unimpaired. 
Deafness  increases  the  appearance  of  stupidity  and  causes  backwardness, 
inattention  and  listlessness.  Moral  degeneracy  has  improved  after  operation. 
The  general  health  and  nutrition  are  impaired  because  of  imperfect  expansion 
of  the  chest  and  deficient  oxygenation.  Malnutrition  may  be  due  to  the 
difficulty  of  sucking.     The  child  cannot  breathe  and  suckle  simultaneously. 

The  chief  indirect  effects  arise  from  imperfect  aeration  of  the  blood 
or  reflex  irritation,  and  include  enuresis  nocturna,  night  terrors,  moaning, 
teeth-grinding,  somnambulism,  frontal  headache  ;  torticollis,  secondary 
to  adenitis  ;  rarely,  a  staggering  ataxic  gait  and  recurrent  vomiting.  Many 
of  these  are  merely  coincident.  Laryngeal  complications  include  "  con- 
genital crowing  "  and  laryngospasm.  Some  of  the  nervous  phenomena  are 
due  to  the  catarrh  and  can  be  cured  by  treatment  of  the  catarrh.  Breathing 
may  be  noisy  from  birth  and  at  times  distressed,  and  the  crowing  very 
loud.  It  persists  day  and  night,  and  must  be  distinguished  from  true 
congenital  stridor. 

Diagnosis. — In  infancy  the  symptoms  of  adenoids  have  to  be  dis- 
tinguished from  those   due  to   other  causes,   notably  simple   post-natal 


The   Throat,   Pharynx,  and  (Esophagus.  241 

catarrh  and  the  snuffles  of  congenital  syphilis.  The  stridulous  breathing 
differs  from  congenital  laryngeal  stridor  in  that  it  is  most  marked  during 
sleep,  when  the  mouth  is  shut,  and  while  suckling.  At  all  ages  the  presence 
of  adenoids  is  diagnosed  by  the  interference  with  breathing  and  the 
functions  of  the  nose  and  naso-pharynx,  and  the  presence  of  enlarged  tonsils. 
The  "  Adenoid  Fades  "  is  merely  the  appearance  due  to  nasal  obstruction 
from  any  cause. 

If  necessary,  the  naso-pharynx  must  be  examined  digitally.  This  is 
difficult  in  infants  because  of  the  small  size,  and  in  older  children  it  is 
unpleasant  and  alarming,  if  they  are  nervous.  The  examiner  stands  on 
the  right  side,  somewhat  behind  the  child,  places  the  left  arm  round  the 
head,  and  depresses  the  lower  jaw  with  the  left  hand  or  pushes  the  left 
cheek  between  the  teeth.  The  index  or  little  finger  is  then  inserted  along 
the  right  faucial  pillar  and  up  into  the  naso-pharynx.  This  mode  of 
examination  is  not  of  very  much  value,  for  the  diagnosis  is  based  mainly 
on  the  symptoms  and  the  advisability  of  operation  on  the  severity  of 
the  symptoms.  It  is  necessary  sometimes,  or  cases  will  be  operated 
on  although  no  adenoids  are  present.  Posterior  rhinoscopy  is  a  better 
method  of  examination  and  is  possible  after  the  third  or  fourth  year,  if 
the  tonsils  are  not  too  large. 

Attention  must  be  directed  particularly  to  mouth-breathing,  snoring, 
nasal  obstruction  even  if  only  nocturnal,  earache,  recurrent  deafness, 
otitis,  otorrhcea  and  adenitis,  together  with  the  effects  on  the  general  health 
and  development  of  the  child,  especially  of  the  thorax.  Nasal  obstruction 
and  deafness  due  to  other  causes  must  be  excluded.  Care  must  be  taken 
not  to  ascribe  backwardness,  physical  or  mental,  to  adenoids,  unless  there 
is  deafness  or  very  definite  obstruction. 

Prognosis. — Adenoids  tend  to  atrophy  at  puberty,  and  the  degree 
of  obstruction  is  reduced  by  the  rapid  enlargement  of  the  throat.  If  they 
are  left  alone  in  early  life,  they  are  liable  to  cause  ear  troubles  and  general 
maldevelopment  of  the  nose,  naso-pharynx,  upper  jaw,  palate  and  chest. 
The  mouth  is  kept  open,  the  upper  lip  raised,  the  incisor  teeth  become 
prominent,  the  teeth  are  more  liable  to  caries,  the  voice  is  nasal,  the  chest 
pigeon-breasted,  growth  stunted,  and  lateral  curvature  not  uncommon. 

The  prognosis  of  operation  depends  upon  the  age  of  the  patient  and 
the  duration  and  degree  of  the  obstruction  before  operation  ;  on  the 
complete  removal ;  on  the  presence  of  other  defects  ;  and  on  the  removal 
of  the  posterior  ends  of  inferior  turbinals,  if  they  are  hypertrophied.  If 
there  is  any  anterior  nasal  obstruction,  it  must  be  treated  first,  otherwise 
mouth-breathing  is  certain  to  persist  after  operation.  In  many  cases  the 
operation  does  not  prevent  mouth-breathing,  for  it  has  become  a  habit  and 
may  be  due  to  other  causes  ;  nor  does  it  always  prevent  deformity  of  the 
jaw  and  ear  troubles.  Too  much  is  usually  expected.  The  best  results 
are  obtained  in  those  cases  in  which  the  obstruction  is  definitely  interfering 

R 


242  Chapter  XXI. 

with  aeration   of  the  blood,   expansion  of  the  chest,   and    the    general 
health. 

Treatment. — Careful  attention  to  catarrhal  conditions  of  the  nose  and 
naso-pharynx  prevents  the  occurrence  of  adenoids.  The  general  treatment 
consists  in  hygiene,  sea  air  or  a  dry  equable  climate,  teaching  the  child  to 
breathe  deeply  and  freely  through  the  nose,  suitable  diet,  and  tonics  such 
as  cod-liver  oil,  arsenic  and  iron.  Lapayer  (1901)  recommended  the 
administration  of  tr.  iodi.  co.,  m.  5-30,  t.d.s.  This  is  an  alcoholic  solution  of 
iodine,  and  is  said  to  cause  atrophy  of  the  vegetations.  An  alkaline  nasal 
lotion  removes  mucus  and  relieves  the  symptoms.  Local  applications  are 
useful  when  the  adenoid  tissue  is  soft  and  gelatinous  from  temporary 
congestion.  The  naso-pharynx  may  be  painted  with  equal  parts  of  liq. 
ferri  perchlor.  and  glycerine,  twice  a  week,  using  a  laryngeal  brush  on  a 
curved  handle,  and  then  once  a  week  ;  or  with  iodine  grs.  2,  pot.  iod. 
grs.  30,  glycerine  oz.  1  ;  or  alum  drs.  2,  tannin  dr.  J.  glycer.  oz.  f,  aqua 
rosarum  ad.  oz.  2.  Sprays  are  of  comparatively  little  value.  If  the  mass 
is  hard  and  fibrous  it  must  be  removed. 

Breathing  exercises,  so  often  recommended,  are  frequently  injurious. 
It  is  by  no  means  uncommon  to  find  an  unfortunate  child  doing  breathing 
exercises  two  or  three  times  a  day,  although  on  every  inspiration  the  ribs 
sink  in  and  the  sternum  is  protruded  ;  or  perhaps  the  lower  part  of  the 
sternum  and  the  cartilages  are  sucked  in.  They  are  only  justifiable  and 
useful  when  the  chest  is  fully  and  normally  expanded  on  deep  inspiration. 
The  child  stands  in  the  erect  posture  and  slowly  elevates  the  extended  arms 
until  the  hands  meet  above  the  head,  taking  at  the  same  time  a  deep  nasal 
inspiration  with  the  mouth  closed.  This  is  repeated  8-10  times  a  minute 
for  15  minutes,  twice  a  day.  Breathing  exercises  may  improve  breathing, 
but  they  will  not  cure  hypertrophy  of  adenoid  tissue. 

Operation. — There  are  several  objections  to  the  unhesitating  recom- 
mendation of  operative  treatment.  It  is  an  operation  which  causes  anxiety, 
trouble  and  expense.  Death  may  result  from  the  anaesthetic  or  haemor- 
rhage, immediate,  recurrent  or  secondary.  Post-operative  haemorrhage  is 
generally  tonsillar.  It  may  depend  on  haemophilia.  Portions  of  growth 
may  get  into  the  air  passages  and  cause  suffocation  or  septic  pneumonia. 
Acute  otitis  media  and  septic  meningitis  are  occasional  sequels.  The 
enlarged  cervical  glands  may  become  infected  and  suppurate.  Septic 
infection  of  the  pharynx  may  occur. 

Age  is  an  important  consideration.  Infancy  is  no  bar.  If  puberty 
is  approaching  the  operation  may  sometimes  be  postponed.  Recurrence 
is  more  likely  in  infants,  but  this  is  no  objection  if  the  operation  is  necessary 
on  account  of  interference  with  suckling  or  otitis.  It  is  practically  devoid 
of  danger,  and  adenoids  produce  the  greatest  evil  effects  in  infancy.  If 
there  is  any  nasal  obstruction,  the  operation  should  be  done  before  the 
commencement  of  the  second  dentition.     Catarrhal  swelling,  due  to  colds 


The  Throat,  Pharynx,  and  (Esophagus.  243 

or  fevers,  may  subside  after  a  few  weeks  or  months  of  local  and  general 
treatment. 

The  chief  indications  for  operation  are  the  duration,  persistence  and 
severity  of  the  effects,  notably  habitual  mouth-breathing ;  imperfect 
development  or  deformity  of  the  chest ;  deafness,  depressed  tympanum, 
earache  and  otitis  ;  constant  or  recurrent  nasal  discharge  and  nasal  ob- 
struction ;  irritating  cough,  suffocative  attacks,  bronchitis  and  asthmatic 
symptoms  ;  catarrhal  affections  of  the  fauces,  and  adenitis.  In  older 
children  it  is  advisable  in  order  to  improve  the  singing  voice. 

Recurrence  is  rare,  if  the  operation  is  thoroughly  done  after  the 
fourth  year.  If  relief  is  not  obtained  the  nose  must  be  examined  for 
deflected  septum,  hypertrophied  turbinals,  mucous  polypi  and  anterior 
nasal  stenosis.  After  operation  there  is  no  immediate  recovery,  for  the 
iabit  of  mouth-breathing  and  the  speech  defects  are  only  slowly  cured, 
and  may  persist  throughout  life  if  operation  has  been  unduly  postponed. 
General  treatment  and  breathing  exercises  are  useful  at  this  time. 

The  operation  is  done  under  anaesthesia,  A.C.E.  or  C1E2  mixture, 
but  not  nitrous  oxide  gas,  with  the  child  in  the  dorsal  position  on  a  flat 
table.  The  tonsils  may  be  removed  afterwards,  unless  so  large  as  to 
interfere  with  operation  ;  and  the  posterior  ends  of  the  inferior  turbinah 
are  removed,  if  they  are  hypertrophied.  Kirstein's  modification  of 
Gottstein's  curette  and  St.  Clair  Thomson's  adenoid  curette  are  the  best 
instruments,  and  generally  preferable  to  the  finger  nail,  the  steel  nail  or 
forceps.  Subsequent  to  operation  swallowed  blood  may  be  vomited ; 
and  snoring  may  persist  and  be  worse  for  2  or  3  nights,  or  until  blood  and 
stagnant  discharges  are  cleared  away.  The  child  is  kept  in  bed  2-4  days, 
given  an  aperient  on  the  second  day,  soft  food  for  3  days,  and  light  diet  for 
a  week.  An  antiseptic  alkaline  lotion  is  used  for  nasal  stuffiness  and 
•offensive  breath,  as  a  spray  or  mild  douche. 

If  there  is  glandular  enlargement,  it  is  advisable  to  put  the  child  on  a 
•course  of  arsenic  before  operation.  The  arsenic  seems  to  render  the  glands 
less  susceptible  to  septic  infection  and  suppuration,  an  accident  which 
sometimes  follows  operation.  Occasionally  a  nasal  tone  after  operation  is 
•due  to  paresis  of  the  soft  palate,  and  is  cured  by  cold  water  gargles. 

Retro-Pharyngeal  and  Retro-CEsophageal  Abscess.— The  true  retro- 
pharyngeal abscess  is  situated  between  the  bucco-pharyngeal  aponeurosis 
and  the  prevertebral  fascia.  The  tuberculous  abscess  of  cervical  caries  is 
posterior  to  the  prevertebral  fascia.  It  begins  insidiously  in  the  middle 
line  and  spreads  slowly  outwards.  The  post-adenoid  abscess  (p.  238) 
is  in  the  middle  line  anterior  to  the  bucco-pharyngeal  aponeurosis.  The 
■ordinary  retro-pharyngeal  abscess  is  due  to  infection  of  the  glands  in  the 
pharyngeal  connective  tissue,  from  septic  conditions  of  the  naso-pharynx 
and  tonsils,  injury  by  fish  bones,  and  specific  fevers,  such  as  measles  and 
-scarlet  fever.    It  is  an  intra-pharyngeal  abscess  starting  behind  the  posterior 


244  Chapter   XXI. 

pillar  of  the  fauces,  spreading  backwards  to  the  posterior  wall  and  then 
inwards.  In  its  early  stage  the  small  rounded  swelling  can  be  felt  and  often 
seen  behind  the  tonsil,  and  the  child  is  ill.  As  the  swelling  enlarges,  becoming 
tense  and  elastic,  it  give  rise  to  salivation,  dysphagia  and  muffled  cry  ; 
and  the  head  is  thrown  back  or  to  one  side.  Then  the  signs  of  obstructive 
dyspnoea  develop,  but  stridor  and  croup  are  generally  absent. 

The  onset  is  gradual,  with  catarrh  of  the  nose  and  throat  and  often 
a  purulent  rhinitis.  The  child  is  generally  brought  for  anorexia  or 
dysphagia,  vomiting,  cough,  croup  or  bronchitis.  The  tongue  is  furred,  the 
fauces  red  and  covered  with  mucus,  and  the  tonsils  enlarged,  one  perhaps 
pushed  forward.  The  head  is  retracted  and  the  neck  stiff  or  rigid,  and 
looks  swollen  because  of  unilateral  or  bilateral  secondary  adenitis.  Dyspnoea 
is  inspiratory  at  first  and  later  expiratory,  with  recession.  It  may  be 
paroxysmal.  The  cry  and  voice  are  altered,  hoarse  or  crowing,  cough 
spasmodic,  and  snoring  present  when  the  child  is  in  the  prone  position. 
The  dysphagia  varies  with  the  size  and  position  of  the  abscess.  Sometimes- 
food  regurgitates  through  the  nose.  The  child  looks  ill,  is  restless,  sweating,, 
pale  or  cyanosed,  with  the  mouth  open,  rapid  pulse,  and  temperature  up 
to  104°  F.    It  refuses  food  because  of  anorexia  or  difficulty  in  swallowing. 

If  the  abscess  is  in  the  upper  part  of  the  pharynx,  the  signs  are  mainly 
an  open  mouth,  snoring,  snuffling,  nasal  cry  and  interference  with  nasal 
breathing.  If  the  abscess  is  low  down,  the  cry  is  laryngeal,  breathing 
stridulous,  the  respiratory  murmur  diminished,  and  there  are  many  moist 
sounds. 

These  cases  generally  occur  between  6  and  12  months  of  age  and  are- 
rare  after  the  third  year.  Bokay's  figures  are  296  in  the  first  year,  78  in 
the  second,  and  93  afterwards.  They  are  extremely  fatal  if  untreated;, 
death  resulting  from  asthenia,  asphyxia,  glottic  spasm  or  vagus  inhibition. 
Rupture  is  rare,  and  may  cause  suffocation  or  inspiratory  pneumonia. 
Ulceration  has  taken  place  into  the  carotid  artery  and  into  the  middle  ear 
or  external  auditory  meatus.  About  5  per  cent,  of  those  treated  by  incision 
do  not  recover. 

Diagnosis. — Extra-pharyngeal  abscess  is  due  to  suppuration  in  deep 
cervical  glands  and  preceded  by  glandular  enlargement  in  the  neck.  There 
is  more  external  swelling.  The  abscess  bulges  but  rarely  bursts  into  the 
lateral  wall  of  the  pharynx.  It  seldom  causes  serious  obstruction  to 
breathing  or  swallowing.  Large  mucous  cysts  and  a  retro-pharyngeal  blood 
cyst,  in  purpura,  cause  symptoms  like  those  of  retro-pharyngeal  abscess. 
Cases  have  also  to  be  diagnosed  from  croup,  oedema  of  the  glottis,  laryn- 
geal obstruction,  foreign  bodies,  enlarged  tonsils  and  adenoids,  diphtheritic, 
palsy,  and  pharyngitis  or  rhinitis,  if  high  up.  The  rigidity  of  cervical 
caries  is  distinguished  by  its  long  duration  ;  that  of  simple  abscess  comes 
on  suddenly  and  is  often  absent.  Palpation  is  more  reliable  than  inspection. 
The  pharynx  is  explored  from  above  downwards  and  from  side  to  side- 


The  Throat,  Pharynx,  and  (Esophagus.  245 

A  gag  must  not  be  used,  as  it  may  cause  rupture  of  the  abscess.  The 
swelling  is  lateral,  larger,  and  usually  lower  than  that  of  post-adenoid 
abscess. 

Treatment. — The  preventive  treatment  is  that  of  tonsillar  and  naso- 
pharyngeal affections.  The  abscess  must  be  opened  through  the  mouth, 
and  the  child  turned  on  its  face  as  soon  as  the  incision  is  made.  Use  a 
straight  scalpel,  £  in.  long,  and  no  ansesthetic  ;  open  the  mouth  with  the 
finger  or  tongue  depressor,  but  not  very  wide.  If  the  erect  position  is 
chosen,  bend  the  child  forward  immediately  after  the  incision  is  made. 
Sudden  respiratory  failure  may  arise  from  manipulation  of  the  pharynx 
or  the  use  of  a  tongue  depressor.  Other  accidents  at  operation  are  sudden 
syncope,  spasm  of  the  glottis,  haemorrhage  from  a  branch  of  the  carotid, 
and  entrance  of  pus  into  the  air  passages.  Secondary  infection  is  rare. 
The  abscess  may  require  re-opening  and  expression.  An  extra-pharyngeal 
abscess  and  that  due  to  cervical  caries  are  opened  by  incisions  through 
the  neck,  generally  along  the  posterior  border  of  the  sterno-mastoid. 

Retro-  (Esophageal  Abscess  is  due  to  spinal  caries,  diphtheritic  pharyn- 
gitis, a  caseous  mediastinal  gland,  or  extension  of  suppuration  from  other 
parts.  The  correct  diagnosis  may  be  impossible.  Dyspnoea  is  present  to 
a  certain  extent  in  all  cases,  and  in  many  is  a  prominent  and  urgent  symptom, 
with  recession.  The  voice  is  little  or  not  at  all  affected.  Cough  is  present, 
perhaps  for  some  months,  and  may  be  croup-like  or  metallic,  suggesting 
laryngeal  mischief,  stenosis  or  pressure  lower  down.  Unless  the  abscess 
is  partly  retro-pharyngeal  dysphagia  is  absent,  for  the  oesophagus  is  easily 
pushed  to  one  side.  It  may  occur  temporarily  from  rupture  into  the 
oesophagus.  There  may  be  swelling  in  the  neck  on  both  sides,  tenderness, 
pain  on  movement  and  fever.  Some  of  these  abscesses  burst  into  the 
oesophagus  or  burrow  into  the  tissues  of  the  neck.  Eupture  into  the 
oesophagus  may  be  followed  by  secondary  stenosis  or  a  diverticulum. 
The  abscess  must  be  opened  at  the  posterior  edge  of  the  sterno-mastoid, 
and  the  child  fed  nasally,  if  unable  to  swallow. 

The  (Esophagus. —  Congenital  Malformations — Inflammation —  Ulcer — 
Foreign  Bodies. — The  oesophagus  appears  in  the  foetus  at  the  end  of  the 
fifth  week  as  a  cylindrical  tube.  In  birds,  fishes  and  reptiles  it  persists 
as  an  impervious  cord  for  a  long  time.  Complete  absence  has  been 
recorded  in  5  cases  up  to  1902.  More  commonly  it  is  obliterated  or  partially 
stenosed.  Other  malformations  are,  a  double  tube  with  reunion  at  the 
lower  end — very  rare  ;  diverticula  or  pouches,  situated  in  the  middle 
line  and  not  causing  symptoms  till  late  in  life,  but  possibly  of  primary 
congenital  origin  ;  fistulous  communication  with  the  trachea  or  bronchus, 
generally  associated  with  atresia  ;  fistula  of  the  neck,  due  to  imperfect 
closure  of  the  second  and  third  branchial  arches  involving  the  oesophagus  ; 
the  lower  end  opening  into  the  trachea  just  above  the  bifurcation,  while 
the  upper  one  ends  in  a  dilated  cul-de-sac. 


-246  Chapter   XXL 

Atresia  or  Occlusion  is  more  frequent  than  supposed.  Hirschsprung 
collected  14  cases.  11  verified  post  mortem,  of  which  no  less  than  7  occurred 

in  the  Copenhagen  Lying-in  Hospital  during  16  years.  Thomas  (1904) 
added  6  more  ;  and  YiUeniin  (1904)  another  one.  The  occlusion  is  situated 
at  the  junction  of  the  oesophagus  with  the  pharynx,  or  in  any  portion  of  the 
tube.  In  the  most  common  variety  the  upper  part  ends  in  a  dilated  blind 
pouch,  and  the  lower  one  opens  into  the  bronchus  or  trachea,  generally 
just  above  the  bifurcation  or  below  the  larynx.  In  the  less  common  type 
the  segments  are  united  by  a  fibrous  or  muscular  cord  \-l  in.  long.  It  is- 
due  to  maldevelopment  of  the  tracheo-cesophageal  septum,  and  is  often 
associated  with  other  defects  of  the  gut. 

The  child  regurgitates  all  its  food  through  the  mouth  and  nose,  and 
has  severe  choking  fits  with  cyanosis  from  entrance  of  food  into  the  larynx. 
It  is  hungry,  micturition  scanty,  the  bowels  cease  to  act.  and  it  dies  from 
inanition  in  a  few  days.  Life  may  be  prolonged  by  rectal  feeding  and 
gastrostomy.  The  diagnosis  is  confirmed  by  the  finger  in  the  pharynx 
or  by  passing  a  bougie. 

Stenosis  or  Stricture  is  congenital  or  acquired.  Diffuse  dilatation  is 
rare  and  may  be  due  to  muscular  atony  and  cardiospasm.  A  congenital 
stricture  is  commonly  situated  at  or  below  the  bifurcation  of  the  trachea. 
It  varies  in  length,  usually  about  -J-l|-  ins.,  and  is  fibrous  in  structure. 
Above  the  stricture  the  tube  is  more  or  less  dilated.  More  rarely  a  partial 
stenosis  is  due  to  a  fold  of  mucous  membrane,  like  a  diaphragm,  at  the 
upper  or  lower  end.  The  minimum  diameter  of  the  oesophagus  in  the 
newborn  is  4  mm.,  and  the  distance  from  the  gums  to  the  cardiac  end  of  the 
stomach  is  17  cm.  A  soft  catheter  is  passed  for  diagnosis.  It  may  go  into 
the  trachea.  Symptoms  rarely  develop  until  6-18  months  after  birth,  and 
consist  of  regurgitation  of  food,  without  nausea  and  often  mistaken  for 
vomiting.  Food  is  generally  retained  unless  regurgitated  at  once  ;  that 
brought  back  has  an  alkaline  reaction,  unless  acid  to  start  with.  The  appetite 
is  D'ood,  but  the  child  becomes  pale  and  emaciated. 

Acquired  stricture  is  most  common  at  3-9  years  of  age,  due  to  swal- 
lowing  caustic  potash  (lye).  In  Norway  and  Sweden,  where  lye  is  used 
instead  of  soap  for  cleaning  purposes,  it  is  drunk  by  children  in  mistake 
for  milk.  The  burns  on  the  lips,  tongue  and  pharynx  may  be  slight  and 
even  absent,  though  marked  in  the  middle  or  lower  end  of  the  oesophagus. 
The  stricture  is  ring-like  or  tube-like,  and  usually  in  the  upper  third.  It 
may  be  complete  and  cause  rapid  inanition  ;  or  incomplete  and  intermittent, 
partly  due  to  spasm  on  deglutition.  Symptoms  come  on  after  2  or  3  weeks. 
A  bougie  may  be  used  3  or  4  weeks  after  the  injury,  and  then  3  times  weekly 
for  6  months.  The  general  treatment  of  stricture  is  dilatation  by  bougies, 
preceded  by  gastrostomy  and  dilatation  from  below  upward,  if  the  stricture 
is  complete  and  the  tube  dilated  above. 

Oesophagitis  ma.y  be  caused  by  infectious  disease,  but  is  more  commonly 
due  to  caustics,    acids  and  hot    water.       Diphtheria    causes    longitudinal 


The   Throat,  Pharynx,  and  (Esophagus.  247 

erosions  with  sharp  cut  edges  covered  with  membrane,  or  the  whole 
tube  is  covered.  In  scarlet  fever  the  inflammation  is  diffuse  and  secondarv 
ulceration  ragged.    It  is  due  to  extension  from  the  throat  and  mav  end  in 

stenosis.  Slight  burns  produce  superficial  nee:  sis.  Severe  ones  cause 
extensive  destruction.,  ulceration,  cicatrisation  and  stricture.  Bloodv 
mucus  and  even  portions  of  mucous  membrane  are  brought  up.  L~e 
is  fatal  in  25  per  cent.,  sulphuric  acid  in  50  per  cent.  (v.  Hacker).  Serious 
stricture  follows  in  50  per  cent.,  of  which  one-third  are  fatal.  Sloushinsr, 
haemorrhage,  perforation,  cellulitis,  media  stinitis,  pyopneumothorax 
and  emphysema  of  the  skin  may  occur. 

Ulcer  may  be  due  to  perforation  bv  a  caseous  gland  or  to  a  broken-down 
pock  in  variola.  More  extensive  ulceration  follows  on  inflammation. 
Simple  ulcer  is  rare,  and  is  probably  a  peptic  ulcer  dependent  on  frequent 
vomiting.  A  few  cases  are  on  record  in  which  a  simple  ulcer  has  been 
found  just  above  the  cardia,  or  at  its  junction  with  the  oesophagus,  in  the 
first  few  days  of  life  ;    death  being  due  to  haematemesis  or  melaena. 

Foreign  Bodies  are  often  passed,  per  amun,  without  trouble  after  a 
period  of  time  varying  with  the  nature  of  the  object  and  the  age  of  the 
patient.  Sometimes  they  stick  in  the  pharynx,  or  more  often  just  behind 
the  level  of  the  upper  notch  of  the  sternum.  Occasionally  they  pass  through 
the  stomach  or  intestine  into  the  subcutaneous  tissue  of  the  abdominal 
wall,  and  even  to  more  distant  parts.  Sometimes  they  are  wilfully  intro- 
duced, e.g.,  corks.  The  most  common  foreign  body  is  a  coin  which  has  been 
put  in  the  mouth  and  accidentally  swallowed.  Coins  lodge  at  the  commence- 
ment of  the  oesophagus,  just  above  the  cardia  or,  most  frequently,  oppc - : 
the  bifurcation  of  the  trachea  at  the  level  of  the  upper  limit  of  the  sternum 
and  the  junction  of  the  seventh  cervical  and  first  dorsal  vertebrae.  Here 
there  is  a  slight  fusiform  dilatation,  due  to  constriction  by  the  transverse 
aorta  passing  just  below.  The  coin  lies  against  the  anterior  wall  and 
fluid  food  can  pass  behind.  The  distance  from  the  upper  incisors  in  infants 
to  the  lower  end  of  the  coin  is  15  cm.  It  may  give  rise  to  brassy  cough, 
regurgitation  of  food,  inability  to  swallow  solids,  fever  and  symptoms  of 
ulceration,  such  as  foul  smelling  material  brought  up  at  intervals.  Although 
coins  have  been  retained  for  months  and  even  years,  and  then  vomited  or 
coughed  up.  the  dangers  of  ulceration  are  so  grave  that  they  should  bo 
removed  at  once.  The  child  is  examined  and  the  coin  removed  while  in  a 
sitting  posture  in  front  of  the  X-ray  screen,  or  anaesthetised  and  horizontal. 
Bougies,  probangs  and  coin  catchers  are  dangerous  in  cases  of  long  standing, 
and  in  recent  ones  may  push  the  coin  further  down.  Forceps  or  Kirrnesson*s 
single  hook  should  be  used:  sometimes  ceso]  :: :. _.:omy  is  necessary.  A 
recently  swallowed  foreign  body  may  sometimes  be  dislodged  by  inducing 
forcible  ret;hing  with  a  tongue  depressor  or  by  emetics.  Such  treatment 
is  dangerous  if  the  body  is  rough  or  pointed.  Substances,  such  as  a 
bolus  of  unmasticated  food,  stuck  in  the  fauces  can  be  dislodged  by  the  finger, 


CHAPTER    XXII. 

THE    STOMACH. 

Malformations  —  Dilatation  —  Gastric  Contents  —  Signs  of  Gastric  Disease 
—  The  Appetite  —  Pica —  Vomiting  —  Regurgitation  —  Rumination — 
Functional  and  Inflammatory  Disorders — Gastric  and  Duodenal  Ulcer. 

At  birth  the  stomach  is  almost  cylindrical  and  is  placed  obliquely  in 
the  epigastrium.  The  cardiac  end  is  just  to  the  left  of  the  tenth  dorsal 
vertebra.  The  pylorus  is  in  the  middle  line  and  is  the  lowest  segment  when 
the  stomach  is  empty.  The  fundus  is  relatively  flat,  gradually  develops 
and  becomes  more  and  more  transverse.  The  gastric  capacity  is  discussed 
in  the  chapter  on  diet  (p.  52).  Malformations  are  rare.  Sometimes  the 
stomach  is  situated  in  the  thorax  as  part  of  a  diaphragmatic  hernia. 
Hour-glass  contraction  is  a  pathological  curiosity,  probably  secondary  to 
ulceration.  It  is  usually  in  the  middle  third,  less  often  near  the  pylorus. 
It  has  not  been  found  in  the  foetus.  Post  mortem  constriction  must  not  be 
mistaken  for  true  hour-glass  contraction.  Diverticula  have  been  found 
arising  from  or  near  the  pyloric  Canal,  and  containing  pancreatic  tissue. 
Accessory  pancreatic  tissue  is  not  uncommon  in  the  walls  of  the  stomach 
and  duodenum. 

Acute  Dilatation  is  rare.  It  may  occur  from  no  apparent  cause.  A 
healthy  breast-fed  infant,  9  months  old,  was  found  dead  in  bed  two  hours 
after  being  suckled.  The  stomach  was  enormously  distended  with  gas 
and  contained  a  small  quantity  of  clotted  milk  (Belilos,  1903).  A  healthy 
bottle-fed  infant,  11  months  old,  was  laughing  and  playing  on  its  mother's 
knee  shortly  after  being  fed,  when  it  seemed  to  stop  breathing,  "  made  a 
noise  in  its  throat,"  and  died.  The  stomach  contained  19  oz.  of  fairly 
thick  Mellin's  food  and  gas  (P.  E.  Cooper,  1903).  Similar  dilatation  may 
occur  in  acute  diseases,  e.g.,  scarlatina,  typhoid,  pneumonia  and  pericar- 
ditis ;  and  less  often  in  chronic  illness.  It  is  a  rare  sequel  after  chloroform 
anaesthesia,  probably  due  to  paralysis  of  the  solar  plexus.  This  variety  causes 
enormous  distension,  excessive  green  vomiting  and  constipation.  Some- 
times the  pylorus  and  duodenum  are  also  widely  dilated.  It  is  treated  by 
lavage,  strychnia  sub  cutem,  and  no  fluid  by  mouth. 

Chronic  Dilatation  in  a  mild  form  is  almost  invariable  in  the  bottle-fed, 
from  excess  of  food.  Rickets  is  an  important  cause.  The  unsuitable 
food  which  has  caused  the  disease  is  liable  to  undergo  fermentation  and 


The  Stomach.  249 

set  up  catarrh,  and  the  muscle  wall  is  atonic.  Dilatation  is  common  in  all 
pulmonary  affections  in  infants  and  may  prove  fatal  by  upward  pressure 
on  the  diaphragm.  It  is  a  characteristic  feature  in  pyloric  obstruction 
(q.v.).  Symptoms  may  be  limited  to  those  of  chronic  dyspepsia,  unless 
there  is  pyloric  obstruction,  when  characteristic  vomiting  and  visible 
peristalsis  ensue.  The  outline  of  the  greater  curvature  is  easily  seen. 
The  treatment  is  that  of  the  cause,  plus  lavage  and  strychnia. 

Gastric  Contents. — The  reaction  is  neutral  or  feebly  alkaline  after 
human  milk,  and  slightly  acid  or  alkaline  after  cow's  milk.  It  is  distinctly 
acid  in  15  minutes,  but  free  HC1  is  said  by  some  observers  to  be  only 
found  in  the  fasting  stomach.  In  the  full  stomach  the  acid  is  partly  trans- 
formed into  acid  salts.  Fatty  acids  are  often  present,  lactic  acid  some- 
times, and  rennet  ferment  always.  In  suckling  infants  the  contents  are  not 
infrequently  streaked  with  altered  blood,  due  to  slight  congestion  from 
unusual  digestive  processes.  Organisms  are  much  more  numerous  in  the 
bottle-fed  than  the  breast-fed.  They  are  insufficiently  numerous  to  affect 
digestion,  and  vary  little  in  number  at  different  periods  of  digestion.  The 
most  frequent  are  B.  lactis,  staphylococci,  B.  subtilis,  B.  butyricus  (if 
cow's  milk  is  given),  and  o'idium  albicans  (if  there  is  thrush). 

In  dyspepsia  tough  mucus  is  frequently  present,  together  with  lactic, 
acetic  and  butyric  acids.  The  percentage  of  HC1  may  be  abnormally 
high  in  subacute  attacks.  Atony  is  due  to  dyspepsia  and  persists  for  some 
days  after  symptoms  have  subsided.  Food  stays  an  abnormally  long 
time  in  the  stomach.  Examination  of  the  gastric  contents  after  lavage 
affords  information  as  to  the  nature  of  the  contents,  degree  of  digestion, 
and  the  mobility  of  the  stomach.  The  conclusions  drawn  must  not  be 
dogmatically  insisted  upon  as  reliable. 

The  Signs  of  Abdominal  Disease  include  not  only  those  indicative  of 
gastric  disturbance,  but  also  those  of  intestinal  and  peritoneal  origin. 
Inspection  may  show  umbilical  peculiarities,  general  distension  or  retrac- 
tion, dilatation  of  superficial  veins,  ecchymoses,  peristalsis  and  the  outlines 
of  the  stomach,  small  intestine  and  colon.  The  abdomen  is  normally 
prominent  in  the  child  up  to  about  puberty,  on  account  of  the  relatively 
narrow  thorax,  flat  pelvis  and  large  liver.  The  protuberance  is  exaggerated 
by  intestinal  fermentation  and  muscular  weakness.  Palpation  reveals 
local  tenderness,  enlarged  glands  or  tumours,  and  the  position  of  normal 
organs.  Sometimes  it  must  be  done  in  a  warm  bath  or  under  anesthesia. 
Percussion  is  always  necessary  and  rectal  examination  frequently. 
Note  alterations  in  the  shape  of  the  abdomen,  unilateral  swelling, 
general  distension  by  gas  {tympanites)  and  by  fluid  (ascites),  and  local 
distension. 

The  Symptoms  include  anorexia,  flatulence,  nausea,  vomiting,  hamiat- 
•emesis,  alterations   in   frequency  and  character  of  the  stools,  and  pain. 


250  Chapter   XXII. 

Pain  may  be  of  extra-abdominal  origin.  The  pain  of  spinal  caries  may  be 
referred  to  the  epigastrium  ;  that  of  pneumonia  or  pleurisy,  especially 
diaphragmatic  pleurisy,  to  the  epigastrium  or  iliac  fossa,  and  if  on  the 
right  side  it  may  be  mistaken  for  appendicitis  ;  and  that  of  hip-disease 
referred  to  the  iliac  fossa.  Kheumatic  myalgia  may  produce  paroxysmal 
attacks  of  pain  in  one  or  other  hypochondrium.  Intra-abdominal  pain 
(Gastralgia  or  Enteralgia)  is  more  commonly  due  to  intestinal  than  to 
gastric  causes.  Gastric  pain  is  due  to  hyperacidity,  dyspepsia,  inflammation 
and  ulceration. 

The  Appetite. — Refusal  of  food  is  due  to  anorexia  or  dysphagia.  Anor- 
exia depends  on  lack  of  appetite,  and  this  is  present  in  febrile  and  toxaemic 
affections,  in  digestive  and  gastric  disorders,  and  mere  debility.  Swal- 
lowing is  difficult,  painful  or  impossible  in  affections  of  the  mouth,  fauces 
and  pharynx  ;  in  malformations  of  these  regions  ;  in  dyspnoea  due  to 
nasal  obstruction  in  infancy  ;  from  diphtheritic  palsy  and  inco-ordination 
of  the  muscles  of  swallowing,  possibly  sometimes  congenital ;  and  in  mental 
defects.  Increased  appetite  (Bulimia)  is  produced  by  thirst,  persistent 
over-feeding,  acid  dyspepsia,  and  occasionally  by  cerebral  tumour. 

Pica,  dirt  eating  or  depraved  habit,  is  a  curious  perversion  of  taste 
which  begins  at  6-18  months  of  age,  or  even  later.  The  child  eats  earth,, 
gravel,  coals,  cinders,  sand,  paper,  hair,  wool,  plaster,  paint  off  toys  and 
even  faeces.  All  babies  do  so  to  a  certain  extent,  through  putting  every- 
thing they  get  hold  of  into  the  mouth.  The  habit  is  due  to  a  neurotic 
heredity,  mental  defect,  lack  of  normal  instinct,  hallucination  of  taste, 
or  alimentary  disturbance  and  worms.  It  is  increased  by  ennui,  and  may  be 
limited  to  a  single  article.  When  indulged  in  to  excess  or  in  variety,  it 
causes  ill-health,  wasting,  sallowness,  anaemia,  colic  and  diarrhoea.  If  the 
habit  is  inveterate,  it  indicates  a  morbid  perversion  of  taste,  but  must  not 
by  itself  be  regarded  as  proof  of  imbecility.  It  tends  to  spontaneous 
recovery  in  the  third  or  fourth  year  of  life,  when  the  interests  widen,  though 
it  may  persist  up  to  puberty  or  adolescence.  Keep  the  child  away  from 
the  desired  article.  Attend  to  the  digestion  and  general  health.  Remove 
worms.  Change  the  surroundings  and  keep  the  patient's  mind  occupied  and 
interested. 

Vomiting. — True  vomiting  is  accompanied  by  pallor,  nausea,  facial 
distortion  and  violent  effort.  In  functional  or  nervous  vomiting  the 
contents  of  the  stomach,  usually  fluid,  are  brought  up  without  effort. 
Regurgitation  or  Over-flow  Vomiting  in  infancy  is  due  to  overdistension  of 
the  stomach,  followed  by  contraction.  The  food  is  brought  up  in  mouth- 
fuls,  without  effort  and  without  nausea,  a  few  minutes  after  it  has  been 
swallowed  and  perhaps  for  sometime  after.  At  first  it  only  occurs  imme- 
diately after  feeding  and  the  food  brought  back  is  unchanged.  Later,  it 
may  be  altered,  sour  and  acrid,  and  contain  curds,  mucus  and  even  bile. 
All  the  signs  of   infantile  dyspepsia  ensue,  viz.  pallor,  restlessness,  pain, 


The  Stomach.  251 

flatulence  anorexia  and  malaise.  The  stomach  is  dilated  and  its  motility 
impaired.  Organic  acids  and  bacteria  are  increased,  and  free  HC1  is  absent. 
Regurgitation  is  also  induced  by  eructations  of  gas,  by  pressure  on  the 
stomach,  and  by  up-and-down  jogging  movements  after  food.  Sometimes 
a  whole  feed  is  regurgitated  at  once,  the  result  of  it  being  swallowed  too 
quickly.  Regurgitation  is  associated  with  constipation  at  first,  and  later 
on  with  diarrhoea,  often  green  stools,  from  fermentation.  Uncontrollable 
vomiting  in  infants  may  be  due  to  some  undiscoverable  quality  in  the 
mother's  milk.  Habit  Vomiting  is  an  exaggerated  kind  of  regurgitation 
which  may  persist  for  years.  Occasionally  it  is  associated  with  chronic 
dyspepsia  and  a  dilated  stomach.  In  some  respects  it  is  analogous  to 
rumination.  It  is  painless,  quiet  and  easy,  without  nausea,  loss  of  appetite 
or  gastric  affection.  Some  babies  seem  able  to  make  themselves  sick  on  the 
least  provocation,  and  are  difficult  to  get  on  to  more  solid  diet  because  of  it. 
They  may  have  to  be  fed  many  times  in  succession,  although  each  feed  is 
vomited,  in  order  to  overcome  the  habit.  Such  babies  are  neurotic,  excitable 
children  who  have  been  rather  badly  managed.  A  trained  nurse  may  be 
necessary  for  some  days.  The  treatment  for  regurgitation  in  its  mildest 
form  consists  in  reducing  the  quantity  of  each  feed  and  giving  it  more 
slowly.  Starvation  and  lavage  are  only  necessary  if  there  is  secondary 
gastric  irritability. 

Rumination  or  Merycism  is  a  variety  of  regurgitation  in  which  the 
food  is  returned  into  the  mouth,  after  a  meal,  in  definite  and  limited 
amounts,  and  is  again  chewed  and  swallowed.  "  Merycism  "  is  derived 
from  a  Greek  word,  meaning  "to  chew  the  cud."  The  first  case  was 
described  by  Fabricius  ab  Aquapendente,  in  1618.  It  has  been  said  to 
be  associated  with  rudimentary  horns  on  the  forehead.  Out  of  100  cases, 
collected  by  Sachs,  of  such  horns  only  one  was  a  ruminant.  It  occurs  in 
all  classes  ;  is  more  or  less  hereditary  (5  generations  ;  Brockbank,  1907), 
and  affects  both  sexes.  It  generally  dates  from  early  childhood  or  infancy, 
or  does  not  begin  until  10-20  years  of  age.  It  has  been  acquired  by  imitation, 
and  has  followed  infectious  disease  and  stomach  troubles.  It  is  an  involun- 
tary act,  sometimes  under  the  control  of  the  will,  beginning  a  few  minutes 
after  a  meal  and  continuing  for  an  hour  or  more.  It  may  be  influenced  by 
diet,  and  is  most  apt  to  follow  meat  and  eating  too  quickly.  The  process  is 
quite  pleasant  unless  the  stomach  is  out  of  order. 

Vomiting  is  a  symptom  of  many  conditions  and  is  caused  by  direct 
action  on  the  gastric  mucosa,  reflex  stimulation  of  the  vagus  centre  in  the 
medulla  or  direct  stimulation  of  it  by  the  blood,  alterations  in  blood 
pressure  and  by  impulses  from  higher  parts  of  the  brain,  e.g. — 

(1)  Unsuitable  ingesta.    Overfeeding.    Dietetic  errors. 

(2)  Inflammatory   affections    and   functional    disorders    of   stomach, 

intestines  and  peritoneum. 


252  Chapter   XXII. 

(3)  Obstructive  disorders  of  the  alimentary  canal  : — 

(a)  In  the  lumen — foreign  bodies,  impacted  faeces,  worms. 

(b)  Stenosis  or  atresia. 

(c)  Intussusception,  volvulus,  hernia. 

(d)  Pressure  on  the  gut  from  without. 

(i)  Toxaemia  : — 

(a)  Uraemia.     Ptomaine  poisoning.     Febrile  states.     Anaesthetics. 

(b)  Diphtheria.     Acetonaemic  states  (q.v.). 

(5)  Febrile  Vomiting — chiefly  toxic,  partly  due  to  arrested  digestion. 

(6)  Mechanical — due  to  paroxysmal  cough. 

(7)  Nervous  : — 

(a)  Functional— Habit    vomiting,    hysteria,    anorexia     nervosa, 

migraine  (?),  recurrent  vomiting  (?). 
(6)  Organic — Tumours,  meningitis,  hydrocephalus,  concussion. 

(c)  Keflex — Pharyngeal  irritation,  teething,  irritants  in  stomach 

and   intestines,    intestinal    obstruction,    passage    of    calculi, 
worms  (?). 

(8)  Excessive  heat  or  cold. 

(9)  Offensive  sights  or  smells,  and  violent  emotion. 

(10)  Disturbances  of  equilibrium  : — 

(a)  Vertigo,  swinging,  mal  de  mer. 

(b)  Travelling  by  rail,  etc.,  especially  with  the  back  to  the  direction 

of  progress. 

The  treatment  of  vomiting  is  primarily  starvation.  Other  measures 
are  lavage,  counter-irritants,  drugs  and  nutrient  enemata.  Eecourse  may 
be  had  to  bismuth  and  alkalies,  dilute  HC1  and  nux  vomica,  cocaine  gr. 
Ttre-A  in  dr.  1  of  water  hourly,  creosote  gr.  2V  to  with  sugar  and 
aq.  anethi  two  hourly,  chloretone  gr.  -|,  tinct.  iodi  m.  1-5  in  glycerine 
and  water  hourly,  vin.  ipecac,  m.  |-1  or  liq.  arsenicalis  m.  1  before  food, 
resorcin  grs.  £-2  every  two  hours,  strong  black  coffee,  sips  of  very  hot  water 
or  iced  water.    Apply  a  mustard  leaf  to  the  epigastrium. 

Lavage. — Use  a  soft  rubber  No.  10-14  catheter  with  solid  end,  and  an 
internal  diameter  5  mm.  and  external  diameter  8  mm.,  attached  to 
a  rubber  tube  about  2  feet  long  and  a  funnel.  Pass  it  through  the  mouth, 
not  the  nose,  into  the  stomach  and  irrigate  with  boric  acid  or  sodium 
chloride  dr.  1  to  lukewarm  water  1  pint,  or  benzoate  of  soda  1-2  per  cent, 
strength.  Introduce  the  fluid  slowly.  Empty  the  stomach  and  repeat 
the  process  until  the  fluid  returns  clear.  The  baby  must  be  well  wrapped 
up,  including  the  arms,  for  lavage  often  causes  the  bowels  to  act.  Take 
the  child  on  the  lap,  and  support  it  with  the  left  hand  and   arm   while 


The  Stomach.  253 

passing  the  tube  with  the  right  hand.  For  older  children  the  sitting  posture 
and  a  gag  may  be  necessary,  and  two  people,  one  holding  the  child  with  the 
legs  between  the  knees,  and  the  head  steadied  by  the  left  hand  on  the 
forehead  and  pressed  against  the  chest.  Careful  lavage  is  very  rarely 
injurious.  In  rare  instances  it  has  caused  cessation  of  breathing  and 
convulsions. 

Gastric  Digestion. — Gastric  juice  in  babies  has  a  relatively  high 
acidity  and  recently  Sedgwick  has  found  in  the  stomach  contents  a  ferment, 
lipase,  which  splits  up  milk  fats  into  free  fatty  acids  producing  this  high 
acidity.  Ibrahim  (1909)  has  found  lipase  in  the  gastric  contents  and 
mucosa.  The  secretion  of  HC1  is  decreased  or  suppressed  in  slight  dis- 
turbances of  digestion  and  in  ill-health.  Normally  in  the  breast-fed  babe 
free  acid  appears  about  1J  hours  after  a  meal ;  in  the  bottle-fed,  2  hours. 
Though  secreted  immediately,  it  combines  at  first  with  the  protein  and 
alkaline  salts.  These  substances  are  greater  in  amount  in  cow's  milk  and, 
therefore,  the  acid  is  longer  appearing  in  the  free  state.  The  combined 
acid  has  no  bactericidal  power,  but  free  acid  has  an  inhibitory  effect  on 
microbial  growth.  Consequently  micro-organisms  will  grow  more  readily 
in  the  bottle-fed  than  in  the  breast-fed.  The  intervals  between  meals  should 
be  sufficiently  long  to  permit  the  secretion  of  free  acid  ;  and  longer  in  the 
bottle-fed  infants.  The  administration  of  diluted  HC1  after  a  meal  is  sound 
treatment  for  the  prevention  of  microbial  growth. 

Hyperchlorhydria  has  not  been  sufficiently  investigated  to  afford 
reliable  proof  of  the  actual  existence  of  an  excess  of  HC1.  The  total 
acidity  is  an  insufficient  test,  for  it  may  be  due  to  lactic  and  other  organic 
acids.  The  acidity  of  the  gastric  juice  is  decreased  by  any  condition  which 
increases  the  secretion  of  mucin.  The  rennet  enzyme  is  always  present 
and  pepsin  is  rarely  deficient.  The  action  of  rennet  ferment  on  cow's 
milk  differs  from  that  on  human  milk.  The  latter  does  not  clot  at  all  unless 
a  little  HC1  is  added,  and  then  it  only  forms  a  fine  flocculent  coagulum. 
Fresh  undiluted  cow's  milk  forms  a  coherent  clot  but,  if  it  is  sufficiently 
diluted  and  agitated,  the  clot  is  similar  to  that  formed  in  human  milk. 
Biedert  states  that  the  coagulation  of  cow's  milk  in  the  stomach  is  similar 
to  that  of  human  milk,  if  the  ratio  of  fat  to  protein  is  the  same.  Dilution 
with  egg  albumin,  gelatine  or  a  cereal  decoction  has  a  similar  effect  on  the 
clot.  It  is  dependent  on  the  degree  of  dilution  and  reduction  of  acidity 
rather  than  on  the  nature  of  the  diluent.  Some  chemists  have  ascribed  to 
rennet  the  power  of  dehydrating  peptone  and  converting  it  into  an  albumin. 
The  change  is  said  to  take  place  in  the  mucous  membrane  of  the  stomach 
and  intestines,  the  various  products  of  protein  digestion  being  converted 
into  a  substance  named  "  plastein,"  from  which  protein  tissues  are  built 
up.  According  to  Rotondi  the  rennet  ferment  acting  on  casein  splits 
off  a  protein  body,  which  is  soluble  in  acetic  acid  and  is  not  coagulable 
by  heat. 


254  Chapter  XXII. 

The  general  conclusions  from  the  study  of  gastric  digestion  in  babies  are 
that  rennet  ferment  is  always  present ;  that  pepsin  is  almost  invariably 
present ;  and  that  HC1  acid  is  often  decreased  in  amount,  sometimes  is 
entirely  suppressed,  and  occasionally  is  excessive. 

Dyspepsia. — In  dyspepsia  or  gastric  indigestion  the  secretory  function 
may  be  defective.  This  can  be  estimated  by  test  meals,  lavage  and 
chemical  tests.  The  gastric  juice  or  the  HC1  is  at  fault.  Dietetic  treatment 
depends  on  the  kind  of  disturbance.  Egg-white,  starch  and  sugar  are  inert, 
milk  and  gelatine  little  stimulating,  and  fat  actually  inhibits  secretion. 
Stimulants  of  secretion  include  salt,  meat  extracts,  condiments,  spices, 
alcohol,  and  palatable  food  generally  through  its  psychical  effect.  Bitters 
are  of  little  use  and  are  generally  disliked.  Equal  parts  of  the  tinctures  of 
nux  vomica,  orange  peel,  gentian  and  aniseed  are  sometimes  well  taken,  and 
useful  as  a  stimulant  for  the  appetite.  One  drop  in  water  should  be  given  to 
babies  before  breakfast  and  dinner.  Strychnia  gr.  ^^  can  be  given  in  syrup 
of  liquorice.  HC1  or  alkalies  before  meals  are  often  useful.  Bromides  and 
belladonna  reduce  secretion.      Burnt   magnesia  neutralizes  hyperacidity. 

If  the  defect  is  a  motor  one  it  is  due  to  hypotonicity,  defective  motility 
the  result  of  atony,  or  excessive  motility  set  up  by  pyloric  spasm.  The 
spasm  can  occasionally  be  relaxed  by  local  heat.  Atony  is  treated  by  small 
meals  of  soft  food,  strychnia  or  nux  vomica,  mineral  acids,  alcohol,  massage, 
douches  and  electricity. 

Sensory  disturbance  causes  hyperesthesia  and  is  treated  by  diet,  heat 
locally,  bismuth,  hydrocyanic  acid  and  bromides.  Anorexia  may  depend 
on  deficient  sensibility. 

Dyspepsia  in  the  Neivborn  gives  rise  to  slow  digestion  and  the  presence 
of  curds  in  the  stools,  or  the  vomiting  of  curdled  milk  in  1^-2  hours,  when  it 
shculd  have  passed  through  the  pylorus.  It  is  commonly  due  to  debility, 
erroneous  feeding,  and  dilatation  of  the  stomach  ;  and  it  sets  up  marasmus, 
if  unrelieved.  Lavage  generally  shows  that  the  gastric  juice  is  deficient  in 
HC1.  Dyspepsia  in  Infants  is  also  due  to  dietetic  causes  or  general  weakness, 
frequently  coincides  with  dilatation  of  the  stomach,  and  ends  in  marasmus. 
In  acute  cases  the  infant  should  be  starved  for  12  hours,  and  then  fed  on 
whey,  albumin  water,  barley  water,  weak  tea,  weak  broth  or  malted  milk. 
As  the  symptoms  subside  it  is  given  peptonised  milk,  and  finally  milk  and 
barley  water.  Teaspoonful  doses  of  lime  water  and  cinnamon  water  (p.a.) 
prevent  vomiting. 

Acute  Dyspepsia  or  Acute  Gastric  Indigestion  causes  pain  and  discom- 
fort, distension,  eructations  and  vomiting.  It  is  often  preceded  by  fever 
and  prostration  ;  or  by  languor,  discomfort  and  flatulence  ;  and  in  infants 
by  collapse.  Vomiting  occurs  some  hours  after  feeding  and  food,  mucus 
and  bile  are  brought  up.  The  chief  predisposing  factors  are  general  delicacy, 
rickets,  liability  to  catarrh,  chills  and  teething.  The  exciting  causes  are 
stale    and    indigestible    food,    foreign    bodies,    drugs,    and    exaggerated 


The  Stomach.  255 

irritability  of  the  mucous  membrane.  Overfeeding  in  infants  and  too  rich 
food  are  common  causes.  Some  attacks  follow  exposure  to  cold.  The 
nervous  symptoms  are  restlessness,  dulness  or  stupor,  and  convulsions 
which  may  be  fatal  in  infancy.  The  pulse  is  weak,  pupils  sometimes  con- 
tracted, and  prostration  severe.  The  tongue  is  furred  and  appetite  lost. 
Fever  rarely  lasts  more  than  a  few  hours,  but  may  be  very  high.  Attacks 
may  be  followed  by  gastric  catarrh,  colic  and  diarrhoea,  or  chronic  dyspepsia. 
Infants  waste  rapidly. 

General  treatment  consists  in  an  emetic  of  warm  water  or  lavage, 
heat  or  counter-irritants  to  the  epigastrium,  and  an  aperient  of  grey  powder 
or  calomel,  with  temporary  starvation  and  regulation  of  the  diet.  The 
child  is  quite  well  in  1-3  days,  but  is  liable  to  relapses  from  trivial  causes. 
Keturn  to  ordinary  diet  must  be  gradual. 

Chronic  Dyspepsia  in  Infants  is  a  common  infantile  ailment,  especially 
in  congenital  syphilis,  tuberculosis  and  marasmus.  Improper  diet  is 
the  great  cause.  The  tongue  is  furred  and,  later  on,  becomes  red  and 
dry.  Thirst,  wasting  and  constipation  are  frequently  present,  together 
with  regurgitation  of  food,  acid  eructations,  vomiting,  excess  of  mucus  in 
the  gastric  secretion,  abdominal  distension  and  pain.  The  infant  is  restless, 
has  a  variable  appetite,  frequently  develops  thrush,  and  suffers  from 
general  malnutrition.  The  disease  may  terminate  in  exhaustion,  anaemia, 
sudden  collapse,  thrombosis,  convulsions  and  coma,  just  as  in  marasmus 
from  other  causes.  Apart  from  prevention  the  treatment  depends  upon 
good  hygiene  and  nursing,  daily  lavage,  small  suitable  meals,  and  the 
administration  of  HC1.  Possibly  pepsin  is  beneficial,  and  sodium  salicylate 
if  there  is  much  flatulence. 

Chronic  Dyspepsia  in  Older  Children  is  often  overlooked  or  ascribed 
to  more  serious  disease.  Vomiting  is  uncommon,  constipation  predominant 
and  wasting  considerable.  It  is  especially  apt  to  follow  chills  from  insuffi- 
cient or  badly  applied  clothing,  notably  bare  legs  and  arms.  The  secondary 
indirect  or  reflex  symptoms  may  be  so  prominent  as  to  mask  the  true  cause. 
Some  children  come  under  observation  for  headache,  especially  in  the  morn- 
ing, giddiness,  disturbed  sleep,  pavor,  teeth  grinding  and  mental  depression. 
Palpitations,  cardiac  irregularity,  and  anginal  attacks  raise  the  fear  of 
heart  mischief.  In  other  cases  an  evening  rise  of  temperature  and  dry 
hacking  cough  suggest  early  phthisis.  Flatulent  distension  may  be  great, 
cause  pain,  and  give  rise  to  resistance  on  examination.  If  it  is  combined 
with  fever,  wasting,  and  alternate  diarrhoea  and  constipation,  it  suggests 
tuberculous  peritonitis,  but  the  doughy  feeling  of  the  abdomen  is  absent. 
The  association  of  headache,  mental  apathy,  teeth  grinding,  constipation, 
vomiting  and  irregularity  of  the  bowels  is  suspiciously  like  the  onset  of 
tuberculous  meningitis.  More  especially  is  this  the  case,  if  there  are  fits. 
Night  terrors  are  common.  Sometimes  there  are  syncopal  attacks.  Petit 
mal  must  be  carefully  excluded.     Occasionally  asthmatic  attacks,   with 


256  Chapter   XXII. 

cyanosis  and  rapid  breathing,  are  entirely  due  to  gastric  catarrh.  Often 
the  symptoms  are  ascribed  to  worms,  which  may  be  present  because  of  a 
chronic  catarrhal  condition  of  the  intestines. 

There  are  two  types  of  chronic  dyspepsia  :  (1)  Gastric  ;  (2)  Intestinal. 
Both  may  be  present  in  the  same  child.  It  is  often  difficult  to  distinguish 
between  them,  and  the  symptoms  as  described  above  are  partly  those  of 
gastric  conditions  and  partly  those  of  the  intestinal  affection.  The  latter 
disease  will  be  considered  more  fully  later.  In  the  differential  diagnosis 
considerable  stress  must  be  laid  upon  the  presence  of  the  furred  tongue, 
discomfort  after  meals,  and  gastric  dilatation  in  chronic  gastric  dyspepsia  ; 
and  the  absence  of  these  symptoms  in  that  of  intestinal  origins.  Gastric 
dyspepsia  is  very  frequent  in  marasmic  infants,  but  comparatively  rare  in 
older  children,  except  as  a  purely  temporary  condition  lasting  a  few  days 
or  a  complication  of  more  serious  illness.  On  the  other  hand  intestinal 
dyspepsia  is  seen  at  any  age  and  is  common  in  childhood. 

Simple  measures  of  treatment  are  sufficient  for  most  cases.  Light 
diet,  fresh  air,  exercise  and  hygiene  are  the  ordinary  measures  adopted. 
Grey  powder  and  rhubarb  are  given  every  2  or  3  days  ;  and  a  mixture  of 
sod.  bicarb.,  nux  vomica  and  tr.  rhei,  or  of  gentian,  soda  and  rhubarb, 
3  times  a  day  before  food  ;  or  a  HC1  mixture  after  meals.  Bicarbonate  of 
sodium  in  hot  water  or  Vichy  water,  on  rising  and  an  hour  before  meals, 
washes  out  the  stomach  and  dissolves  mucus,  and  thus  improves  the 
digestion.  No  syrups  should  be  prescribed  because  of  the  liability  to 
fermentation. 

Achylia  Gastrica  is  comparatively  rare  before  puberty.  It  gives  rise 
to  general  malnutrition,  abdominal  pain  and  chronic  diarrhoea,  though  the 
appetite  remains  good.  The  stools  are  liquid  or  pultaceous,  foetid  and  clay 
coloured.  They  contain  no  starch,  exceedingly  few  fat  droplets,  small  white 
granules  of  fatty  acid  needles,  little  connective,  tissue,  undigested  meat 
fibres  and  trypsin.  Examination  of  the  gastric  contents  after  a  test 
meal  shows  absence  of  rennet  and  HC1,  and  that  pepsin  is  either  greatly 
deficient  or  absent.  The  affection  is  a  disturbance  in  digestion  of  meat, 
but  not  of  fat. 

Acute  Gastritis  is  catarrhal,  ulcerative  or  membranous.  The  acute 
catarrhal  variety  is  due  to  cold,  unsuitable  diet,  alcohol  and  irritants. 
It  may  come  on  at  any  age,  even  in  babies,  and  is  sometimes  set  up  by 
champagne.  Occasionally  small  follicular  ulcers  are  formed  (follicular 
gastritis).  The  symptoms  are  those  of  acute  dyspepsia,  but  are  more 
severe  and  prolonged.  The  temperature  is  often  high  and  the  vomiting 
constant. 

Furred  tongue,  anorexia,  thirst,  languor  and  debility,  and  epigastric 
pain  and  tenderness  are  present,  just  as  in  acute  gastric  dyspepsia.  But 
the  vomiting  is  more  persistent,  the  thirst  more  intense,  and  the  local 
signs    are    exaggerated.      Sometimes    there    is    profound    collapse.      The 


The  Stomach.  257 

abdominal  pain  and  tenderness  may  be  so  severe  as  to  suggest  peritonitis. 
The  fever  and  acute  symptoms  are  worst  at  the  onset  and  subside  in  a  day 
or  two.  The  usual  duration  of  a  properly  treated  attack  is  3-7  days,  but 
it  may  be  prolonged  by  bad  management,  too  early  return  to  ordinary  diet, 
and  end  in  chronic  gastritis.  The  ulcerative  variety  is  secondary  to  a 
phlegmonous  gastritis,  with  necrosis  of  the  mucosa,  set  up  by  corrosive 
poisons  or  infectious  diseases,  such  as  smallpox,  measles,  scarlatina,  etc., 
and  pysemia.  The  necrosed  mucosa  may  be  vomited.  It  is  generally  fatal, 
if  due  to  corrosive  poisons.  The  treatment  of  acute  gastritis  is  by  alkalies 
bismuth,  and  the  methods  adopted  for  acute  dyspepsia.  For  corrosive 
poisoning  the  proper  antidote  is  given  and  then  oily  fluids,  milk  and 
albumin  water  ;   morphia  sub  cutem  ;   but  no  lavage. 

Membranous  Gastritis  is  characterised  by  the  formation  of  a  false 
membrane  over  all  or  part  of  the  mucosa.  The  membrane  is  composed  of 
exudation,  fibrin,  blood  cells  and  microbes.  A  boy,  18  months  old, 
admitted  under  my  care  for  rickets  and  constipation,  developed  bacteriuria, 
albuminuria,  nasal  discharge,  debility  and  vomiting.  A  small  dirty  yellow 
patch  was  present  on  the  tonsils  for  two  days  before  death.  The  oeso- 
phagus contained  much  membrane  in  the  upper  third.  In  the  stomach 
almost  surrounding  the  pyloric  half,  but  not  quite  reaching  the  pylorus, 
that  is  in  the  pyloric  vestibule,  was  an  intensely  engorged  hemorrhagic 
area,  partly  covered  with  adherent  yellow  membrane.  Diphtheria  bacilli 
were  recovered  from  the  oesophagus  and  the  stomach. 

A  false  membrane  in  the  stomach  has  been  recorded  in  about  12  cases 
of  diphtheria,  4  of  pneumonia,  and  2  of  pulmonary  phthisis.  Diphtheritic 
inflammation  is  probably  always  secondary  to  diphtheria  of  the  throat  or 
respiratory  tract.  It  occurs  almost  exclusively  in  children  but  has  been 
reported  in  young  adults.  It  produces  isolated  patches  in  the  fundus ; 
streaks  of  membrane  radiating  from  the  fundus  to  pylorus  ;  and,  rarely, 
extensive  ulceration  or  a  universal  false  membrane.  Deficiency  of  HC1 
may  explain  the  preponderance  of  cases  in  the  young,  and  the  fact  that 
separation  of  the  membrane  takes  place  least  rapidly  at  the  pyloric  half. 
Probably  all  other  cases  of  membranous  gastritis  are  pneumococcal,  though 
a  few  may  be  due  to  other  organisms  or  to  aphtha?. 

Symptoms  may  be  absent,  or  variable  in  severity  up  to  distressing 
thirst,  frequent  and  uncontrollable  vomiting  and  bad  epigastric  pains, 
grafted  on  those  of  the  primary  disease.  Casts  or  shreds  of  membrane 
may  be  vomited.  Apart  from  this,  the  affection  cannot  be  diagnosed,  and 
usually  the  gastric  symptoms  are  put  down  to  the  severity  of  the  primary 
disease.  The  prognosis  is  bad.  Griinbaum's  (1902)  case,  probably  diph- 
theritic, recovered.  The  treatment  is  that  of  acute  gastritis  ;  allaying 
vomiting  and  feeding  by  rectum. 

Hair  Balls  are  not  uncommon  in  the  stomach  of  animals  which  lick 
themselves,  such  as  cows,  lambs  and  cats.     They  are  rare  in  human  beings, 

s 


258  Chapter   XXII. 

and  usually,  though  not  invariably,  in  girls  or  women  with  weak  intellects. 
The  habit  of  pulling  out  the  hair  may  develop  as  early  as  the  fifth  month 
of  life.  "Pernet  has  given  it  the  name  of  "  trichotillomania.''''  The  hair  is 
swallowed  and  by  the  action  of  the  stomach  is  felted  into  rounded  masses 
of  variable  size,  some  being  small  enough  to  pass  through  the  pylorus  and 
per  anum.  They  are  called  aegropiles.  They  may  form  a  complete  cast 
of  the  stomach.  The  symptoms  are  those  of  dyspepsia,  of  colic  and  diarrhoea, 
or  may  be  entirely  absent ;  the  hard  lump  in  the  stomach  being  dis- 
covered quite  accidentally.  Sometimes  there  are  vomiting  and  anorexia. 
Analogous  habits  are  those  of  eating  wool  off  blankets,  chewing  grass  or 
paper,  and  "  pica  "  or  dirt  eating.  The  diagnosis  is  easy,  if  the  condition 
is  suspected  and  the  habit  known  ;  otherwise  the  tumour  may  be  mistaken 
for  something  more  serious. 

Gastric  Ulcer. — Sim-pie  erosion,  due  to  haemorrhagic  extravasation,  is 
not  uncommon.  The  mucous  membrane  often  exhibits  hsemorrhagic 
patches,  with  blackish  centre  and  irregular  edges,  and  numerous  spots 
of  ecchymosis.  Minute  follicular  ulcers,  circular  and  multiple,  are  caused  by 
necrosis  of  solitary  glands.  They  are  common  in  infants  with  follicular 
gastritis,  frequent  in  children,  and  rare  in  adults.  Hoamatemesis  and  melsena 
neonatorum  may  be  due  to  erosions  or  follicular  ulcers.  Diffuse  ulceration 
is  produced  by  scalds,  corrosive  fluids,  poisons  and  diphtheria.  Severe 
scalds  cause  much  destruction  and  are  rapidly  fatal,  while  slighter  ones 
may  induce  cicatricial  contraction. 

Tuberculous  ulcers  are  of  two  types.  Some  are  minute,  round,  with 
thickened  edges,  and  perhaps  multiple  ;  others  are  large  and  irregular. 
The  small  ones  are  probably  due  to  a  blood  infection,  and  may  be  found  in 
any  fatal  case  of  tuberculosis.  The  large  ones  are  rare.  The  small  ones  are 
unimportant. 

The  simple  peptic  ulcer  is  acute  or  chronic.  An  acute  ulcer  is  circular 
or  oval,  sharply  defined,  more  or  less  perpendicular,  sometimes  funnel- 
shaped,  with  soft  edges,  no  surrounding  inflammatory  thickening  and  a 
base  in  the  muscular  or  serous  coat.  The  chronic  ulcer  is  large,  irregular, 
with  sloping  and  indurated  edges,  and  a  base  often  adherent  to  subjacent 
structures.  Chronic  ulcers  are  most  frequent  at  the  pyloric  and  acute 
ones  at  the  cardiac  end.  They  may  be  on  the  anterior  or  posterior  wall  ; 
on  the  lesser  or  greater  curvature.  In  number  they  vary  from  one  to  many, 
usually  single,  and  in  size  from  |-1  in.  or  more.  Under  the  age  of  10  years 
both  sexes  are  equally  liable.  The  simple  ulcer  is  most  common  in  the  first 
two  weeks,  and  rare  after  the  first  two  years  of  life. 

Etiology. — Some  cases  are  congenital,  due  to  a  natal  or  ante-natal  cause. 
Charcot  found  2  ulcers  in  the  stomach  of  a  G  months  foetus  affected  with 
smallpox.  Asphyxia  at  birth  may  induce  congestion  of  the  mucosa  and 
secondary  necrosis  or  haemorrhagic  erosion.  Subsequently,  an  ulcer  may  be 
due  to  an  acute  infection.    Thus  it  has  been  found  in  infectious  disease,  such 


The  Stomach.  25D 

as  varicella,  measles,  typhoid,  smallpox,  diphtheria,  noma,  empyema, 
pneumonic  affections,  and  after  burns.  Many  of  the  recorded  cases  have 
occurred  within  the  first  few  days  or  months  of  life. 

Symptoms  are  often  indefinite  and  irregular,  and  may  be  entirely  absent, 
an  unexpected  ulcer  being  found  after  death.  During  the  first  month  of 
life  there  may  be  hasmatemesis  and  melsena,  or  merely  restlessness  and 
signs  of  indigestion  or  gastric  catarrh.  After  this,  dyspepsia,  pain  and 
vomiting  are  more  common.  The  pain  is  situated  in  the  epigastrium,  is 
paroxysmal,  usually  not  severe,  comes  on  after  food  and  causes  vomiting. 
It  may  be  mistaken  for  colic.  It  is  relieved  by  vomiting.  Intense  pain 
indicates  bleeding  or  perforation.  In  older  children  the  pain  may  be  referred 
to  the  last  dorsal  or  the  first  lumbar  vertebra.  It  may  be  uninfluenced  by 
food.  Vomiting  is  most  common  if  there  is  follicular  gastritis.  In  older 
children  it  is  preceded  by  nausea,  occasionally  by  profuse  salivation,  and 
comes  on  when  the  pain  is  severe.  Hsematemesis  is  less  frequent  than 
vomiting.  It  may  follow  food,  exercise  or  emotion.  It  varies  in  quantity, 
may  occur  without  vomiting  and  give  rise  to  melaena.  The  vomited  blood 
is  bright  red,  brown  or  even  black.  The  tongue  is  generally  clean,  the 
appetite  unimpaired,  and  the  bowels  confined.  Sometimes  there  is  chronic 
dyspepsia  or  gastric  catarrh,  with  furred  tongue,  anorexia,  flatulence, 
pyrosis  and  dilated  stomach.  Diarrhoea  is  present  in  about  half  the  acute 
cases.  Fever  is  not  infrequent,  because  of  the  associated  infection.  The 
child  becomes  anemic,  emaciated  and  stunted.  On  examination  of  the 
abdomen  a  tender  spot  may  be  found  in  the  epigastrium  or  at  the  tip  of  the 
ensiform  cartilage,  and  in  chronic  cases  some  dilatation  of  the  stomach. 
Perforation  may  be  the  first  indication.  The  haematemesis  must  not  be 
mistaken  for  that  due  to  other  causes,  notably  blood  swallowed. 

Course  and  Prognosis. — Except  in  infants  fatal  haemorrhage  is  rare, 
but  may  occur  even  from  follicular  ulcers.  Perforation  and  secondary 
peritonitis  are  rare  in  newborns.  Fever  and  fits  may  be  due  to  peritonitis. 
Cases  have  ended  in  adhesion  to  the  diaphragm,  perforation  and  empyema ; 
in  death  from  chronic  malnutrition  and  asthenia,  peritonitis,  haemorrhage, 
or  some  intercurrent  disease.  In  Chvostek's  case  symptoms  began  at 
4  months  and  the  child  died,  small  and  emaciated,  at  18  years.  The 
stomach  was  enormously  dilated  and  there  was  some  pyloric  stenosis, 
with  a  chronic  ulcer  near  the  pylorus  and  a  recent  ulcer  near  the  cardiac 
end.  Donner  has  reported  a  healed  ulcer  at  3  years  of  age.  Probably 
75  per  cent,  recover,  though  most  of  the  cases  on  record  are  the  fatal 
ones.  Constitutional  debility  from  any  cause  helps  to  produce  an  ulcer 
as  well  as  prevent  its  cure.  Adhesion  to  neighbouring  organs  is  probably 
injurious  by  preventing  contraction  of  the  ulcer.  Hyperacidity  is  not 
necessarily  present,  but  is  harmful. 

Complications  include  dilatation  of  the  stomach,  pyloric  stenosis, 
haemorrhage,  perforation,  peritonitis,  local  abscess,  and  perforation  of  the 


260  Chapter  XXII. 

diaphragm.  Both  severe  bleeding  and  perforation  may  be  ushered  in  by 
great  pain.  Perforation  is  common  in  acute  cases  and  not  rare  in  chronic 
ones.  It  gives  rise  to  sharp,  sudden  abdominal  pain,  collapse  and  vomiting, 
and  may  end  fatally  in  two  hours.  In  one  case  it  caused  death  from  con- 
vulsions and  fever. 

The  treatment  is  similar  to  that  of  adults,  and  consists  of  careful  diet 
and  rectal  feeding.  The  chief  drugs  are  alkalies,  calcined  magnesia  and 
bismuth,  with  the  addition  of  small  doses  of  morphia  or  opium  for  the 
relief  of  pain.  The  beneficial  effects  of  horse  serum,  by  mouth  or  rectum, 
on  haemorrhagic  conditions  in  older  patients  render  it  worth  a  trial  in  these 
cases.    Perforation  is  treated  on  ordinary  surgical  principles. 

Duodenal  Ulcer. — A  considerable  number  of  cases  of  duodenal  ulcer 
have  been  found  in  melsena  neonatorum,  and  a  few  in  older  children,  but 
it  is  uncommon  after  the  first  two  weeks  and  quite  rare  after  the  first  year 
of  life.  Males  are  twice  as  often  affected  as  females.  The  ulcer  is  usually 
single,  situated  in  the  first  part  of  the  duodenum  just  below  the  papilla, 
and  of  the  simple  type.  Many  are  of  septic  origin  or  follow  extensive 
burns.  In  a  boy  of  8  months  haeniatemesis  and  perforation  ensued  on  acute 
eczema  becoming  impetiginous  (Borland,  1903).  In  a  child,  aged  10  months, 
the  ulcer  was  a  sequel  of  catarrhal  colitis  (Vanderpoel).  Others  are  possibly 
due  to  a  duodenitis,  of  septic  or  bacillus  coli  origin,  or  produced  by  hyper- 
acidity of  the  chyme  acting  on  a  patch  of  haemorrhagic  infiltration  or 
thrombosis. 

Symptoms  may  be  entirely  absent.  Restlessness,  constant  crying, 
meteorism,  abdominal  pain,  the  hands  placed  over  the  abdomen,  and 
rapid  emaciation  may  be  noted  in  infants.  There  may  be  melaena,  alone 
or  associated  with  haematemesis.  In  older  children  the  pain  comes  on  about 
2-4  hours  after  food,  and  is  due  to  contact  of  the  ulcer  with  the  acid  con- 
tents of  the  stomach.  It  extends  round  the  right  hypochondrium  and 
through  to  the  back.  Sometimes  a  tender  spot  is  found  a  little  above  and 
to  the  right  of  the  navel.  Constipation  and  anorexia  may  be  marked. 
In  other  cases  the  appetite  is  good,  pain  is  relieved  by  food,  and  the  symp- 
toms are  those  of  dyspepsia.  Perforation  may  be  the  first  sign.  Nephritis 
is  not  infrequent. 

It  may  lead  to  duodenal  stenosis,  obstruction  of  the  bile  and  pan- 
creatic ducts,  secondary  disease  of  the  gall  bladder  and  pancreas,  con- 
striction of  the  portal  vein,  and  local  abscess.  Operation  is  contra-indicated 
by  profuse  haemorrhage,  for  such  cases  die  in  a  few  hours.  The  treatment 
is  similar  to  that  of  gastric  ulcer.  Attacks  may  be  followed  by  periods  of 
latency. 


CHAPTER    XXIII 

THE    PYLORUS. 

Pyloric  Spasm — Congenital  Hypertrophic  Stenosis. 

Atresia  of  the  pylorus  is  almost  unknown.  Simple  congenital  stenosis 
has  been  put  forward  as  the  explanation  of  gastric  dilatation,  dyspeptic 
symptoms  and  vomiting,  which  have  started  in  infancy  and  persisted  into 
adult  life  ;  the  pyloric  canal  being  found  abnormally  small  at  operation. 
Such  a  small  canal  might  be  blocked  by  a  plug  of  inspissated  mucus  or 
swollen  mucous  membrane  in  gastric  catarrh.  Hall  (1906)  reported  the 
case  of  a  child,  aged  7  months,  who  had  persistent  vomiting  from  birth 
and  died  after  gastro-enterostomy.  A  plug  of  mucus  due  to  chronic  gastritis 
blocked  the  pylorus.  The  intestines  were  empty.  Pyloric  obstruction, 
due  to  enlarged  glands,  dermoids  or  new-growth ;  to  polypus  of  the  mucous 
membrane  ;  and  obstruction  by  impacted  food  or  foreign  bodies,  are  so 
rare  as  to  be  practically  negligible  in  children. 

Pyloric  Spasm  is  characterised  by  severe  and  continued  vomiting. 
Usually  the  food  is  brought  up  at  once,  but  a  considerable  quantity  may 
be  kept  down  and  then  violently  ejected.  This  type  of  vomiting  may 
begin  shortly  after  birth,  or  even  some  months  later,  and  continue  although 
the  child  is  apparently  properly  fed.  It  is  generally  started  by  improper 
feeding.  A  typical  case  was  that  of  a  breast-fed  girl  who  began  vomiting 
three  days  after  birth.  Vomiting  persisted,  with  constipation  and  wasting, 
for  11  weeks.  She  was  then  anaemic  and  emaciated,  but  no  dilatation  of 
the  stomach,  peristalsis  or  palpable  pylorus  could  be  demonstrated.  She 
died  the  next  day,  although  she  had  retained  26  oz.  of  whey.  The  pylorus 
showed  no  trace  of  stenosis  or  hypertrophy.  Similar  cases  may  start  at 
any  period  during  the  first  year  of  life,  but  in  my  experience  are  uncommon 
after  the  third  month. 

The  etiology  of  the  affection  is  doubtful.  It  is  probably  due  to  hyper- 
esthesia of  the  pyloric  mucosa,  started  in  the  first  instance  by  unsuitable 
food  or  local  erosion,  and  the  spasm  is  secondary  to  the  hyperajsthesia. 
These  cases  are  curable  by  a  diet  of  whey  or  albumin  water,  and  frequent 
small  doses  of  cocaine.  In  one  instance  it  was  necessary  to  give  the  child 
cocaine  and  teaspoonful  feeds  of  raw  meat  juice  every  £  hour  for  2  days, 
before  the  vomiting  stopped.  This  was  a  boy,  7  months  of  age,  who,  while 
breast-fed,  began  vomiting  in  the  seventh  week  of   life    and  continued 


262  Chapter  XXIII. 

until  breast-feeding  was  entirely  omitted  in  the  fifteenth,  week.  The 
severe  attack  might  be  regarded  as  a  recrudescence  of  a  milder  one  in 
earlier  life. 

The  most  important  point  in  these  cases  is  the  complete  absence  of 
pyloric  stenosis  or  hypertrophy  on  post  mortem  examination.  In  the  only 
two  fatal  cases  under  my  notice  the  pyloric  canal  was,  if  anything,  larger 
than  normal.  Some  of  them  may  exhibit  a  dilated  stomach  and  a  moderate 
degree  of  peristalsis  during  life.  The  successful  results  of  treatment  support 
the  hypothesis  put  forward  as  to  their  pathology. 

Congenital  Hypertrophic  Stenosis. — This  affection  has  been  described 
under  the  names  of  the  "  congenital  gastric  spasm,"  "  congenital  pyloric 
spasm"  "  congenital  pyloric  stenosis"  and  "  infantile  hypertrophy  of  the 
pylorus."  The  name  "  congenital  hypertrophic  stenosis  "  is  justifiable 
because  the  affection  is  congenital,  hypertrophy  or  hyperplasia  is  the 
main  feature,  and  it  leads  to  stenosis.  It  is  the  hypertrophy  that  is  con- 
genital not  the  stenosis. 

The  first  case  in  infancy  was  recorded  by  Williamson  in  1841.  In 
1898  I  collected  20  definite  cases,  including  2  of  my  own  ;  and  4  years  later, 
in  a  conjoint  paper  with  C.  T.  Dent,  we  were  able  to  collect  over  50.  Now 
there  are  probably  150  to  200  on  record,  and  references  in  the  literature  to 
anatomical  specimens  from  many  others.  Of  these,  21  have  come  under 
my  own  observation,  the  diagnosis  being  verified  at  operation  or  after 
death.  The  affection  is,  therefore,  by  no  means  uncommon,  and  must  be 
frequently  overlooked. 

Symptoms. — The  characteristic  features  of  a  typical  case  are  the  age 
of  the  child,  the  vomiting,  constipation,  wasting,  visible  peristalsis,  dila- 
tation of  the  stomach  and  a  palpable  pylorus. 

These  babies  are  normal  at  birth  ;  a  few  have  been  premature. 
Males  preponderate  to  a  remarkable  extent.  Only  5  out  of  21  were  females. 
They  come  under  observation  during  the  first  3  months  of  life.  The  symp- 
toms may  begin  within  a  few  hours  or  days  of  birth,  or  not  appear  until 
the  third  or  fourth  week  ;  occasionally  not  till  the  second  month  ;  rarely 
or  never  at  a  later  date.  Usually  they  begin  in  the  second  week.  They 
develop  just  as  readily  in  the  breast-fed  as  in  those  brought  up  in  other 
ways.  If,  as  often  happens,  partial  bottle-feeding  has  been  begun,  vomiting 
is  almost  always  ascribed  to  the  diet.  It  is  not  uncommon  for  a  child  to 
start  life  as  "  a  fine  baby  born,"  to  gain  weight  rapidly  for  2  or  3  weeks, 
and  then  to  begin  vomiting.  Lack  of  appetite  is  the  first  sign.  The  child 
does  not  take  the  breast  readily  or  is  very  soon  satisfied. 

Vomiting  is  likely  to  be  mistaken  for  regurgitation  at  first.  Later 
on  it  becomes  more  characteristic  and  forcible,  like  that  seen  in  older 
children.  The  contents  of  the  stomach  may  be  violently  ejected  to  a 
distance  of  three  feet.  In  typical  cases  two  or  more  meals  are  kept  down, 
and  then  the  whole  lot  is  brought  up  forcibly,  gushing  through  nose  and 


The  Pylorus.  263 

mouth,  or  shot  out  as  through  a  pump.  It  causes  some  pain,  but  the  babe 
is  more  comfortable  with  the  stomach  empty.  There  is  no  nausea  and 
food  may  be  taken  almost  immediately  afterwards.  If  the  stomach  is 
washed  out  twice  a  day,  and  it  is  already  chronically  dilated,  there  may 
be  no  vomiting.  The  absence  of  vomiting,  in  cases  treated  by  lavage,  is 
apt  to  be  misleading.  Vomiting  is  also  modified  by  the  degree  and 
acuteness  of  the  stenosis.  In  some  instances  there  is  little  obstruction 
and  no  vomiting,  if  appropriate  diet  is  given.  In  acute  obstruction  it 
may  be  as  severe  as  in  acute  gastritis  or  intestinal  obstruction,  withhsemat- 
emesis  of  coffee-ground  material.  The  vomited  matter  consists  of  the 
stomach  contents  and  is  free  from  bile.  It  often  contains  mucus,  from 
secondary  gastric  catarrh,  and  lactic  acid  or  hydrochloric  acid.  If  the 
stomach  is  washed  out  and  a  fresh  meal  given,  the  whole  may  be  recovered 
at  the  end  of  two  hours,  though  it  ought  to  have  passed  onward  into  the 
intestines. 

The  tongue  remains  clean  and  the  breath  sweet,  unless  gastric  catarrh 
is  set  up.  The  appetite  is  poor,  except  when  the  stomach  is  emptied.  Then 
food  may  be  taken  ravenously.  Pain  is  caused  by  over-distension,  if  food 
is  given  when  the  stomach  is  already  full. 

Constipation  is  marked  and  increases  in  severity.  The  stools  are  often 
devoid  of  faecal  material  and  resemble  brownish  or  dark  green  paint,  or 
meconium.  Occasionally  they  are  tarry.  They  consist  of  epithelial  debris, 
intestinal  secretions,  altered  bile  and  perhaps  blood.  If  the  obstruction  is 
not  continuously  complete,  faecal  matter  is  present,  and  the  stools  may  be 
many  and  watery  ;  the  result  of  enteric  catarrh  set  up  by  irritant  stomach 
contents.  It  is  quite  common  for  large  normal  stools  to  be  passed  during 
the  first  week  or  two  of  life,  and  the  constipation  to  then  develop  gradually. 

The  child  wastes  progressively,  sometimes  with  extraordinary  rapidity. 
The  body  surface  is  cold,  temperature  subnormal ;  the  pulse  small,  frequent, 
and  weak  ;  and  the  general  appearance  one  of  whining  lethargy  with  half- 
open  eyes  and  sunken  fontanelles. 

Visible  peristalsis  is  an  important  physical  sign.  It  is  best  elicited  by 
giving  a  fair  sized  meal,  or  "  a  comforter  "  to  suck,  by  flicking  the  stomach 
wall  with  a  finger,  or  by  the  application  of  a  cold  object.  The  stomach 
bulges  forward,  forming  a  swelling  about  the  size  of  half  a  golf  ball  in  the 
left  hypochondrium,  and  the  swelling  flows  over  like  a  wave  from  left  to 
right  to  the  pylorus  ;  and  occasionally  passes  onward  down  the  duodenum, 
showing  a  marked  constriction  and  a  momentary  stoppage  at  the  pylorus. 
The  unyielding  linea  alba  gives  the  stomach  during  peristalsis  an  hour-glass 
appearance.  The  peristalsis  is  most  marked  in  cases  of  long  duration. 
If  the  stomach  is  much  dilated  and  the  walls  weakened,  the  wave  does  not 
cause  so  marked  a  bulging  of  the  abdominal  wall.  A  mild  degree  of  peris- 
talsis is  often  visible  in  the  dilated  stomach  of  emaciated  children,  and 
must  not  be  mistaken  for  peristalsis  of  this  type. 


2G4  Chapter   XXIII. 

Dilatation  of  the  stomach  is  present  in  advanced  stages.  It  depends 
on  the  degree  and  duration  of  obstruction.  In  the  early  stages  it  is  absent, 
for  food  is  ejected  as  soon  as  the  stomach  is  over-distended.  Gradually  the 
stomach  becomes  dilated  and  holds  as  much  as  14  oz.  in  the  third  month  of 
life.  It  bulges  forward  the  epigastrium,  and  gives  the  lower  half  of  the 
abdomen  an  empty  or  retracted  appearance.  The  greater  curvature  is 
visible  through  the  thin  parietes  and  reaches  the  level  of  the  navel. 

The  pylorus  is  palpable  as  a  hard  lump  about  the  size  and  shape  of  a 
filbert,  sometimes  more  rounded  and  feeling  like  a  small  marble.  I  am 
convinced  that  it  does  not  alter  definitely  in  hardness  or  become  more 
palpable  during  peristalsis,  though  that  portion  of  the  stomach  adjacent 
to  it,  known  as  the  pars  pylorica  ventriculi  or  pyloric  vestibule,  may  contract 
and  give  rise  to  the  sensation  of  a  tumour.  In  the  adult  the  pars  pylorica 
has  been  seen  at  operation  to  contract  up  into  a  hard  tumour-like  mass, 
even  during  deep  chloroform  narcosis,  and  such  spasm  may  last  for  a  few 
seconds  only  or  continue  for  days,  but  there  is  no  true  hypertrophy.  This 
is  probably  the  explanation  of  some  cases  in  which  the  pylorus  is  said  to  be 
palpable  at  one  time  and  not  at  another.  In  infants  operated  on  for 
pyloric  hypertrophy,  a  wave  of  peristalsis  may  be  seen  at  the  time  of 
operation  to  pass  from  the  stomach  to  the  pylorus  without  causing  the 
least  change  in  its  consistency  or  appearance.  The  pylorus  is  felt  about 
J  in.  to  the  right  of,  and  §  in.  above  the  umbilicus,  roughly  midway  between 
the  umbilicus  and  the  costal  margin.  Occasionally  it  is  lower  down  and 
may  be  mistaken  for  an  enlarged  gland.  Sometimes  it  is  buried  beneath 
a  large  liver,  though  even  then  it  can  generally  be  felt.  It  is  more  or  less 
palpable  in  practically  every  case,  though  it  is  impossible  to  be  absolutely 
positive  in  well-nourished  infants.  The  examination  must  be  conducted 
with  warm  hands,  the  tips  of  the  fingers  being  gently  pressed  deeply  in  the 
pyloric  region,  and  slowly  moved  up  and  down.  In  wasted  babies  it 
may  be  possible  to  grasp  the  lump  between  the  fingers  in  front  and  the 
thumb  behind. 

Varieties. — Cases  may  be  divided  into  three  types.  The  majority  are 
typical  ones,  such  as  above  described.  Rarely  the  obstruction  is  acute, 
probably  in  consequence  of  oedema  of  the  mucous  membrane  of  the  pylorus, 
set  up  by  rapid  contraction  of  the  hypertrophied  muscle.  In  the  third 
variety  there  is  less  hypertrophy  and  the  muscle  does  not  contract  suffi- 
ciently to  cause  complete  obstruction.  Cases  of  this  type  may  live  for  years, 
e.g.,  4  years  (Hezekiah  Beardsley,  1788)  ;  5  years  (Sonnenberg)  ;  and 
11  years  (Hansy).  Probably  the  hypertrophic  stenosis  of  adults  is  due 
to  persistence  of  the  infantile  condition. 

Morbid  Anatomy. — The  normal  pylorus  is  a  constriction,  the  thickness 
of  an  old-fashioned  wedding  ring,  formed  by  the  circular  muscular  fibres. 
In  hypertrophic  stenosis  it  forms  a  hard,  elongated,  cylindrical  tumour, 
f-1  in.  long,  and  about  1J  in.  in  circumference  ;    a  solid  tumour  about  the 


The  Pylorus.  265 

size  of  the  last  joint  of  the  female  little  finger.  In  advanced  cases  it  is  hard, 
white  and  bloodless.  It  terminates  abruptly  at  the  duodenal  end,  projecting 
into  the  duodenum  much  as  the  os  uteri  projects  into  the  vagina,  and 
looking  like  it  when  viewed  from  the  duodenal  aspect.  On  the  gastric  side 
it  is  more  funnel-shaped,  but  ends  abruptly.  Microscopical  examination 
shows  that  the  enlargement  is  due  to  a  great  increase  in  the  circular 
muscular  fibres.  I  have  examined  many  specimens  and  am  convinced 
that  all  other  changes  are  secondary.  The  mucous  membrane  is  thrown 
into  folds  from  1-5  in  number.  Sometimes  one  fold  projects  as  a  ridge- 
like promontory  along  the  whole  length  of  the  canal,  in  the  same  way  as  the 
verumontanum  in  the  urethra.  It  may  be  congested  in  acute  cases.  It  is 
to  the  folds  of  the  mucous  membrane  that  the  complete  obstruction  is  due  ; 
and  these  folds  are  produced  by  the  gradual  or  spasmodic  contraction  of 
the  hypertrophicd  muscle.  No  stages  of  muscular  hyperplasia  are  found 
intermediate  between  the  normal  pylorus,  or  the  pylorus  of  infants  who 
suffer  apparently  from  pyloric  spasm,  and  that  of  infants  with  true 
hypertrophy.  Gastric  catarrh,  oedema  of  the  pyloric  mucosa  and  gastric 
dilatation  are  all  absent  at  the  onset  of  the  initial  symptoms. 

Pathology. — It  is  probable  that  nature,  in  her  extreme  anxiety  to 
provide  an  efficient  pyloric  sphincter,  has  produced  too  great  a  quantity 
of  muscular  tissue.  In  other  words  there  is  a  true  hyperplasia,  a  simple 
redundancy  of  foetal  growth.  The  pylorus  begins  to  be  formed  during  the 
third  month  of  foetal  life,  so  there  is  plenty  of  time  for  hyperplasia  to  take 
place  before  birth.  Such  hyperplasia  has  been  found  by  C.  T.  Dent  in  a 
7  months  foetus.  Possibly  it  represents  a  reversion  to  an  earlier  type  of 
pylorus,  for  the  circular  muscle  is  well  marked  in  the  pylorus  of  many 
mammals.  It  has  been  suggested  that  the  hypertrophied  pylorus  is 
analogous  to  the  "  gastric  mill  "  of  Crustacea,  the  "gizzard"  of  birds,  and 
the  "  gastric  mill"  of  edentata,  closely  resembling  that  of  the  great  ant- 
eater  and  some  armadilloes.  The  early  appearance  of  symptoms  and  the 
degrees  of  hypertrophy  present  in  cases  dying  within  a  few  weeks  of  birth, 
seem  quite  incompatible  with  post-natal  development.  Operation  within 
the  first  few  days  of  life  has  shown  the  presence  of  as  much  hyperplasia 
as  in  the  second  or  third  month. 

Thomson  holds  that  "  the  essential  lesion  is  not  a  muscular  but  a 
nervous  one  ;  a  functional  disturbance  of  the  stomach,  and  pylorus  leading 
to  ill-coordinated  and  therefore  antagonistic  action  of  their  muscular 
development."  This  hypothesis  assumes  the  occurrence  of  ill-coordination  ; 
it  assumes  that  antagonistic  muscular  action  and  muscular  hypertrophy 
are  the  result ;  and  it  assumes  that  this  nervous  derangement  can  occur 
in  foetal  life.  Thomson  suggests  that  it  is  set  up  in  foetal  life  by  liquor 
amnii,  which  may  be  swallowed.  It  is  difficult  to  understand  why  spasm 
should  only  occur  and  produce  hypertrophy  in  the  first  three  months  of 
life  and  not  at  a  later  age.     In  the  rare  cases  that  come  under  observation 


2G6  Chapter   XXIII. 

after  the  third  month,  the  symptoms  have  dated  from  early  infancy.  Spasm 
will  not  explain  the  cases  in  which  there  is  hypertrophy  and  little  or  no 
vomiting.  Those  adults,  whose  symptoms  are  put  down  to  pyloric  spasm, 
do  not  show  evidence  of  pyloric  hypertrophy  at  operation  or  after  death. 

There  is  no  evidence  that  the  spasm  is  set  up  by  erroneous  feeding  or 
by  hyperacidity.  Observations  by  Miller  and  Willcox  (1907)  are  of  value 
in  this  connection.  They  found  that  in  marasmus  or  atrophic  dyspepsia, 
the  acidity  and  ferment  activity  of  the  gastric  contents  was  diminished, 
and  that  there  was  neither  mucin  nor  retention  of  food  in  the  stomach. 
In  5  cases  of  hypertrophic  stenosis  the  acidity  was  variable  and  tended 
to  be  diminished,  varying  with  the  amount  of  gastritis.  Ferment  activity 
was  markedly  increased,  mucin  in  excess,  and  food  retained  in  the  stomach. 
These  results  were  absent  in  early  stages,  were  modified  by  systematic 
lavage,  and  depended  on  secondary  effects.  In  pyloric  spasm  or  acid 
dyspepsia,  there  was  neither  mucin  nor  retention  of  food  in  the  stomach  ; 
the  ferment  activity  was  normal  or  subnormal ;  and  the  acidity  was 
increased.  The  test  meals  consisted  of  2-3  oz.  of  diluted  milk,  withdrawn 
in  20  minutes  ;  and  the  rennet  activity  of  the  filtered  gastric  juice  was 
estimated  by  adding  O^Ol-O'S  c.c.  to  5  c.c.  milk  at  40°  C.  These  carefully 
conducted  investigations  are  in  favour  of  the  view  that  spasm  may  be  due 
to  hyperacidity,  and  that  in  hypertrophic  stenosis  spasm,  if  present,  is 
produced  by  some  other  cause,  ?  toxins  of  decomposing  food.  In  some 
patients  there  is  very  little  evidence  of  spasmodic  obstruction  ;  for  vomiting 
is  slight  or  absent,  there  is  little  peristalsis,  and  food  passes  readily  through 
the  pylorus.  In  such  cases,  on  the  hypothesis  of  spasm,  we  should  be  driven 
to  assume  that  spasm  had  existed  and  produced  a  certain  degree  of  hyper- 
trophy, and  that  it  had  then  ceased  and  left  behind  it  a  certain  degree  of 
mechanical  obstruction.  A  more  justifiable  hypothesis  is  that  there  exists 
a  considerable  hyperplasia  or  hypertrophy,  that  this  gradually  contracts 
and  produces  obstruction,  and  that  it  may  be  exaggerated  by  attacks  of 
pyloric  spasm.  Hence,  in  mild  degrees  of  hypertrophy  recovery  may  take 
place  if  spasm  is  absent  or  ceases  under  treatment.  A  hypertrophied  pylorus 
does  not  necessarily  contract  sufficiently  to  cause  serious  obstruction. 

There  is  no  proof  that  spasm  of  the  pylorus  produces  hypertrophy.  In 
long  continued  anal  spasm  no  hypertrophy  results.  Normally  the  pylorus 
is  contracted  and  only  opens,  like  a  closed  door,  to  permit  the  passage  of 
chyme  in  response  to  the  duodenal  reflex,  when  the  acid  chyme  which  has 
passed  through  has  been  neutralized.  Consequently  very  little  extra 
exertion  would  be  necessary  to  counteract  the  tendency  to  relaxation  or  to 
maintain  contraction  ;  certainly  not  sufficient  to  produce  this  great  hyper- 
trophy. Moreover,  if  spasm  can  produce  hypertrophy,  we  ought  to  find 
post  mortem  evidence  of  all  degrees  of  hypertrophy,  up  to  the  extreme 
amount  present  in  these  peculiar  cases,  in  babies  of  all  ages.  Furthermore, 
few  of  these  cases  are  amenable  to  medical  treatment,  even  if  they  come  under 


The  Pylorus.  267 

observation  at  the  earliest  possible  age.  Anti-spasmodic  drugs  are 
unavailing.  A  large  number  of  post  mortem  specimens  accumulate  under 
purely  medical  treatment. 

Diagnosis.  —  Simple  regurgitation,  gastric  catarrh,  vomiting  and 
constipation  from  unsuitable  food,  and  habit  vomiting  must  be  excluded  ; 
so,  too,  rare  forms  of  stenosis  from  other  causes.  The  diagnosis  often 
rests  on  a  careful  study  of  the  history,  symptoms  and  course  of  the  illness, 
and  the  age  of  the  patient.  The  presence  of  peristalsis  and  a  palpable 
pylorus  are  the  most  reliable  physical  signs  ;  but  it  is  not  necessary  to  wait 
until  the  pylorus  can  be  felt  with  absolute  certainty  before  coming  to  a 
definite  conclusion.  It  is  most  important  to  distinguish  pyloric  spasm  from 
hypertrophy.  In  spasm  the  vomiting  is  much  less  characteristic,  peristalsis 
is  slight  or  absent,  the  stomach  rarely  dilated,  pronounced  constipation 
unusual,  diarrhcea  may  be  present,  and  there  is  no  tumour.  Dilatation 
of  the  stomach  is  common  in  babies.  If  it  is  associated  with  vomiting, 
wasting  and  a  certain  degree  of  peristalsis,  the  diagnosis  is  very  difficult. 
The  presence  of  hyperacidity  is  in  favour  of  spasm  rather  than  stenosis. 
In  case  of  doubt,  the  results  of  medical  treatment  are  of  assistance.  On 
the  whole  the  character  of  the  vomiting,  typical  peristalsis,  and  complete 
constipation  or  meconium-like  stools,  are  the  most  reliable  signs  in  early 
stages.  The  presence  of  fecal  matter  in  the  stools  is  in  favour  of  spasm  or 
of  spasm  'plus  hypertrophy.  Stenosis  cannot  b3  complete  and  medical 
treatment  may  be  given  a  further  chance. 

Prognosis.— A.  study  of  my  cases  affords  valuable  information  about 
prognosis  and  treatment.  One  out  of  the  21  is  omitted  for  it  was  only 
seen  in  consultation,  subsequent  to  operation.  All  the  8  patients  who  were 
not  operated  on,  died  in  the  second  to  the  fourth  month  of  life.  One  of  these 
died  at  the  age  of  14  weeks  from  enteritis.  While  under  treatment  there 
were  periods  during  which  he  gained  weight.  A  large  almost  normal  stool 
was  passed  8  days  before  death,  and  normal  faeces  were  found  in  the  intes- 
tines in  considerable  quantities  after  death.  During  the  10  days  he  was  in 
hospital  the  pylorus  was  palpable,  peristalsis  was  only  observed  once, 
the  stomach  was  little  dilated,  and  there  was  no  characteristic  vomiting. 
The  appearance  of  the  pylorus  after  death  was  quite  typical.  This  case 
shows  that  hypertrophy  alone  does  not  necessarily  produce  obstruction. 
Of  5  private  patients  operated  on  at  ages  varying  from  28-45  days,  4 
recovered  completely  and  have  remained  well.  The  fifth  was  treated  on 
medical  principles  as  the  parents  were  opposed  to  operation,  but  even- 
tually they  decided  on  having  the  operation  done  as  a  forlorn  hope.  The 
child  never  rallied  and  died  17  hours  later.  Two  other  cases,  seen  in  con- 
sultation and  sent  into  hospital  for  operation,  also  recovered.  Of  the 
5  remaining  hospital  cases  1  recovered,  and  died  3  months  later  from 
summer  diarrhcea  ;  another  recovered  from  the  operation  and  progressed 
favourably  for  a  time,  but  succumbed  to  enteritis  54  days  later.    These 


268  Chapter    XXIII. 

may  justly  be  claimed  as  surgical  successes  and  medical  failures.  A  third 
died  from  the  anaesthetic  and  shock  ;  a  fourth  died  suddenly  from  syncope 
on  the  fourth  day,  while  apparently  progressing  well,  and  no  cause  could 
be  found  post  mortem  ;  and  the  fifth  died  from  adhesive  peritonitis  6  days 
after  the  operation,  he  had  suffered  from  irregular  pyrexia  during  the 
9  days  before  he  was  operated  on.  In  all  but  one,  the  too-late  case,  pylo- 
roplasty was  performed,  and  8  out  of  1 1  treated  by  pyloroplasty  recovered. 
From  the  above  results  it  is  clear  that  the  outlook  is  extremely  bad  if  the 
treatment  is  purely  medical,  even  though  obstruction  is  incomplete. 
At  a  meeting  of  the  Clinical  Society  of  London  (1906)  Voelcker  stated  that 
out  of  39  cases  observed  at  the  Hospital  for  Sick  Children,  Great  Ormond 
Street,  34  died.  Ashby,  of  Manchester,  had  made  necropsies  on  11  cases, 
only  one  of  which  had  been  operated  on.  Still  ("  Common  Disorders  of 
Childhood,"  1909)  claims  19  recoveries  out  of  42  cases.  Of  the  19  cured, 
11  were  treated  medically.  Of  20  fatal  cases,  6  were  treated  by  operation. 
Thus  the  operative  mortality  was  6  out  of  14  ;  three  cases  were  lost  sight  of ; 
and  14  out  of  25  died  under  medical  treatment.  John  Thomson,  who  has 
done  so  much  towards  attracting  attention  to  this  disease  ("  Clinical 
Examination  of  Sick  Children,"  1908)  states  that  he  has  seen  41  cases  since 
1894.  Omitting  one  which  was  under  treatment,  his  results  were,  4  recov- 
eries out  of  17  treated  medically,  and  8  out  of  23  which  were  operated  on. 
In  3  instances  no  autopsy  was  obtained  ;  in  33  the  diagnosis  was  verified 
at  operation  or  after  death.  These  results  are  very  different  from  those 
obtained  by  Still,  and  support  the  view  that  it  is  difficult  to  differentiate 
between  spasm  and  true  hypertrophy. 

The  prognosis  of  operation  depends  chiefly  upon  the  state  of  the  child 
and  the  subsequent  treatment.  The  greater  the  marasmus  and  dilatation 
of  the  stomach,  the  less  is  the  chance  of  recovery.  After  successful 
operation  the  prognosis  is  that  of  the  marasmus.  It  is  quite  possible  that 
mild  cases,  and  even  some  of  considerable  severity,  may  recover  under 
medical  treatment,  if  the  obstruction  is  due  to  spasm  grafted  on  hyper- 
trophy rather  than  to  hypertrophy  alone.  It  is  practically  certain  that 
many  of  the  recorded  cures  are  of  this  type  or  merely  cases  of  pyloric  spasm. 
Ibrahim,  of  Heidelberg,  wrote  me  that  two  cases,  which  showed  typical 
peristalsis,  had  recovered.  One  of  these  died  6  months  later  from  pneu- 
monia, and  the  hypertrophy  of  the  pylorus  was  still  present.  In  those 
few  instances  of  recovery,  in  which  the  diagnosis  of  hypertrophy  was  certain, 
the  prolonged  and  dangerous  illness,  apart  from  almost  certain  failure, 
far  outweighs  in  risk  the  dangers  of  operative  treatment.  One  might  almost 
as  well  wait  for  an  intussusception  to  be  cured  by  spontaneous  reduction 
or  by  sloughing,  as  postpone  operation  because  instances  of  recovery  have 
been  recorded.  After  operation  the  child  is  practically  well  in  10-14  days. 
A  child  left  with  the  condition  unoperated  on  is  for  the  remainder  of  life 
liable  to  further  pyloric  obstruction  and  dilatation  of  the  stomach. 


The  Pylorus.  269 

Treatment. — In  a  doubtful  case  put  the  child  under  careful  observation 
and  on  a  simple  diet  of  breast-milk,  ass's  milk,  whey,  albumin  water  or 
Allenbury  No.  1  Food.  Give  the  food  in  small  quantities  at  intervals  of 
2  hours.  In  addition  give  cocaine  gr.  x^o,  or  tr.  opii.  m.  §-J,  every  hour. 
If  there  is  no  improvement  in  24  hours,  wash  out  the  stomach  once  or 
twice  a  day  with  a  weak  alkaline  solution.  This  line  of  treatment  may  be 
continued  for  several  days  or  even  weeks,  if  the  child  is  not  losing  ground. 
It  is  not  advisable  to  persevere  with  it  until  the  child  is  so  wasted  that  the 
chance  of  recovery  from  operation  is  infinitesimal,  although  it  has  been 
asserted  that  the  child  goes  on  losing  weight  until  4  or  5  months  of  age,  or- 
is almost  moribund,  and  then  suddenly  rounds  the  corner.  Lavage  is 
beneficial  by  washing  away  irritating  gastric  contents,  the  products  of 
decomposition  of  food  retained  long  in  the  stomach.  If  spasm  is  due  to 
this  cause,  it  may  be  relieved  by  lavage.  One  occasional  complication,  even 
in  cases  treated  on  these  lines,  is  tetany  ;  and  even  convulsions  have 
occurred.  These  nervous  phenomena  are  not  unusual  in  chronic  dilatation 
of  the  stomach.  Lavage  is  further  advantageous  in  helping  to  prevent  over- 
distension of  the  stomach,  provided  that  it  is  done  systematically  twice 
a  day,  and  that  small  feeds  are  given  in  the  intervening  periods.  It  is 
certain  that  a  greatly  dilated  stomach  adds  to  the  difficulties  of  treatment 
after  operation;  and  it  seems  likely  that  such  a  stomach,  full  of  liquid  food, 
may  drag  on  the  pylorus  and  cause  a  definite  amount  of  kinking,  and  thus 
increase  the  obstruction.  This  mode  of  treatment  is  almost  certain  to  cure 
acid  dyspepsia  and  simple  spasm.  It  will  relieve  and  assist  in  the  cure  of 
gastric  catarrh.  But  it  is  difficult  to  believe  that  it  can  in  the  least  degree 
affect  the  hypertrophy  of  the  muscle  fibres  or  be  of  the  least  value,  except 
in  those  cases  in  which  the  obstruction  is  due  to  secondary  effects,  grafted 
on  a  primary  hyperplasia  of  moderate  severity.  The  choice  of  operation 
lies  between  pyloroplasty,  Loreta's  stretching  operation,  and  posterior 
gastro-enterostomy.  The  stretching  operation  is  somewhat  analogous 
to  forcible  rupture  of  urethral  stricture.  For  complete  success  it  is  necessary 
to  rupture  some  or  all  of  the  circular  muscle  fibres,  and  the  peritoneal  coat 
is  liable  to  be  ruptured  as  well.  This  has  been  followed  by  fatal  peritonitis. 
If  the  pylorus  is  merely  dilated,  it  is  liable  to  contract,  and  a  second 
operation  may  be  and  has  been  necessary.  Posterior  gastro-enterostomy 
is  satisfactory  as  regards  the  maintenance  of  nutrition,  but  does  not 
affect  the  condition  of  the  pylorus.  Morse  has  reported  a  case,  treated  by 
this  method,  which  died  from  another  cause  6|  months  later,  aged  8  months. 
The  pylorus  was  found  in  exactly  the  same  condition  as  at  the  time  of 
operation  ;  a  conclusive  proof  that  spasm  had  nothing  to  do  with  the 
hypertrophy  or  the  stenosis.  Pyloroplasty  is  the  most  scientific  method  of 
treatment,  for  the  pylorus  can  no  longer  contract  after  operation  and 
there  is  no  fear  of  recurrence.  Its  difficulties  are  overrated,  for  it  can  be 
done  by  a  reasonably  good  surgeon  in  20  minutes.    It  is  important  to  have 


270  Chapter  XXIII. 

a  skilled  anaesthetist.  Immediately  after  the  operation  the  child  should  be 
given  a  rectal  feed  of  2  oz.  of  peptonised  milk  and  water,  p. a.,  and  10-20 
drops  of  brandy.  Rectal  feeds  should  be  given  every  4  hours  for  2  days, 
every  6  hours  for  2  days,  and  twice  a  day  for  2  days.  A  teaspoonful  of  hot 
water  must  be  given  by  mouth  every  J  hour,  while  awake,  for  a  period  of 
12  hours,  and  after  that  a  similar  quantity  of  whey.  Subsequently  the 
whey  is  increased  to  2  teaspoonfuls  every  J  hour,  a  tablespoonful  every 
^  hour,  1  oz.  hourly,  and  finally  2  oz.  every  2  hours.  After  that  it  is 
strengthened  by  the  addition  of  cream  ;  and  gradually  replaced  by  pep- 
tonised milk  and  water,  or  milk  and  water  with  cream,  until  the  child  is 
on  an  ordinary  diet.  Vomiting  usually  persists  for  2-6  days,  and  some 
altered  blood  is  brought  up  a  few  hours  after  the  operation.  There  may 
be  a  little  fever  for  2  or  3  days.  As  a  rule  the  vomiting  subsides  in  a  couple 
of  days  ;  food  passes  through  the  pylorus  in  24-48  hours,  and  is  found 
in  the  rectal  wash  on  the  third  day  ;  and  the  child  is  discharged  cured  at 
the  end  of  a  fortnight.  Great  care  must  be  taken  not  to  overfeed  these 
children  in  the  early  stages  of  convalescence,  on  account  of  the  liability  to 
enteritis.  This  is  especially  apt  to  occur  in  marasmic  infants,  and  is 
probably  dependent  upon  nutritional  changes  in  the  intestinal  mucosa, 
consequent  on  starvation.  (Edema  is  another  complication  occasionally 
seen.    It  is  due  to  overfeeding  or  to  renal  inadequacy. 

Though  recognising  the  possibility  of  cure  in  mild  cases  without 
operation,  my  experience  leads  me  to  assert  that  operation  is  the  best 
possible  treatment  to  advise  and  that,  if  done  early,  its  risk  is  comparatively 
small.  It  is  essential  that  the  after-treatment  is  left  in  the  hands  of  the 
physician,  and  not  entrusted  to  the  surgeon,  for  on  this  the  life  of  the 
child  is  most  likely  to  depend.  There  is  grave  danger  of  ascribing  to 
pyloric  hyperplasia  the  symptoms  due  to  pyloric  spasm  only,  and  thus 
acquiring  an  unduly  favourable  idea  of  the  prognosis  in  the  more  serious 
disease.  An  almost  equivalent  danger  is  that  of  diagnosing  hypertrophy 
and  operating,  when  the  affection  is  purely  spasmodic. 


CHAPTER    XXIV. 

INTESTINAL   DIGESTION. 

The  Stools — Tympanites — Colic — Reflex   Colic  and    Diarrhoea — Intestinal 
Dyspepsia —  Carbohydrate  Fever. 

The  Stools. — Meconium  is  passed  during  birth,  or  a  few  hours  after, 
and  for  a  period  of  1-4  days.  If  passed  before  birth  it  indicates  sometimes, 
but  not  always,  ante  partum  asphyxia.  The  total  amount  is  2-3  07.  It 
is  odourless,  homogeneous,  viscid  and  tenacious,  sterile,  weakly  acid, 
and  semi-solid.  In  colour  it  is  greenish,  greenish-black,  dark  brown  or 
brownish-black.  It  is  composed  of  various  intestinal  materials,  namely 
epithelium,  mucus,  bile  and  cholesterin,  and  the  substances  swallowed  with 
the  liquor  amnii,  such  as  squamous  cells,  fat  globules  and  lanugo.  The 
meconium  corpuscles  are  oval  or  round,  and  greenish  yellow  ;  probably 
bile-stained  altered  epithelium  cells.  Bile  begins  to  be  secreted  in  the  third 
month  of  foetal  life.  Meconium  is  found  in  the  small  intestine  and  appendix 
about  the  middle  of  the  fourth  month  of  foetal  life,  and  in  the  large  intestine 
in  the  beginning  of  the  fifth  month.  After  the  seventh  month  it  distends 
the  whole  large  intestine.  It  has  been  found  in  the  appendix  although 
the  caecum  was  practically  empty. 

During  the  first  2  or  3  days  after  birth  from  2-4  stools  of  meconium 
are  passed.  By  the  fourth  or  fifth  day  the  golden  yellow  colour  of  ordinary 
milk  fasces  is  acquired.  Sometimes  the  meconial  character  persists  for  a 
week  or  more. 

The  normal  amount  of  faeces  passed  daily  by  a  breast-fed  infant  is 
1-3  oz.,  or  about  2  per  cent,  of  the  weight  of  milk  ingested.  The  dried 
residue  has  been  estimated  at  15-20  per  cent. ;  consisting  of  organic  sub- 
stances 90,  and  inorganic  10  per  cent.  One-third  of  the  inorganic  sub- 
stances consists  of  calcium  salts.  The  reaction  is  acid  or  neutral.  In  colour, 
consistency  and  general  appearance,  the  faeces  resemble  the  yolk  of  an 
egg,  and  they  vary  in  colour  according  to  the  percentage  of  fat,  as  much  as 
•do  the  yolks  of  eggs,  without  being  abnormal.  The  colour  is  due  to  bili- 
rubin, and  becomes  greenish  on  exposure  to  air  by  conversion  into  biliverdin. 
The  stools  are  mainly  composed  of  fat ;  perhaps  25-35  per  cent,  of  the 
•dried  solids  is  in  the  form  of  neutral  fats,  fatty  acids  and  soaps.  The  acid 
reaction  and  slightly  sour  smell  are  due  to  these  acids,  chiefly  lactic  acid. 
The  proteins  of  breast-milk  are  almost,  but  not  entirely,  absorbed.    Mucus 


272  Chapter   XXI  V. 

and  intestinal  epithelium  are  present  in  considerable  quantity,  and  the 
other  constituents  are  bile  pigments,  cholesterin,  lime  salts  and  other 
inorganic  salts,  and  rarely  indol.  Hydrobilirubin  is  not  often  found, 
because  of  the  rarity  of  putrefactive  intestinal  changes.  The  gaseous 
discharges  consist  of  hydrogen  and  carbonic  acid  gas.  Sulphuretted 
hydrogen  and  marsh  gas  appear  later  in  life.  Micro-organisms  are  soon 
present  in  large  numbers.  The  streptococcus  acidi  lactici  is  the  chief  organism 
in  the  small  intestine,  and  both  it  and  B.  coli  are  found  in  the  meconium 
10-12  hours  after  birth.  This  organism  sours  milk  and  restrains  the  growth 
of  pathogenic  bacteria.  In  the  large  intestine  the  B.  bifidus  is  the  most 
important  organism.  It  is  anaerobic  and  found  in  the  stools  after  the 
meconial  stage.  The  absence  of  a  putrefactive  odour  is  partly  due  to  the 
rapid  passage  of  the  food  through  the  alimentary  tract ;  to  the  fact  that 
milk  does  not  usually  undergo  putrefaction,  and  a  milk  diet  lessens 
intestinal  putrefactive  processes  ;  and  to  the  fact  that  fermentation  has  a 
•similar  effect.      Putrefaction  depends  chiefly  on  the  intestinal  flora. 

In  infants  fed  on  cow's  milk  the  stools  are  larger  in  amount,  equal  to 
about  one-fourth  of  the  milk  ingested,  and  contain  casein.  They  are  whitish 
or  pale  yellow  in  colour,  and  turn  greyish  yellow  or  white  on  exposure. 
The  odour  is  cheesy  or  offensive,  and  the  reaction  alkaline.  The  addition 
of  carbohydrates  to  the  diet  renders  the  stools  more  yellow  in  colour,  acid 
in  reaction,  and  free  from  the  smell  of  decomposition.  The  acid  reaction, 
due  to  the  fermentative  changes  of  carbohydrates,  prevents  putrefaction. 
The  common  organisms  present  are  the  Streptococcus  acidi  lactici,  B.  coli., 
B.  lactis  aerogenes  and  B.  bifidus,  all  of  which  cause  fermentation  but 
have  no  proteolytic  or  peptonising  action. 

Curds  of  two  types  are  found  in  infantile  stools.  Fat  Curds  are 
small,  soft,  whitish  lumps,  sometimes  pin-head  in  size,  yellowish,  and 
looking  like  yellow  sandy  particles  or  biliary  concretions.  They  are 
composed  of  fat  in  the  form  of  fatty  acids  and  calcium  soaps.  They 
contain  little  nitrogen.  Casein  Curds  are  in  the  form  of  smooth  white 
flakes,  or  large  and  tough  lumps,  and  sink  in  water.  They  contain  much 
nitrogen,  little  soap,  and  consist  chiefly  of  casein.  If  there  is  no  excess  of 
casein  in  the  milk  given  to  infants,  the  stools  may  be  the  same  as  in  the 
breast-fed.  Gradually  as  the  diet  becomes  more  mixed,  the  stools  acquire 
the  adult  characters,  and  become  brownish  and  usually  formed  by  the 
end  of  the  second  year.  The  healthy  child  passes  2-4  stools  daily  during 
the  first  fortnight  and  after  that  2  a  day,  or  a  number  varying  from  1-4  or 
more.  Occasionally  the  breast-fed  infant  passes  a  large  number  of  normal 
stools,  even  12  or  13  daily,  and  yet  gains  weight  rapidly. 

Abnormalities  of  the  Stools. — They  may  be  frothy  ;  too  liquid  or  too 
solid  ;  acid  or  alkaline  ;  variable  in  colour  and  odour,  in  size  and  in 
composition  ;    and  may  contain  parasites. 

As  a  general  rule,  the  paler  the  yellow  colour,  the  less  is  the  amount 


Intestinal    Digestion.  273 

of  fat  present.  Large  colourless  stools  may  be  due  to  failure  of  pancreatic 
digestion.  They  are  acid  and  contain  an  excess  of  fat,  chiefly  fatty  acid. 
Stercobilin  is  usually  present  and  abundant  though  the  stools  are  colourless. 
This  condition  is  associated  with  a  distended  abdomen,  anaemia,  great  and 
often  rapid  emaciation,  and  frequently  a  sore  tongue,  aphthae  and  ulcers. 
Possibly  there  is  pancreatitis  of  a  mild  type.  Milk  diet  is  useless.  The 
child  must  be  fed  upon  pounded  beef,  eggs,  chicken,  liver  soup,  jellies  and 
barley  water  ;  vegetables  are  added  later.  In  some  respects  it  is  analogous 
to  Sprue,  for  which  santonin  and  ipecac,  sine  emetin  are  useful.  In  this 
affection  also  milk  diet  is  useless,  though  milk  and  strawberries  are  beneficial. 
White  stools  have  been  ascribed  to  excess  of  milk  curd  ;  to  absence  of  bile, 
giving  rise  to  offensive  smell  ;  or  excess  of  fat,  causing  an  odour  of  rancid 
butter.  Some  infants  overfed  with  cow's  milk,  but  under-nourished,  pass 
stools  which  are  dry,  neutral  or  faintly  alkaline,  very  pale  or  even  almost 
white,  like  those  of  acholia.  These  stools  are  not  free  from  bile,  but  are  the 
result  of  perverted  liver  function  or  change  in  the  bile  pigment.  Bilirubin 
is  changed  into  colourless  urobilinogen  instead  of  urobilin.  With  an  acid 
solution  of  dimethylamido-azobenzaldehyde  urobilinogen  produces  an 
ntense  red  colour.  Probably  it  is  derived  from  hydrobilirubin  in  an 
alkaline  medium,  and  the  hydrobilirubin  is  due  to  putrefactive  processes. 
Faeces  containing  the  latter  pigment  turn  red  with  a  saturated  solution  of 
corrosive  sublimate.  If  bilirubin  is  present  it  is  converted  into  biliverdin, 
and  the  colour  is  green.  Some  of  these  stools  are  more  the  colour  of  clay 
or  putty  ;  and  perhaps  due  to  a  similar  cause,  acholia,  an  excess  of  starch, 
or  gastro-intestinal  catarrh.  Starch  can  be  recognised  under  the  microscope 
or  by  its  reaction  with  iodine. 

Intestinal  fermentation,  if  excessive,  as  it  may  be  from  excess  of  starch 
or  carbohydrate  food,  gives  rise  to  frothy  stools  with  a  sour  smell.  Intes- 
tinal putrefaction  is  due  to  decomposition  of  protein,  and  the  stools  are 
putrid  and  offensive.  In  all  pathological  states,  especially  catarrhal  con- 
ditions of  the  intestine,  the  secretion  of  mucus  is  excessive.  It  is  extra- 
ordinarily liable  to  decomposition,  and  produces  an  alkaline  reaction  in  the 
stools  and  a  foul  smell.  Clinically  these  effects  are  of  great  importance. 
Excessive  or  abnormal  fermentation  may  be  set  up  by  unsuitable  food, 
too  large  or  too  frequent  meals,  and  give  rise  to  fermentative  dyspepsia 
with  tympanites  and  the  evacuation  of  numerous  frothy  acid  stools. 
In  moderation  this  process  can  be  used  as  a  curative  agent,  for  the  preven- 
tion of  intestinal  putrefaction  and  decomposition  of  protein.  The  lactic 
and  other  organic  acids  destroy  or  inhibit  the  growth  of  intestinal  proteo- 
lytic and  peptonising  organisms. 

Green  stools  may  be  green  before  or  shortly  after  being  passed,  in 
consequence  of  the  conversion  of  bilirubin  into  biliverdin  by  an  alkali 
in  the  canal  or  the  oxygen  in  the  atmosphere.  The  colour  has  also  been 
ascribed  to  the  administration  of  alkalies  by  the  mouth,  and  to  intestinal 


274  Chapter   XXI  V. 

flora.  More  probably  the  conversion  is  due  to  an  oxidizing  ferment  in  the 
mucus  or  leucocytes.  Wernstedt  claims  that  he  has  identified  such  a 
ferment.  The  green  colour  is  always  associated  with  the  secretion  of  mucus  ; 
the  ferment  action  is  secondary.  Slimy  or  mucoid  stools  are  those  in  which 
there  is  excess  of  mucus.  If  it  is  mainly  from  the  colon,  the  stools  may  con- 
sist of  little  more  than  mucus.  The  stools  may  vary  in  colour  from 
slatey  blue  or  grey  to  black,  due  to  the  action  of  iron,  bismuth,  tannic  acid 
or  blood.  They  are  often  brown  or  greyish  and  offensive  from  the  ingestion 
of  raw  meat  juice  ;  and  may  be  bright  red  or  black  and  tarry,  due  to  blood 
from  various  parts  of  the  alimentary  tract.  In  rare  instances  membrane 
is  present,  for  instance  in  membranous  colitis.  Worms  and  their  eggs, 
parasites,  pus,  undigested  cellulose,  and  various  foreign  bodies  may  be 
found  and  give  valuable  information  as  to  the  cause  and  nature  of  the 
illness. 

Examination  of  the  Stools. — Food  passes  from  mouth  to  anus  in  20 
hours  for  lean  meat  (Strauss)  ;  24  hours  for  mixed  diet  (Kozieskowski)  ; 
36-48  hours  for  milk  diet  (Maurel).  Delay  may  be  due  to  atony  or  a 
dilated  sigmoid  ;  and  may  occur  in  the  stomach  or  small  intestine,  leading 
to  auto-intoxication  and  attacks  of  bilious  vomiting  though  the  bowels 
act  daily.  Give  one  or  two  Belloc's  pastilles  of  vegetable  charcoal  at 
breakfast ;  delayed  appearance  of  the  charcoal  in  the  stools,  if  frequent, 
indicates  that  the  diarrhoea  is  due  to  causes  low  down.  In  examining  for 
occult  blood  exclude  all  hsemoglobin  from  the  diet  and  make  an  ether  extract 
of  the  fasces.  Mucus  is  recognised  by  mixing  the  stool  with  water  and 
examining  it  against  a  black  surface.  Undigested  connective  tissue,  meat 
fibres,  starch  grains,  ova  of  worms,  etc.,  are  found  by  microscopic 
examination. 

Intestinal  Dyspepsia. — The  chief  symptoms  of  intestinal  dyspepsia  are 
tympanites  and  colic.  These  may  be  associated  with  constipation  cr 
diarrhoea,  lientery,  and  general  malnutrition.  Not  infrequently  there  are 
nervous  symptoms,  either  toxaemic  or  reflex  in  causation,  such  as  irritability 
and  fretfulness,  violent  and  prolonged  outbreaks  of  temper,  teeth  grinding, 
pavor  and  somnambulism. 

Tympanites. — Distension  of  the  abdomen,  due  to  abnormal  production 
of  intestinal  gases,  is  a  chronic  condition  of  gradual  onset,  or  so  rapid  in 
its  development  as  to  deserve  the  name  of  "  acute  abdominal  distension.'- 

The  chief  causes  are  more  or  less  associated  in  action,  namely,  excessive 
production  of  gas  and  intestinal  muscular  atony  with  imperfect  peristalsis. 
Over-production  of  gas  is  due  to  bad  feeding,  carious  teeth,  imperfect 
mastication,  bolting  food,  insufficient  exercise,  constipation,  and  fermen- 
tative processes.  Intestinal  atony  is  common  in  rickets,  and  in  malnutrition 
from  any  cause,  and  is  assisted  by  weakness  of  the  abdominal  walls. 
Imperfect  peristalsis  depends  upon  an  insufficient  supply  of  fluid  and  waste 
matter  in  the  food,  failure  of  pancreatic  digestion,  intestinal  catarrh,  abuse 


Intestinal   Digestion.  275 

of  purgatives  ;  paralytic  conditions  from  peritonitis,  mechanical  obstruction 
and  nerve  palsies,  such  as  diphtheritic  paralysis  and  affections  of  the 
spinal  cord. 

Acute  distension  is  not  very  uncommon  under  3  years  of  age.  It  is 
a  serious  sign  in  grave  illness  and  often  appears  part  of  the  act  of  dying. 
It  is  most  often  seen  in  diseases  of  the  lungs  and  pleura,  and  greatly  inter- 
feres with  the  breathing  and  the  action  of  the  heart,  by  upward  pressure 
on  the  diaphragm.  In  older  children  distension  is  frequently  chronic  and 
the  result  of  dyspepsia  and  bad  feeding,  often  associated  with  constipation. 
The  normally  prominent  abdomen  of  childhood  must  not  be  ascribed  to 
this  condition.  Intestinal  distension  is  general,  except  when  arising  from 
localised  mechanical  obstruction. 

In  chronic  cases  anti-fermentative  drugs  are  given,  but  the  treatment 
is  mainly  that  of  the  local  or  constitutional  state.  Immediate  measures  are 
necessary  in  acute  distension.  The  finger  must  be  passed  through  the 
anus  and  the  sphincter  dilated  if  there  is  any  spasm.  An  enema  of  soap  and 
water,  turpentine  or  asafoetida,  is  then  given.  The  back  and  shoulders 
must  be  supported,  strychnia  injected,  and  brandy  given  by  the  mouth. 

Colic  or  Enteralgia  is  paroxysmal  intestinal  pain  from  spasm  of  the 
intestinal  muscles.  In  babies  it  is  caused  by  flatulence  from  excess  of  pro- 
tein, sugar  or  starches ;  the  pain  being  due  to  distension  and  spasm.  In 
older  children  it  chiefly  follows  the  ingestion  of  hard  or  unsuitable  food, 
•or  poisons  such  as  lead.  Vague  pains  are  sometimes  associated  with  worms, 
and  may  be  referred  to  the  navel  or  iliac  fossa.  Pain  in  the  iliac  region 
after  exertion,  such  as  hurrying  to  school  after  breakfast,  may  be  due  to 
•chronic  appendicitis.  Colic  is  also  set  up  by  intestinal  and  peritoneal 
inflammation,  appendicitis,  intussusception,  intestinal  obstruction  and 
scybala  ;  or  it  may  arise  simply  from  cold  feet,  chills,  and  drinking  iced 
water.  Infantile  colic  is  characterised  by  moaning,  screwing  up  of  the 
face  and  paroxysmal  cry  ;  and  in  bad  attacks,  by  pallor,  sweating,  cold 
•extremities  and  collapse.  The  knees  are  drawn  up,  the  arms  bent  and  the 
hands  clenched.  The  abdomen  is  tense  and  hard,  and  the  scrotum  retracted. 
There  is  no  local  tenderness  or  fever.  The  attack  is  of  short  duration 
and  relieved  by  the  expulsion  of  wind.  The  cry  differs  from  that  of  hunger 
in  its  loud  and  paroxysmal  character,  and  it  is  associated  with  other  signs  of 
pain.  The  pain  is  lessened  by  food  temporarily,  but  soon  returns  in  pro- 
bably a  worse  form.  Simple  colic  must  be  distinguished  from  colic  due 
to  other  causes,  notably  renal  colic,  intussusception  and  tuberculous 
adhesions. 

Treatment. — The  injection  of  warm  water  2-6  oz.,  or  glycerine  dr.  A- 
in  1-2  oz.  of  cold  water,  generally  leads  to  evacuation  of  wind  and 
affords  relief.  During  the  attack  apply  warmth  to  the  abdomen  and  feet ; 
give  mild  laxatives  and  carminatives,  such  as  sp.  chlorof.,  tr.  card,  co., 
tr.  zingib.,  sp.  vini.  rect.,  dill  water  and  peppermint  in  hot  water  ;    small 


276  Chapter  XXIV. 

doses  of  belladonna,  hyoscyamus  and  codeia  are  useful  for  recurrent  colic, 
or  minim  doses  of  Fowler's  solution  just  before  meals.  Between  the 
attacks  attend  to  the  digestion,  avoid  excess  of  starch,  greens,  fruit  and 
vegetables  containing  cellulose.  See  that  the  clothing  is  sufficient  and  pro- 
perly distributed. 

Reflex  Colic  and  Diarrhoea. — These  names  are  more  appropriate  than 
';  lienteric  diarrhoea,"  for  they  indicate  the  causation  of  the  trouble  and 
the  appropriate  lines  of  treatment.  "  Lientery  "  is  derived  from  Greek 
words  meaning  "  a  smooth  intestine."  It  is  defined  in  the  New  Sydenham 
Society's  Lexicon  of  Medicine  as  "A  species  of  diarrhoea,  or  looseness,  in 
which  the  food  passes  rapidly  through  the  bowel  undigested,  and  nearly  in 
the  same  condition  as  it  was  when  taken  ...  so  called  because  the  food 
seems  to  have  slipped  over  a  smooth-lined  intestine." 

It  occurs  at  any  age,  but  more  especially  in  the  sixth  year  of  life. 
This  may  be  because  dentition  leads  to  bolting  of  food  and  imperfect 
digestion.  It  is  quite  common  in  infants,  each  feed  being  followed  by  an 
immediate  action  of  the  bowels.  The  presence  of  undigested  food  in  the 
stools  does  not  mean  that  the  food  has  passed  through  the  alimentary 
tract  in  the  short  time  which  elapses  between  ingestion  and  defsecation, 
but  that  it  passes  out  of  the  stomach  and  through  the  intestines  too  rapidly 
to  be  properly  digested,  and  consequently  appears  in  an  undigested 
form  in  the  stools.  Although  gastric  digestion  is  not  essential  in  infancy, 
it  is  necessary  that  the  food  should  stay  sufficiently  long  in  contact  with  the 
digestive  juices,  and  not  be  hurried  through  the  gut  by  unduly  rapid 
peristalsis.  Reflex  peristalsis  is  set  up  as  soon  as  food  enters  the 
stomach,  is  followed  by  griping  pains  or  colic,  and  causes  almost  imme- 
diate evacuation  of  the  lower  bowel.  The  stools  consist  of  undigested 
food  and  mucus. 

These  children  are  generally  of  the  nervous  type,  excitable,  neurotic,, 
highly  strung  and  variable  in  temper.  Attacks  are  induced  by  food 
unsuitable  in  quantity  and  quality,  given  at  too  high  or  too  low  a  tempera- 
ture, or  too  rapidly.  The  habit  of  bolting  the  morning  meal  in  order  to 
hurry  out  to  school  or  play,  combined  with  sudden  exposure  to  change  of 
temperature  on  leaving  the  house  and  hurried  bodily  movements,  is  a 
common  cause  in  children.  In  its  simplest  form  it  is  induced  by  taking  cold 
water  or  ice  into  the  stomach,  when  heated.  Colicky  pains  are  at  once 
induced  and  the  bowels  act  profusely,  with  abdominal  discomfort  and 
even  severe  pain.  Such  attacks  are  easily  relieved  by  warmth  and  tem- 
porary abstinence  from  food  and  drink.  Reflex  colic  is  more  difficult  of 
diagnosis  when  it  is  not  severe  enough  to  cause  action  of  the  bowels.  It  has 
to  be  differentiated  from  the  colicky  attacks  of  appendix  origin,  renal. 
calculus,  tuberculous  adenitis  or  adhesions,  gastric  or  duodenal  ulcer,  and 
such  like  causes.  The  prognosis  is  excellent.  Untreated  cases  may  continue 
for  many  months. 


Intestinal   Digestion.  277 

Treatment  is  simple.  Food  should  be  easily  digestible,  neither  hot  nor 
cold,  and  taken  slowly.  A  certain  amount  of  rest  after  meals  must  be 
insisted  on.  The  child  must  be  warmly  clad,  especially  as  regards  the 
extremities  ;  cold  and  wet  feet  being  injurious.  The  most  efficacious  drug 
is  Fowler's  solution,  m.  ^-1  in  water  dr.  1,  before  meals.  Sometimes 
carminative  digestive  mixtures  are  required,  if  there  is  gastric  catarrh. 
If  these  measures  fail,  recourse  must  be  had  to  bismuth,  bromide,  codeia 
or  small  doses  of  Dover's  powder.  Bad  cases  are  generally  cured  by 
change  of  climate  and  surroundings. 

Acute  Intestinal  Indigestion,  when  sudden  in  onset,  gives  rise  to 
fever  for  12-24  hours.  In  children  the  temperature  rises  to  100-101°  F., 
and  in  infants  102-105°  F.  Colicky  pains  are  severe  and  cause  screaming, 
restlessness,  and  drawing  up  the  limbs.  Tympanites,  diarrhoea,  prostration 
and  nervous  disturbance  are  commonly  present.  In  older  children  the 
pain  is  situated  about  the  umbilicus  and  followed  in  a  few  hours  by 
diarrhoea.  It  is  often  diagnosed  with  difficulty  from  appendicitis.  Recovery 
rapidly  follows  the  administration  of  castor  oil,  a  mercurial  purge,  or  an 
enema. 

Intestinal  Dyspepsia  has  been  described  by  Eustace  Smith  under 
the  name  of  "Mucous  disease,"  and  by  other  observers  as  "  Lithcemia," 
"  Neurasthenia,"  and  "  chronic  dyspepsia  in  children.''''  These  differences 
in  nomenclature  have  given  rise  to  much  confusion,  and  it  is  doubtful 
whether  the  name  of  "  intestinal  dyspepsia  "  is  sufficiently  precise  to 
include  all  the  cases  of  this  type.  The  characteristic  feature  is  mal- 
nutrition or  deficient  growth,  associated  with  alimentary  symptoms 
and  others  of  a  more  or  less  neurotic  type.  There  is  certainly  some  error 
of  absorption  or  metabolism,  not  dependent  upon  stomachic  conditions. 

Etiology. — The  predisposing  factors  are  a  family  history  of  neuroses, 
gout,  tuberculosis  or  digestive  weakness  ;  lowered  general  health  from 
measles  or  whooping  cough  ;  overcrowding,  bad  hygiene,  defective  teeth, 
insufficient  exercise,  etc.  Boys  are  more  liable  than  girls  in  the  pro- 
portion of  about  2-1.  Race,  social  position  and  residence  have  little  effect. 
The  age  varies  from  3-12,  most  commonly  5-8,  the  period  of  commencing 
second  dentition.  The  teeth  are  often  carious  and  septic  matter  is  swallowed. 
Partly  on  this  account  and  partly  because  of  the  age,  food  is  bolted.  The 
exciting  causes  are  school  life  and  an  unsuitable  diet  containing  an  excess 
of  carbohydrates. 

Symptoms.— The  onset  may  be  acute  with  headache,  vomiting  and 
loose  stools,  but  more  often  is  indefinite.  The  child  is  languid,  especially 
in  the  morning,  is  disinclined  to  get  up,  and  "  lays  about  "  or  "  has  no 
life  in  it."  At  night  there  is  restlessness  in  the  early  part,  teeth  grinding, 
talking  in  the  sleep,  pavor,  sometimes  somnambulism  and  night  sweats. 
This  is  followed  by  a  deep  lethargic  slumber.  The  nocturnal  restlessness  is 
most  common  in  school  children  and  associated  with  constipation.      In 


278  Chapter   XXIV. 

contrast  to  the  lethargy,  these  children  are  said  to  be  very  nervous, 
excitable,  crying  on  the  least  provocation,  starting  at  the  slightest  noise, 
afraid  of  being  alone  even  in  the  daytime,  and  to  blush  or  grow  pale  on  the 
least  emotional  disturbance.  These  attacks  of  pallor  are  common  and  most 
characteristic.  The  child  "  comes  over  white,"  with  black  rings  round  the 
eyes,  and  the  feeling  of  faintness  lasts  for  several  minutes  but  actual 
syncope  is  rare.  The  hands  and  feet  are  often  cold,  and  the  attacks  may  be 
associated  with  abdominal  pain  or  worms.  They  are  ascribed  to  entero- 
spasm  or  intestinal  distension,  and  they  have  to  be  distinguished  from 
fainting  attacks  and  petit  mal. 

More  or  less  headache  is  generally  present,  usually  frontal.  It  may 
occur  at  any  time,  especially  in  the  morning  or  after  school,  and  can 
sometimes  be  traced  to  visual  defects.  A  slight  or  hacking  cough,  perhaps 
barking,  worst  in  the  morning,  is  often  present  and  probably  due  to 
pharyngeal  congestion.  Pains  are  felt  in  the  epigastrium  or  in  either  hypo- 
chondrium,  and  "  stitch  "  in  the  side  is  frequent  on  exertion. 

The  appetite  is  lost,  poor  or  ravenous.  Vomiting  rarely  occurs 
except  from  exacerbations,  which  are  usually  described  as  "  bilious  attacks" 
or  "  attacks  of  gastric  fever."  They  are  ushered  in  by  headache,  vomiting 
and  diarrhoea,  anorexia,  epigastric  pains,  high  fever  and  even  delirium. 
They  vary  in  severity  and  duration,  perhaps  consisting  only  of  vomiting 
and  headache.  Often  they  last  for  a  few  days,  and  are  followed  by  a  period 
of  good  health  and  constipation.  Gradually  the  appetite  becomes  ravenous, 
more  signs  of  the  affection  develop,  and  finally  another  acute  attack. 
This  description  must  be  compared  with  that  of  recurrent  vomiting  (p.  158). 
Mild  attacks  are  more  prolonged  than  severe  ones.  The  bowels  are  usually 
normal  in  appearance  ;  occasionally  grey  and  often  very  offensive.  Some- 
times the  stools  are  large,  offensive,  and  consist  of  scybala.  Occasionally 
there  is  lienteric  diarrhoea.  Mucus  is  commonly  present,  if  there  is  con- 
stipation or  diarrhoea.  Fever  occurs  in  attacks  in  which  the  temperature 
ranges  from  100-105°  F.,  and  together  with  the  symptoms  suggests  typhoid 
fever.  Gradually  the  child  wastes,  though  this  is  not  very  noticeable  to  a 
stranger  for  the  face  suffers  little. 

On  physical  examination,  the  child  is  pale  or  sallow,  may  have  a  slight- 
icteric  tinge  or  actual  jaundice,  with  dark  rings  round  the  eyes,  and  seems 
intensely  languid  or  tired.  On  excitement  he  readily  flushes  up  and  looks 
quite  healthy.  Generally  nutrition  is  poor,  but  the  wasting  rarely  amounts 
to  emaciation ;  the  muscles  are  soft  and  flabby.  The  tongue  has  a  whitish 
yellow  fur  far  back  on  the  dorsum  and  anteriorly  is  covered  with  mucoid 
secretion.  It  may  be  generally  white  and  sodden,  with  prominent  fungiform 
papillae.  The  teeth  are  usually  carious.  Large  tonsils  and  adenoids  are 
present  in  about  half  the  cases,  but  it  is  doubtful  whether  they  have  any- 
thing to  do  with  the  disease.  Chronic  pharyngitis  is  almost  constant.  The 
chest  is  often  flattened,  shoulders  round,  abdomen  pot-bellied,  and  the 


Intestinal   Digestion.  279 

liver  somewhat  enlarged.  The  urine  contains  an  excess  of  urates.  Some- 
times there  is  cyclic  albuminuria.  All  varieties  of  worms  have  been  noted, 
but  thread  worms  are  the  most  common.  There  is  no  fever  except  during 
the  acute  attacks. 

Carbohydrate  Fever,  food  fever,  acute  febrile  or  recurring  gastric 
catarrh,  is  almost  certainly  one  of  this  group  of  cases  and  does  not  require; 
differentiation  as  a  special  entity.  The  name  has  been  given  to  attacks  o£ 
fever  in  children  with  more  or  less  digestive  disturbance,  liability  to 
recurrence,  and  no  apparent  origin.  Some  of  them  have  been  traced  to 
excess  of  carbohydrate  diet,  and  have  been  cured  by  strict  limitation  of  this 
food  stuff.  The  symptoms  are  an  impaired  appetite,  more  or  less  headache, 
general  malaise,  occasionally  collapse,  and  fever  for  one  to  a  few  days, 
sometimes  reaching  a  maximum  of  104°  F.  Possibly  the  cause  lies  in  the 
products  of  fermentation,  a  kind  of  toxaemia  ;  or  some  catarrh  is  set  up 
;md  the  metabolism  of  the  liver  is  impaired.  The  catarrhal  hypothesis 
is  unlikely  to  be  true  for  a  mercurial  purge  often  cuts  short  the  attack. 

Pathology. — Intestinal  dyspepsia  has  been  ascribed  by  Eustace  Smith 
to  "A  mucous  flux  which  interferes  mechanically  with  ingestion  and 
absorption  of  food."  On  the  other  hand,  in  many  cases,  no  excess  of  mucus 
Las  been  noted  in  the  stools ;  more  probably  it  is  a  result  rather  than  a  cause. 
The  character  of  the  stools  in  some  patients,  the  lithuria,  altered  appetite 
end  wasting  show  that  there  is  a  defect  of  absorption  and  assimilation. 
It  has  been  ascribed  to  lithseniia  or  the  uric  acid  diathesis,  and  undoubtedly 
many  of  the  symptoms  of  lithaemia  are  due  to  intestinal  dyspepsia.  It  has 
also  been  put  down  to  auto-infection ;  and  to  over-stimulation  of  the  glyco- 
genic function  of  the  liver,  because  of  the  hepatic  enlargement. 

The  most  probable  explanation  is  that  these  cases  are  due  to  errors  in 
diet,  chiefly  an  excess  of  carbohydrates  combined  with  a  deficiency  of 
proteins,  and  that  a  catarrhal  condition  of  the  alimentary  tract  is  set  up, 
varying  in  severity.  Consequently  the  secretions  are  altered  in  character, 
the  food  is  not  properly  digested,  by-products  are  formed,  and  there  is 
imperfect  absorption  and  assimilation  of  normal  food  stuffs,  together  with 
auto-intoxication  from  the  absorption  of  the  by-products.  The  lowered 
vitality  and  the  catarrhal  condition  of  the  intestines  permit  the  develop- 
ment  of  worms,  and  account  for  symptoms  such  as  albuminuria  and  those 
due  to  impaired  nutrition  of  the  nervous  system. 

Diagnosis. — This  affection  has  to  be  differentiated  from  tuber- 
culous disease,  especially  the  abdominal  forms.  It  may  occur  as  a  com- 
plication of  tuberculosis.  The  presence  of  adenoids  and  enlarged  tonsils 
is  too  common  in  children  of  this  age  to  have  any  bearing  on  the  diagnosis. 
By  interfering  with  breathing  they  may  accentuate  the  general  mal- 
nutrition and  the  symptoms,  and  account  for  some  of  the  occasional  compli- 
cations, such  as  enuresis.  Acute  attacks  are  apt  to  be  mistaken  for  appen- 
dicitis  or  other  abdominal  mischief.     Headache   and  vomiting  may  be 


280  Chapter   XXI  V. 

"mistaken  for  migraine  ;  and  the  general  symptoms  ascribed  to  neuras- 
thenia rather  than  the  neurasthenic  symptoms  to  the  disease. 

Prognosis. — The  fever  may  last  as  long  as  10  days  and  at  times  sub- 
sides suddenly.  Recovery  is  rapid,  except  in  recurrent  cases.  If  untreated, 
it  may  continue  for  years  in  attacks  of  varying  severity.  It  does  not  prove 
fatal  in  itself,  but  it  lowers  the  general  health  and  decreases  the  resisting 
power  to  other  diseases.  Relapses  are  liable  to  occur.  Regularity  of 
the  bowels  and  the  absence  of  mucus  in  the  stools  are  favourable  features. 

Treatment. — For  acute  cases  give  a  mercurial  purge  and  simple  diet, 
and  rest  in  bed  until  2  days  after  the  fever  has  subsided.  For  chronic  cases 
change  of  air  and  surroundings  is  more  important  than  diet  or  drugs. 
Forbid  all  mental  work,  worry,  excitement  and  entertainments.  Keep  the 
abdomen  and  extremities  warm  and  dry.  Attend  to  the  teeth  and  fauces. 
Adenoids  and  large  tonsils  must  be  removed. 

The  diet  consists  of  regular  meals.  Reduce  or  omit  fermenting  foods, 
sweets,  jam  and  carbohydrates  generally.  Forbid  all  new  bread,  new 
potatoes,  fried  fish,  pickles  and  stringy  vegetables.  Allow  oatmeal  porridge 
and  stale  brown  bread  tentatively.  At  first  limit  the  diet  to  eggs,  fish, 
bacon,  ham,  tongue,  meat,  potted  meats,  butter  and  dripping,  dry  toast 
and  rusks.    Later  on,  add  greens  and  ripe  fruit. 

Cod-liver  oil  and  hypophosphites  are  injurious  unless  the  child  is 
almost  convalescent,  and  even  then  they  may  upset  the  digestion.  Give 
grey  powder,  with  or  without  rhubarb  and  soda,  at  bedtime  ;  in  small 
doses  if  there  is  diarrhoea,  and  larger  doses  if  the  bowels  are  constipated. 
Apenta  water  or  sodium  sulphate  on  waking  is  necessary,  if  there  is  much 
constipation.  A  mixture  of  bicarbonate  of  soda  or  potash,  citrate  of  potash, 
nd  tincture  of  nux  vomica  can  be  given  before  meals.  The  addition  of 
vegetable  bitters  improves  the  appetite.  Decoct,  aloes  co.  dr.  ^-1  before 
meals  may  improve  a  poor  appetite  or  reduce  a  voracious  one.  Give 
bismuth  and  carbonate  of  magnesia  for  diarrhoea  ;  charcoal  and  salol  for  the 
tympanites  and  excess  of  mucus  ;  small  doses  of  calomel,  if  the  stools  are 
white.     Maltine  and  mild  alcoholic  drinks  are  sometimes  useful. 


CHAPTER    XXV. 

DIAKRHCEAL    AFFECTIONS. 

Simple  Diarrhoea — Infective  Diarrhoea — Infantile  Cholera — Ileo- Colitis 
and  Colitis,  catarrhal,  ulcerative  and  membranous  —  Tuberculous 
Enteritis  and  Colitis. 

Diarrhoea  is  merely  a  symptom  of  many  different  affections.  Some 
cases  are  functional,  others  of  organic  origin.  They  are  divisible  into 
two  main  groups  :  (1)  Acute — mild,  severe  and  choleraic  ;  (2)  Chronic — 
(a)  functional ;    (6)  organic. 

On  anatomical  grounds  the  organic  cases  are  divisible  according  to  the 
main  situation  of  the  organic  mischief,  but  many  overlap.  Thus,  we  speak 
of  gastro-enteric  catarrh  and  gastro-enteritis  ;  enteric  catarrh  and  enteritis  ; 
entero-colitis  or  ileo-colitis  ;  and  colitis.  Or  we  may  base  the  classification 
primarily  on  the  grounds  of  etiology,  and  secondarily  according  to  the 
morbid  anatomy  and  severity,  in  the  following  manner  : — 

(1)  Simple  or   N on- Infective   Diarrhoea. 

(a)  Mechanical,  e.g.,  indigestible  food,  foreign  bodies. 
(6)  Dietetic,  e.g.,  unsuitable  food. 

(c)  Nervous— due  to   excessive  peristalsis,   e.g.,   fright,   fatigue, 

reflex  irritation,  atmospheric  conditions. 

(d)  Eliminative. 

(2)  Infective,   Inflammatory,  or    Febrile    Diarrhoea — toxic,  fermental 

epidemic. 

(a)  No   serious   anatomical   change   in   the   mucous   membrane. 

This  includes  most  febrile  cases — mild,  severe  and  choleraic, 
as  well  as  toxic  ones. 

(b)  Serious  inflammatory  or  ulcerative  changes,  secondary  to  the 

inflammation. 

(3)  Sijmptomatic    Diarrhoea. 

(a)  Due  to  gross  anatomical  specific  changes,  e.g.,  tuberculous, 

typhoidal  and  dysenteric. 

(b)  Eliminative,  e.g.,  uraemia  and  the  crises  of  some  febrile  attacks, 

such  as  pneumonia  and  erysipelas. 


282  Chapter   XXV. 

The  difference  between  simple  and  infective  diarrhoea  is  that  in  the 
former  there  is  neither  microbial  infection  nor  any  special  anatomical 
change  in  the  digestive  tract.  According  to  this  the  toxic  cases  must 
be  grouped  with  the  simple  diarrhoeas.  It  must  not  be  forgotten  that  a 
simple  diarrhoea  may  become  infective  through  secondary  infection,  and 
that  in  infective  cases  anatomical  changes  are  not  necessarily  present. 
No  strict  line  of  demarcation  can  be  drawn  between  the  two  types.  Thus,. 
it  is  obvious  that  no  uniform  system  is  quite  satisfactory.  The  name 
sometimes  indicates  the  cause  of  the  attack,  sometimes  the  clinical  picture,, 
and  at  others  the  locality  of  the  pathological  changes.  According  to  the 
nomenclature  of  the  Royal  College  of  Physicians  of  London,  the  infective 
type  should  be  certified  as  "  epidemic  diarrhoea"  "  epidemic  enteritis," 
or  "  zymotic  diarrhoea.''''  The  names  are  unsatisfactory,  for  enteritis  is  not 
always  present  nor  do  the  cases  always  occur  in  epidemics.  "  Summer 
diarrhoea  "  is  an  unsuitable  name,  for  it  includes  many  cases  occurring 
in  hot  weather  which  are  of  the  simple  variety  and  not  infective,  and 
the  infective  type  may  occur  at  other  periods  of  the  year. 

The  Registrar-General  no  longer  recognises  the  names  "  acute  gastro- 
enteritis "  and  "  gastro-enteric  catarrh,"  yet  they  are  not  inappropriate 
by  reason  of  the  clinical  association  of  gastric  and  enteric  symptoms,  though 
there  is  no  affection  of  the  stomach,  "  Enter o-colitis  "  and  "  ileo-colitis  "" 
indicate  that  both  the  small  and  the  large  intestine  are  involved.  In  many 
instances  the  colon  escapes  and  in  others  it  alone  is  affected.  The  name 
::  dysenteric  diarrhoea"  given  when  there  are  mucus  and  blood  in  the  stools,. 
is  unsuitable,  for  it  is  based  merely  on  the  character  of  the  stools  and  has 
nothing  to  do  with  true  dysentery.  ''''Choleraic  diarrhoea,  cholera  nostras,, 
cholera  infantum  and  English  Cholera "  are  names  appropriate  for  a. 
particular  type,  with  profuse  watery  diarrhoea  and  rapid  collapse,  but  they 
are  not  true  cholera.  "Febrile  diarrhoea  "  is  not  a  perfect  name,  for  though 
fever  is  almost  invariable  in  the  infective  type,  it  may  also  be  present  in  non- 
infective  forms.  "Inflammatory  diarrhoea  "  is  equally  unsatisfactory  for 
there  is  often  no  evidence  of  inflammation  after  death.  "Lientery"  or 
" Lienteric  Diarrhoea"  is  an  affection  due  to  reflex  peristalsis  and  is  not 
true  diarrhoea. 

Etiology. — Infants  are  specially  prone  to  diarrhoea  for  the  stools  are- 
normally  liquid  or  semi-solid.  The  food  is  liquid,  peristalsis  active,  and  the 
sphincter  ani  weak.  Consequently  the  fseces  are  not  long  retained  in  the 
colon  and  diarrhoea  may  be  a  mere  exaggeration  of  the  normal  conditions. 
Moreover,  milk  is  a  suitable  nutrient  medium  for  the  growth  of  micro- 
organisms, and  the  deficiency  of  free  hydrochloric  acid  in  the  stomach 
may  enable  them  to  escape  destruction. 

Unsuitable  food  sets  up  catarrhal  conditions  in  the  intestines  and 
causes  increased  peristalsis.  Rickets  also  predisposes  to  catarrh  and  the 
secretion  of  inefficient  digestive  juices.      Heat  affects  the  system  generally 


Diarrheal   Affections.  283 

and  impairs  the  digestion,  for  much  less  food  is  required.  A  deficient  rainfall 
and  long  continued  high  external  temperature  predispose  to  epidemic 
outbreaks.  These  epidemics  have  been  thought  to  depend  upon  the 
temperature  of  the  soil,  4  feet  below  the  surface,  reaching  56°  F.  But  the 
ordinary  factors  that  come  into  play  in  hot  weather  are  quite  sufficient  to 
account  for  the  outbreaks.  The  bulk  of  the  infective  cases  occur  in  the 
hottest  months  of  the  year,  when  the  level  of  the  ground  water  is  low. 
A  heavy  rainfall  reduces  the  number  of  cases  and  raises  the  height  of  the 
ground  water,  but  it  also  reduces  the  temperature.  The  connection  of 
diarrhoea  with  teething  is  discussed  in  the  chapter  on  dentition.  Age  has 
an  important  bearing  on  mortality  and  the  incidence  of  the  attacks.  Most 
cases  occur  between  6  and  18  months  of  age,  and  the  mortality  of  infants 
under  I  year  is  appalling.  This  is  due  to  the  fact  that  additions  to  the 
diet  are  generally  given  about  the  age  of  6  months. 

The  environment  has  an  important  influence  on  epidemic  outbreaks 
and  on  mortality.  Bad  sanitation  and  hygienic  surroundings  lower  the 
vitality  of  the  child  and  exaggerate  the  effects  and  the  dissemination  of 
infection.  Decomposing  material  is  readily  conveyed  by  flies  to  food  or 
directly  to  the  lips  and  mouth  of  the  child.  Unsuitable  dwellings  and 
overcrowding  are  injurious.  The  mortality  among  children  living  in 
"  back  to  back  "  houses  is  higher  than  among  those  living  in  "  through  " 
houses.  Among  the  labouring  classes  improvement  in  their  dwellings  is 
accompanied  by  a  reduction  in  infantile  mortality. 

Anything  which  gives  rise  to  catarrh  in  the  intestines  is  a  predisposing 
factor.  Mere  chill  may  act  as  an  exciting  cause  of  simple  diarrhoea  or 
predispose  to  infective  attacks.  Such  a  chill  may  be  due  to  wet  napkins, 
a  prolonged  hot  bath,  too  cold  water,  short-coating,  insufficient  clothing, 
wet  feet,  etc.  It  is  apt  to  follow  sweating  produced  by  rickets.  The  custom 
of  dressing  children,  so  that  legs  and  arms  are  bare  and  the  neck  exposed, 
is  much  more  likely  to  lower  vital  resistance  and  cause  congestion  of 
internal  organs  than  to  have  a  hardening  effect  upon  the  child.  Intestinal 
parasites  cause  recurrent  attacks  by  setting  up  reflex  peristalsis  or  catarrh 
of  the  mucous  membrane. 

Under  the  age  of  9  months,  and  to  a  less  extent  in  older  children, 
diarrhoea  depends  on  the  mode  of  feeding.  Out  of  1,000  fatal  cases 
(Hope,  1887)  only  30  of  the  infants  had  been  entirely  breast-fed.  The 
mortality  among  infants  brought  up  by  hand  was  22  times  greater  than 
among  an  equal  number  of  those  nursed  or  partly  nursed.  Artificial  feeding, 
whether  on  cow's  milk  or  proprietary  foods,  is  the  great  cause  of  infantile 
mortality  from  diarrhoea.  These  observations  have  been  confirmed  by 
innumerable  physicians.  The  attack  is  due  to  various  causes  connected 
with  the  diet.  The  food  may  be  too  rich  in  quality  or  too  much  in  quantity, 
or  both  factors  may  be  combined.  It  may  be  unsuitable  in  character  to  the 
age  of  the  child.     Many  attacks  are  produced  by  malted  or  starchy  foods 


284  Chapter   XXV. 

in  the  first  few  months  of  life  ;  and  by  indigestible  articles  of  diet  at  all 
ages.  In  other  cases  the  food  is  given  too  often  or  at  irregular  intervals. 
Deleterious  changes  may  have  taken  place  in  it  before  ingestion.  The  milk 
may  have  gone  sour  or  meat  preparations  may  have  "  turned."  Lactic 
acid  is  not  a  cause  of  diarrhoea,  but  in  milk  that  has  turned  sour  other 
organisms  may  have  grown.  The  micro-organisms  may  produce  toxins  or 
ptomaines  in  the  food  before  or  after  ingestion,  or  they  may  set  up  ferment- 
ative or  proteolytic  changes  while  in  the  intestinal  tract. 

In  quite  one- quarter  of  the  cases  other  children  in  the  same  house  are 
attacked.  This  means  that  they  have  been  exposed  to  the  same  exciting 
cause,  or  that  direct  or  indirect  infection  has  occurred.  Even  the  breast-fed 
infant  may  be  infected  by  the  mother's  nipples,  from  lack  of  cleanliness  or 
by  organisms  which  have  made  their  way  up  the  ducts.  Infants,  too,  are 
apt  to  suck  the  fingers,  Job's  comforters,  teething  rings,  etc.,  and  to  put 
anything  within  their  reach  into  the  mouth.  Nevertheless  outbreaks  of 
infective  diarrhoea  in  the  breast-fed  are  comparatively  infrequent,  and  it 
is  quite  likely  that  infection  is  conveyed  by  flies  or  by  neglect  of  cleanliness 
on  the  part  of  the  mother.  Epidemics  have  been  traced  to  infection 
conveyed  by  milk,  water  or  food  at  all  ages.  In  institutions  it  may  be 
conveyed  from  patient  to  patient  by  careless  nurses.  It  is  carried  directly 
by  infected  dust,  or  indirectly  through  the  infective  dust  being  blown  on 
to  milk  and  other  foods.  On  account  of  the  prevalence  of  flies  in  hot  weather 
and  the  rapid  decomposition  of  organic  matter  in  the  room  or  in  the 
neighbourhood,  it  is  more  than  probable  that  the  fly  is  the  main  carrier  of 
infection. 

There  is  a  striking  resemblance  between  infective  diarrhoea  and 
many  outbreaks  of  food  poisoning.  They  are  clinically  indistinguishable 
and  may  occur  at  any  season.  The  simple  form  of  food  poisoning  is  due 
to  toxins  or  ptomaines  produced  by  the  action  of  infective  organisms  in 
the  food  before  it  is  swallowed.  The  symptoms  come  on  rapidly,  in  a  few 
hours  after  the  ingestion  of  the  poison,  and  are  proportionate  in  severity 
to  the  size  and  virulence  of  the  dose  and  the  susceptibility  of  the  individual. 
If  the  infective  organism  is  present  in  the  food  and  gets  into  the  system, 
it  may  develop  there  and  produce  toxins.  The  symptoms  do  not  arise 
as  quickly  but  they  are  more  prolonged  and  often  more  serious  ;  the  case 
is  really  one  of  blood  poisoning.  Often  the  attack  is  due  to  toxins  produced 
before  ingestion  and  a  secondary  microbial  blood  infection  subsequently. 
Here  the  acute  initial  attack  may  pass  off  and  be  followed,  in  the  course 
of  a  few  days,  by  a  febrile  condition  due  to  the  blood  infection. 

Bacteriology. — The  meconium  in  the  newborn  is  sterile,  but  by  the 
second  day  the  streptococcus  acidi  lactici,  B.  lactis  aerogenes  and  B.  coli 
are  abundant.  Some  attacks  are  apparently  due  to  virulent  forms  of  the 
B.  coli  which  get  into  the  milk,  through  faecal  contamination,  and  produce 
toxins.     The  most  dangerous  organisms  are  the  B.  enteritidis  of  Gartner, 


Diarrlceal   Affections.  285 

the  B.  enteritidis  sporogenes  of  Klein,  the  B.  dysenterise  of  Shiga,  the 
paratyphoid  and  the  paracolon  bacilli,  proteus  vulgaris,  and  some  strep- 
tococci. 

Pathology. — In  the  infective  cases  the  nervous  symptoms,  and  to  a 
great  extent  the  systemic  disturbance,  are  due  to  toxaemia.  They  are  often 
out  of  all  proportion  to  the  diarrhoea  and  vomiting,  which  at  first  may  be 
slight  or  absent.  In  other  cases  the  constitutional  symptoms  are  due  to 
excessive  loss  of  fluid.  The  vomiting  is  reflex  in  origin  in  most  forms  of 
simple  diarrhoea  ;  and  in  the  infective  type  sometimes  reflex  and  sometimes 
toxseinic.  The  different  anatomical  lesions  are  due  to  different  poisons  or  to 
special  proclivities  in  the  individual.  They  are  chiefly  found  in  the  caecum 
and  large  intestine,  that  is  in  the  places  where  faecal  material  is  longest 
retained.  The  local  phenomena,  diarrhoea  and  vomiting,  are  not  often  due 
to  actual  structural  changes.  To  a  great  extent  they  are  protective  and 
the  means  of  elimination  of  the  toxins.  Usually  they  are  too  profuse  and 
have  to  be  checked,  and  counteracted  by  the  free  administration  of  fluids. 
(Edema  may  be  the  result  of  renal  inadequacy  from  the  direct  action  of 
toxins  on  the  renal  epithelium.  Broncho-pneumonia  is  generally  due  to 
secondary  infection  of  the  lungs.  Sometimes  in  institutional  epidemics  it 
is  part  of  a  general  septic  infection  of  which  the  diarrhoea  is  also  a  symptom. 

Morbid  Anatomy. — The  more  acute  the  attack  the  less  evidence  of  it 
is  found  after  death.  Often  it  is  impossible,  by  examination  of  the  cadaver, 
to  ascertain  the  cause  of  death.  There  may  be  neither  macroscopic  nor 
microscopic  changes.  In  more  prolonged  attacks  there  is  a  simple  catarrhal 
inflammation  of  the  mucous  membrane,  which  varies  in  severity  and 
distribution.  The  epithelium  is  denuded  and  the  glandular  cells  are 
swollen  and  granular  ;  the  mucous  membrane  throughout  the  whole  of  the 
small  intestine,  more  especially  the  lower  half,  or  in  patches  of  varying 
extent,  is  acutely  inflamed.  Sometimes  the  solitary  follicles  and  Peyer's 
patches  are  swollen  and  stand  out,  much  as  in  the  early  stages  of  typhoid 
fever.  Sometimes  this  condition  is  so  marked  that  bacteriological  examina- 
tion must  be  made  for  the  typhoid  bacillus  in  the  spleen  and  mesenteric 
glands.  Occasionally  the  mucous  membrane  of  the  stomach  is  also  congested. 
In  other  cases,  notably  cholera  infantum,  the  mucous  membrane  throughout 
the  digestive  tract  is  quite  pallid  and  shows  no  signs  of  congestion.  The 
contents  of  the  intestines  vary  much  in  colour,  resembling  the  stools  passed 
during  life,  and  are  offensive  ;  and  theie  is  a  variable  amount  of  gas. 
Coming  to  the  colon  we  may  find  no  definite  anatomical  change  ;  congestion, 
in  patches  or  throughout ;  extensive  proliferation  or  ulceration.  In 
Acute  Catarrhal  Colitis  the  mucosa  is  swollen,  covered  with  mucus,  and 
exhibits  patches  of  haemorrhage  into  its  substance.  In  one  instance  in  a 
girl,  aged  5  years,  the  swelling  was  so  extreme  that  the  colon  formed  a 
thick  and  rigid  tube  ;  this  might  be  spoken  of  as  Acute  Proliferative 
Colitis.    The  thickening  involved  the  whole  wall,  but  especially  affected  the 


286  Chapter   X  X  V. 

mucosa.  The  child  only  lived  8  days.  In  a  brother,  aged  3  years,  who  also 
lived  8  days,  acute  inflammation  was  present  with  similar  haemorrhage  and 
superficial  abrasions,  but  no  abnormal  thickening.  In  prolonged  cases 
of  colitis  the  whole  of  the  wall  is  involved,  covered  with  a  false  membrane, 
and  the  solitary  follicles  are  swollen  and  may  ulcerate. 

Ulceration  of  the  Colon  is  of  varied  type.  In  severe  catarrhal  inflam- 
mation there  is  an  irregular  patchy  erosion  of  the  mucous  membrane,  due 
to  superficial  necrosis,  which  may  extend  in  depth  and  area.  Small  circular 
ulcers  either  commence  as  an  ulceration  of  the  mucosa  covering  the  lymph 
follicles,  or  the  follicles  undergo  necrosis  and  form  minute  abscesses  which 
discharge  through  the  mucous  membrane  and  leave  a  shallow  ulcer. 

Follicular  Colitis  occurs  with  or  without  ulceration  of  the  follicles. 
In  the  milder  type  Peyer's  patches  are  prominent  and  the  follicles  through- 
out the  colon  and,  to  a  less  extent,  in  the  ileum  are  swollen  and  stand  out 
above  the  surface  as  smooth  rounded  elevations,  like  minute  peas  ;  the 
overlying  mucous  membrane  may  or  may  not  be  swollen.  In  more 
advanced  stages  ulceration  begins  at  the  apex  of  the  follicle  and  gradually 
extends  deeper  until  the  whole  of  the  follicle  is  destroyed  and  extruded, 
leaving  a  sharply  cut  shallow  pit-like  ulcer.  The  colon  may  be  honey- 
combed with  such  ulcers  and  some  of  them  may  coalesce  into  large  ones,  an 
inch  or  more  in  diameter.  The  ulceration  extends  down  to  the  muscular 
coat,  the  striae  of  which  can  sometimes  be  seen  at  the  bottom  of  the  larger 
ones.  They  do  not  cause  perforation.  In  cases  of  long  standing  the  ulcers 
may  be  pigmented. 

In  Pseudo-membranous  Colitis  the  colon  is  mainly  involved,  and  the 
lower  2  or  3  feet  of  the  ileum  generally  affected.  The  walls  of  the  gut  are 
rigid  and  thickened.  The  mucous  membrane  is  intensely  engorged,  red, 
swollen,  and  roughened  in  appearance  or  covered  with  a  dirty  greyish 
exudation  of  fibrin,  which  looks  like  membrane.  The  exudation  consists 
of  round  cells,  red  corpuscles  and  micro-organisms  embedded  in  a  network 
of  fibrin.  It  may  infiltrate  both  the  mucosa  and  submucosa,  and  the  false 
membrane  is  then  a  compound  of  exudation  and  necrotic  products.  The 
intense  engorgement  is  primary  and  results  in  a  necrotic  condition  with 
patches  of  false  membrane.  Haemorrhagic  and  petechial  extravasations 
may  occur.  The  other  post  mortem  changes  in  the  various  forms  of  fatal 
diarrhoea  are  broncho-pneumonia,  bronchitis  and  pulmonary  collapse.  The 
liver  may  exhibit  fatty  changes  and  collections  of  inflammatory  cells  round 
the  portal  canals.  It  has  been  suggested  by  Terrien  that  cirrhosis  may 
start  in  this  way.  Cloudy  swelling  and  desquamation  of  cells  in  the  renal 
tubules  have  been  noted,  and  are  due  to  the  fever  or  to  the  direct  action  of 
toxins.  The  brain  may  be  congested  or  anaemic,  and  occasionally  the 
cerebral  sinuses  are  thrombosed. 

Simple  Diarrhoea. — In  the  breast-fed  simple  diarrhoea  is  due  to  colos- 
trum in  the  first  few  days  of  life  ;   to  milk  containing  too  much  fat  or  too 


Diarrhoea!   Affections.  287 

many  salts  ;  or  changes  in  the  milk  due  to  illness,  emotional  disturbance, 
dietetic  errors,  etc.,  in  the  mother.  One  of  the  most  frequent  causes  is  too 
frequent  nursing  at  irregular  intervals.  The  milk  contains  too  much  protein, 
and  the  curds  set  up  irritation  of  the  mucosa,  excessive  peristalsis  and 
diarrhoea.  Chill  is  not  an  uncommon  cause.  The  other  factors  are  those 
already  discussed  in  the  general  etiology  of  diarrhoea. 

The  stools  may  be  green,  the  colour  varying  from  patches  of  light  green 
mixed  with  the  fpeces  to  a  general  watery  green  like  spinach.  The  presence 
of  curds  shows  that  the  milk  contains  an  excess  of  undigested  protein  or  fat. 
Fat  curds  are  readily  disintegrated  by  pressure.  Yellow  stools,  more 
frequent  and  greater  in  quantity  than  natural,  even  thin  and  watery,  are 
due  to  conditions  of  increased  peristalsis  and  perhaps  too  liberal  supply 
of  digestible  food.  They  may  follow  chill  or  may  occur  at  the  onset  of 
infective  diarrhoea.  Profuse  watery  stools  are  also  due  to  too  rapid  peris- 
talsis ;  they  vary  in  colour  from  light  brown  to  green,  or  may  be  clear, 
serous,  like  rice  water.  They  are  often  dirty,  offensive  and  putrid.  Some- 
times they  are  almost  odourless  or  have  a  faint  sickly  smell.  Slimy  cr 
mucoid  stools  from  excess  of  mucus,  are  due  to  catarrh  or  more  serious 
inflammation  of  the  intestines,  especially  the  large  intestine.  Bloody  stools 
occur  in  acute  inflammatory  conditions,  especially  of  the  large  intestine. 
It  is  unusual  for  any  particular  variety  of  stool  to  persist  throughout  the 
illness.  They  vary  in  character  with  the  progess  of  the  case,  as  well  as  with 
the  anatomical  changes. 

In  the  bottle-fed  and  older  children  etiological  factors  are  much  more 
numerous  than  in  the  breast-fed,  though  they  are  chiefly  dietetic  in  origin, 
especially  in  the  simple  cases.  Attacks  are  liable  to  follow  the  ingestion  of 
any  indigestible  kind  of  food,  which  sets  up  excessive  peristalsis  and 
perhaps  some  catarrh  because  of  mechanical  irritation. 

Symptoms. — Simple  diarrhoea  is  often  ushered  in  or  preceded  by 
vomiting  and  a  variable  amount  of  colic.  In  the  infant  the  knees  are 
drawn  up  and  the  child  utters  an  angry  cry  ;  flatulence  is  commonly 
present.  Vomiting,  colic  and  diarrhoea  are  characteristic  symptoms  in  all 
cases.  Often  in  babies  there  is  a  variable  degree  of  fever.  At  all  ages,  more 
especially  in  the  very  young,  there  may  be  considerable  depression  and 
even  collapse  ;  the  child  being  pale,  the  features  pinched  and  drawn,  eyes 
sunken,  skin  cold  and  clammy,  and  the  temperature  subnormal. 

Infective  Diarrhoea. — The  symptoms  are  divisible  into  two  groups  ; 
the  intestinal  or  gastro-enteric,  and  the  nervous  or  toxa?mic.  The  toxaemia 
produces  the  sudden  onset,  marked  restlessness,  incessant  movement, 
sleeplessness,  depression,  prostration,  cardiac  collapse,  vomiting  and 
perhaps  fever.  The  more  acute  the  case  the  less  is  the  fever.  Some  of  the 
symptoms  in  the  gastro-enteric  form  are  due  to  thirst.  The  cases  may  be 
mild,  severe  or  choleraic. 


288  Chapter   XXV. 

Mild  cases  simulate  those  of  diarrhoea  and  vomiting  due  to  unsuitable 
food.  In  babies  the  vomiting  is  slight  and  consists  of  curdled  milk  ;  colic 
may  be  present  and  the  stools  are  unduly  frequent,  5  or  6  per  day,  greenish 
in  colour  and  containing  curds.  They  may  be  sour  and  offensive  and 
contain  blood  and  mucus.  In  2  or  3  days  they  are  even  much  more  frequent 
and  more  watery.  The  child  is  restless  and  irritable,  no  longer  crawls  or 
runs  about,  and  looks  ill.  The  face  is  pale  and  a  little  shrunken,  the  tongue 
furred,  the  pulse  increased  in  frequency,  and  the  muscles  flabby.  Appetite 
is  impaired  or  lost  and  thirst  is  marked.  Water  alone  may  be  taken  readily 
and  retained.  The  temperature  ranges  between  100°  and  102°  F.  These 
patients  recover  in  a  few  days  ;  but  often  in  a  few  hours  may  become 
very  severely  ill,  passing  on  into  the  second  type. 

Severe  cases  are  characterised  by  depression,  collapse,  and  a  temperature 
of  102-104°  F.  Cases  often  begin  as  mild  attacks,  but  the  fever  increases 
instead  of  decreases,  and  all  the  symptoms  are  exaggerated.  Vomiting  is 
severe  and  often  continuous.  At  first  the  vomiting  consists  of  partially 
digested  food,  then  of  watery  fluid  and  bile.  The  stools  are  very  frequent 
more  and  more  like  dirty  green  or  greenish  water  with  brownish  particles  in 
them,  or  perhaps  vivid  green.  Sometimes  they  contain  mucus  and  blood. 
Often  they  are  extremely  offensive,  and  less  frequently  they  are  frothy. 
Tenesmus  and  prolapsus  recti  may  occur.  Restlessness  is  sometimes  a 
marked  feature  from  the  commencement  and  throughout  the  illness.  Thirst 
iS  often,  but  not  always,  extreme  ;  it  gives  rise  to  restlessness,  moaning, 
incessant  movement  of  lips  and  tongue,  and  tossing  of  the  head  from  side 
to  side  ;  even  water  is  vomited.  Gradually  or  rapidly  the  child  becomes 
feeble,  drowsy,  and  takes  no  notice.  The  face  is  drawn  and  pinched, 
expression  anxious,  cheeks  pale  and  hollow,  and  the  naso-labial  folds 
exaggerated.  The  mouth  is  dry  and  the  tongue  raw,  red  and  irritable,  or 
shows  patches  of  fur.  In  colitis  the  tongue  may  remain  clean  throughout. 
The  eyes  are  half-open  and  staring,  sunken,  dull  and  lustreless.  In  late 
stages  mucus  collects  on  the  insensitive  cornea?  and  the  pupils  may  be 
unequal.  The  fontanelle  is  sunken  and  pulsation  barely  palpable.  The 
abdomen  is  swollen  and  tender,  flaccid  and  clammy,  or  even  retracted. 
Abdominal  pain  gives  rise  to  acute  cries,  drawing  up  of  the  legs,  and  rigidity 
of  the  abdominal  muscles.  The  skin  loses  its  elasticity  and  is  wrinkled. 
(Edema  is  not  uncommon  and  general  anasarca  may  occur.  The  urine  is 
scanty,  albuminous,  and  may  contain  hyaline  casts.  The  pulse  is  small, 
frequent  and  running.  At  first  breathing  is  shallow  and  increased  in 
frequency,  but  towards  the  end  it  becomes  slow,  infrequent  and  sighing. 
Cj^anosis  is  sometimes  present.  Finally,  a  comatose  state  results  and 
death  occurs  from  respiratory  failure  or  is  ushered  in  by  convulsions. 
This  comatose  state  is  known  as  " Hydrocephaloid"  or  "False  Hydro- 
cephalus," for  it  resembles  that  of  meningitis.  The  eyes  are  wide  open  and 
staring,  the  cornea?  dull  and  insensitive,  the  pupils  inactive  to  light  and 


Diarrhceal    Affections.  289 

perhaps  unequal ;  but  the  fontanelle  is  deeply  sunken  and  not  bulging 
as  in  true  hydrocephalus.  The  temperature  may  fall  in  the  axilla,  though 
remaining  high  in  the  rectum.  Eecovery  is  extremely  rare  from  the 
hydrocephaloid  state,  and  the  mortality  as  a  whole  is  high.  Cases  which 
recover  usually  end  in  7-10  days,  but  the  diarrhoea  may  persist  3-4  weeks 
or  even  become  chronic. 

Choleraic  or  Fulminating  Attacks  are  sudden  in  onset,  and  soon 
exhibit  grave  toxic  symptoms.  They  occur  in  the  strong  and  healthy  as 
readily  as  in  the  weak  and  delicate,  and  may  terminate  fatally  in  a  few 
hours.  At  first  the  child  is  irritable,  feeble,  and  prostrate.  Soon  it  becomes 
dull  and  apathetic  with  pinched  senile  aspect,  uttering  feeble  whining  cries. 
Wasting  is  extraordinarily  rapid.  A  strong  child  becomes  a  shrivelled 
wreck  in  a  few  hours.  Thirst  is  extreme,  and  even  water  is  almost  im- 
mediately vomited.  The  stools  are  faecal  and  copious  at  the  onset.  Soon 
they  become  watery,  odourless  and  colourless,  consisting  of  serous  fluid 
as  in  true  cholera  ;  or  they  may  be  dirty  brownish  or  greenish.  Pain, 
abdominal  tenderness,  and  tenesmus  are  usually  absent.  The  temperature 
reaches  104-106°  F.  In  some  cases  there  is  hyperpyrexia,  and  in  others 
a  subnormal  temperature  from  collapse.  Often  the  child  is  restless  and 
sleepy,  and  becomes  comatose  towards  the  end.  The  attack  may  begin 
with  or  terminate  in  convulsions.  Quite  three-fourths  of  the  cases  prove 
fatal.  The  duration  varies  from  a  few  hours  to  a  few  days.  Recovery  may 
be  sudden  and  rapid,  even  in  the  apparently  moribund.  Death  may  occur 
before  the  onset  of  the  diarrhoea. 

Colitis  and  Ileo-Colitis. — Cases  of  this  type  are  only  differentiated  from 
those  of  infective  diarrhoea,  by  the  anatomical  changes  found  after  death. 
In  other  words  the  disease  must  be  in  existence  for  a  sufficient  length  of  time 
to  produce  these  changes.  There  is  no  definite  line  of  demarcation,  no 
essential  difference  in  causation,  and  the  one  type  may  terminate  in  the 
other.  On  account  of  the  severity  of  the  anatomical  changes  and  certain 
special  peculiarities  of  the  disease,  an  attempt  must  be  made  to  define  the 
chief  diagnostic  features. 

Nothing  need  be  added  to  what  has  been  discussed  under  the  general 
etiology  of  diarrhoea,  except  to  insist  upon  the  infective  character  of  the 
affection.  It  may  occur  at  any  age,  but  is  most  common  between  6  months 
and  2  years.  It  may  occur  at  any  period  of  the  year,  but  is  most  common 
in  the  hot  months.  Sometimes  it  follows  infectious  diseases,  such  as 
measles,  influenza  and  diphtheria.  There  is  little  doubt  that  it  is  con- 
tagious through  infection  from  the  discharges,  and  that  different  organisms 
may  be  responsible  for  different  epidemics. 

Its  occurrence  in  epidemic  form  is  rare  in  England.  A  well-defined 
outbreak  came  under  my  notice  in  1900.  All  the  cases  occurred  on  one 
staircase  in  certain  barracks.     Four  floors,  with  four  rooms  on  each  floor, 

u 


290  Chapter  XX  V. 

opened  on  to  the  staircase,  and  they  were  occupied  hy  13  women  and 
30  children.  The  outbreak  began  on  the  top  floor,  spread  to  the  ground 
floor,  and  finally  to  the  first  floor.  There  were  12  inhabitants  on  each  of 
these  floors,  and  only  7  on  the  one  which  escaped.  The  outbreak  began 
at  the  end  of  June  and  ceased  at  the  end  of  August.  It  was  probably  due 
to  an  infective  water  supply  from  a  cistern  on  the  top  floor.  Six  children 
were  affected,  and  4  of  them  died.  Three  of  the  women  were  attacked,  but 
less  severely,  and  recovered.  Only  one  infant  under  2  years  was  affected. 
This  was  a  breast-fed  baby,  aged  3  months,  who  was  infected  either  from 
the  mother  or  another  child.  Two  fatal  cases,  a  brother  and  sister,  aged 
3  and  5  years  respectively,  ended  in  8-9  days.  The  anatomical  changes  are 
described  above. 

The  characteristic  symptoms  are  an  acute  onset,  with  vomiting  and 
diarrhoea,  moderate  fever,  frequent  pulse  and  respiration,  great  restless- 
ness and  depression.  The  stools  are  very  numerous,  small,  offensive,  green, 
and  contain  bright  red  blood,  mucus  and  a  little  faecal  matter.  In  these 
cases  there  was  no  abdominal  tenderness  and  no  tenesmus.  In  the  girl  the 
abdomen  was  lax  and  empty  ;  in  the  boy  it  was  a  little  distended.  Vomiting 
was  frequent  and  persistent.  The  tongue  was  somewhat  furred,  and 
tended  to  become  dry  and  brown  in  the  centre,  anorexia  was  marked,  but 
there  was  no  conspicuous  thirst.  The  diarrhoea,  vomiting  and  fever 
persisted,  and  death  ensued  from  exhaustion  due  to  the  toxaemia.  In 
favourable  cases  of  this  type,  the  vomiting  subsides,  the  tongue  remains 
c'ean  throughout  or  soon  becomes  so,  the  character  of  the  stools  improves,  and 
the  signs  of  toxaemia  are  less  profound.  The  blood  disappears  from  the 
stools  ;  next,  the  amount  of  mucus  decreases,  the  faecal  matter  increases, 
the  stools  become  less  frequent,  and  finally  more  solid.  The  offensive 
odour  persists  for  some  time,  even  after  the  stools  are  solid.  As  the 
diarrhoea  ceases  the  fever  subsides  and  the  appetite  returns.  The  ana- 
tomical lesions  are  those  of  acute  catarrhal  colitis,  previously  described. 
At  the  onset  of  these  attacks  the  symptoms  are  probably  put  down  to 
acute  indigestion  or  food  poisoning.  Other  symptoms  are  sometimes 
present,  such  as  great  thirst,  abdominal  pain,  especially  just  before  defae- 
cation,  tenesmus,  tenderness  in  the  course  of  the  colon,  and  prolapsus 
recti.  Although  very  frequent  the  stools  are  usually  small  in  amount, 
perhaps  not  more  than  \  oz.  at  a  time.  The  blood  is  bright  red,  liquid  or  in 
streaks,  and  persists  for  a  few  days.  The  more  the  blood  and  mucus 
present,  the  worse  is  the  case.  The  height  of  the  temperature  and  the 
degree  of  toxaemia  indicate  the  severity  of  the  attack.  In  mild  cases  the 
fever  may  only  last  a  few  days  and  not  reach  more  than  101°  F.  In 
a  severe  case  it  reaches  103°  F.,  or  more,  and  lasts  for  7-10  days.  The 
worst  attacks  prove  fatal  in  a  few  days.  If  it  is  prolonged,  it  is  liable  to  end 
in  catarrhal  ulceration  and  chronic  diarrhoea.  Ulceration  is  most  prone  to 
occur  in  the  ill-nourished,  in  those  badly  treated  at  the  onset,  and  from 


Diarrhoeal   Affections.  291 

too  soon  a  return  to  ordinary  diet.    Even  in  the  mildest  cases  convalescence 
is  slow,  a  matter  of  some  weeks  or  even  months. 

Follicular  Colitis  is  the  most  common  variety.  It  is  rare  under  the 
age  of  6  months  and  after  2  years  ;  and  is  often  found  in  fatal  cases  of 
infective  diarrhoea  in  badly  fed  infants.  The  onset  is  usually  that  of 
infective  diarrhoea  of  a  moderately  severe  type,  with  vomiting  and  fever  ; 
or  it  may  develop  more  gradually.  Probably  it  is  a  primary  catarrhal 
colitis  with  secondary  extension  to  the  lymph  follicles,  which  become 
swollen  and  stand  out  above  the  level  of  the  mucous  membrane.  Peyer's 
patches  are  also  swollen.  As  the  result  of  superficial  necrosis  of  the  mucosa 
covering  the  follicles,  or  necrosis  of  the  follicles  and  secondary  rupture, 
small  ulcers  are  left. 

The  affection  must  be  suspected  in  cases  of  infective  diarrhoea  in  infancy 
in  which  the  fever  has  persisted  for  over  a  week,  and  if  the  stools  contain 
much  mucus  but  no  blood.  In  later  stages,  when  ulceration  has  occurred, 
blood  may  be  present  in  small  quantities.  The  stools  are  not  very  frequent, 
but  they  vary  in  colour  and  are  offensive.  Their  most  characteristic  feature 
is  the  presence  of  mucus.  Pound  cells  may  be  found  on  microscopic 
•examination.  Vomiting  is  not  a  marked  feature,  nor  is  the  fever  high, 
except  perhaps  at  the  onset.  The  appetite  is  lost,  mouth  dry,  tongue  dr}' 
and  furred.  Catarrhal  stomatitis,  thrush  and  simple  ulcers  are  common 
The  abdomen  is  somewhat  full,  or  occasionally  relaxed  and  empty.  Urine 
is  scanty  and  loaded  with  urates.  The  skin  is  wrinkled  and  loses  its 
•elasticity,  and  emaciation  is  steadily  progressive. 

The  course  varies.  There  are  frequently  periods  of  remission  followed 
by  exacerbations  which  are  readily  induced  by  injudicious  feeding.  The 
ulcers  never  perforate,  and  their  presence  cannot  be  positively  diagnosed, 
but  must  be  suspected  in  prolonged  cases  and  if  blood  is  present.  Relapses 
.are  common  and  complete  recovery  rare.  Death  takes  place  in  a  few 
weeks,  usually  3-6,  from  exhaustion  or  from  the  marasmus  secondary 
to  the  disease.  It  may  be  preceded  by  a  hemorrhagic  petechial  eruption 
•on  the  abdomen  and  trunk. 

Pseudo-membranous  Colitis  is  a  very  severe  variety  affecting  infants 
under  2  years.  Clinically  it  is  a  grave  type  of  catarrhal  colitis  with  acute 
■onset,  vomiting,  high  fever,  large  liquid  stools  and  prostration.  Abdominal 
•distension,  tenderness,  severe  pain,  tenesmus,  prolapsus  recti  and  con- 
siderable haemorrhage  are  more  constant  and  more  marked  than  in  the 
•catarrhal  variety.  There  is  no  essential  difference  in  the  stools,  except  that 
perhaps  threads  and  patches  of  false  membrane  may  be  found.  Prostra- 
tion, delirium  and  coma  may  be  so  marked  as  to  quite  mask  the  abdominal 
symptoms.  The  diagnosis  from  catarrhal  colitis  is  based  upon  the  severity 
of  the  symptoms,  the  less  continuous  vomiting,  the  patches  of  false  mem- 
bane  in  the  stools,  and  in  rare  instances  visible  false  membrane  on  the 
prolapsed  mucous  membrane  of  the  rectum.     It  must  be  regarded  as  an 


292  Chapter   X  X  V. 

exceptionally  severe  form  of  catarrhal  colitis  with  fibrinous  exudation  and 
superficial  necrosis.    It  is  almost  invariably  fatal  in  infants. 

It  is  clearly  quite  impossible  to  make  an  exact  diagnosis  of  the  variety 
of  colitis  present,  in  many  cases,  though  it  can  be  assumed  with  a  con- 
siderable degree  of  certainty.  The  changes  in  the  colon  mainly  have  been 
insisted  on.  But  in  about  half  the  cases  there  is  inflammation  of  the 
ileum  as  well.  It  chiefly  affects  the  lower  half,  perhaps  only  2  or  3  feet,  as 
an  acute  catarrhal  inflammation,  general  or  patchy.  Or  it  appears  as  a 
hyperplasia  of  the  lymph  follicles  and  Peyer's  patches. 

Chronic  Colitis  is  divisible  into  chronic  catarrhal,  ulcerative,  and 
membranous  varieties.  The  chronic  catarrhal  form  is  sometimes  called 
mucous,  muco-membranous,  pseudo-membranous  or  membranous  ;  but 
the  term  membranous  should  be  entirely  dropped  for  this  variety.  It  is 
a  simple  catarrhal  inflammation  in  which  the  mucous  membrane  is  swollen, 
red  and  thickened  ;  and  it  is  characterised  by  mucus  in  the  stools.  The 
mucus  is  discharged  in  glairy  masses  like  slime,  jelly  or  white  of  egg  ; 
sometimes  they  are  so  coherent  as  to  float  out  in  water  and  look  like 
membrane,  but  they  are  readily  disintegrated  on  stirring.  The  mucus  is 
generally  on  the  surface  of  the  faeces  and  not  intimately  mixed  therewith. 
It  may  be  occasionally  passed  alone,  in  quantities  as  much  as  a  wine- 
glassful  at  a  time.  Microscopically,  there  are  found  desquamated  epithelial 
cells,  leucocytes,  blood  cells,  triple  phosphates,  and  granular  and  faecal 
debris. 

This  affection  is  quite  frequent  in  children  of  all  ages,  though  it  is 
frequently  overlooked.  It  is  a  sequel  of  an  acute  attack  of  ileo-colitis 
or  of  neglected  constipation,  through  the  irritation  of  the  mucous  mem- 
brane by  scybala.  Subjective  symptoms  are  slight  or  absent.  The  child 
may  appear  perfectly  well.  Frequently  there  is  a  history  of  languor, 
disinclination  to  play,  dark  rings  under  the  eyes,  and  perhaps  a  variable 
appetite.  Often  the  appetite  remains  excellent  throughout.  The  prognosis 
is  good  under  simple  measures  of  treatment. 

Ulcerative  Colitis  is  a  sequel  of  the  catarrhal  variety,  either  acute  or 
chronic,  or  due  to  specific  infection  as  in  tuberculosis,  typhoid  fever  and 
dysentery.  Stercoral  ulcers  result  from  obstruction  and  chronic  con- 
stipation. The  common  variety  of  ulcerative  colitis  is  the  one  in  which 
the  intestine  is  studded  with  many  minute  follicular  ulcers.  These  cases 
have  already  been  referred  to  under  the  name  of  follicular  colitis.  More 
extensive  ulceration  may  be  due  to  the  aggregation  of  several  follicular 
ulcers  but,  in  spite  of  the  frequency  of  follicular  colitis,  extensive  ulceration 
is  rare  in  infancy.  Much  more  probably  it  is  a  sequel  of  the  acute  catarrhal 
variety  or  of  chronic  colitis  secondary  to  constipation.  The  symptoms 
of  the  follicular  variety  are  those  of  follicular  colitis  plus  the  passage  of 
blood.  Ulcerative  colitis,  similar  in  type  to  that  of  adults,  is  comparatively 
rare  in  children,  and  no  fatal  case  has  come  under  mv  observation.     A 


Diarrheal   Affections.  293 

typical  instance  was  that  of  a  boy,  9  years  old,  under  the  charge  of 
Dr.  J.  Smith,  of  Putney.  Eight  months  previously  he  had  an  attack  of 
diarrhoea  and  vomiting  ;  4  months  later  another  and  worse  attack  of  the 
same  nature  from  which  he  had  not  recovered.  The  general  symptoms  were 
slight  febrile  attacks  with  pain  and  vomiting,  followed  by  the  passage  of 
loose,  rather  offensive  stools,  containing  mucus  and  brightish  red  blood. 
Between  the  attacks  the  stools  were  somewhat  the  same  in  character,  but 
less  frequent.  Nothing  abnormal  was  found  on  physical  examination, 
except  slight  pallor  and  a  little  tenderness  along  the  transverse  and 
descending  colon.  Another  case  of  a  milder  type  occurred  in  a  girl,  aged 
6  years,  who  had  been  passing  mucus  and  blood  on  and  off  for  a  year. 
Even  under  treatment  the  condition  persisted  for  8  or  9  months.  The 
general  health  of  these  children  and  the  appetite  remain  good,  and  for  that 
reason  it  is  difficult  to  get  efficient  dieting,  nursing  and  treatment  carried 
out.  It  is  important  in  these  cases  to  make  a  rectal  examination,  sometimes 
with  the  sigmoidoscope,  in  order  to  exclude  local  ulceration,  foreign  bodies, 
polypus,  piles,  angeioma,  papilloma  and  sarcoma. 

Membranous  Colitis  is  still  more  rare  in  children.  It  may  be  secondary 
to  an  acute  attack  ;  possibly  primary  and  due  to  the  pneumococcus  or  other 
organisms.  In  this  condition  there  is  considerable  quantity  of  thick 
membrane  composed  of  a  fibrinous  network,  leucocytes,  epithelial  and 
red  cells.  In  a  case  of  a  boy,  3  months  old,  with  apparently  simple  catarrhal 
colitis,  membrane  was  first  found  7  months  later,  and  for  a  year  longer  the 
lower  bowel  continued  to  form  and  discharge  it  in  considerable  quantities 
at  intervals  of  a  few  weeks.  Even  6  years  later  occasional  shreds  were 
passed,  although  the  boy  was  in  good  health.  This  variety  differs  in  no 
respect  from  the  chronic  catarrhal  form,  except  in  the  character  of  the 
membrane,  which  must  be  distinguished  from  the  muco-membranous  casts 
of  catarrhal  colitis.  It  is  almost  certainly  a  variety  of  this,  with  more 
infiltration  and  destruction  of  the  mucous  membrane. 

Tuberculosis  Enteritis  and  Colitis. — Tuberculous  ulceration  may,  or  may 
not,  give  rise  to  diarrhoea,  according  to  the  situation  and  extent  of  the 
ulceration.  Probably  diarrhoea  only  ensues  on  secondary  ileo-colitis, 
toxaemia  or  malnutrition.  Most  extensive  ulceration  may  be  found  in 
the  small  or  large  intestine  after  death,  although  in  life  there  has  been  no 
diarrhoea.  An  interesting  case  is  that  of  a  girl,  aged  4  years,  who  had  been 
ill  for  11  months.  For  6  months  she  had  loss  of  appetite  and  wasting  ; 
then  pain  in  the  abdomen  and  diarrhoea  began  and  continued  in  spite  of 
treatment  ;  for  2  weeks  there  had  been  blood  in  the  stools.  The  child 
was  very  wasted,  anaemic,  and  her  liver  was  enlarged.  The  abdomen 
was  a  little  distended,  but  at  times  was  lax  and  empty,  with  no  tenderness 
or  local  resistance.  Vomiting  was  frequent  and  there  was  a  little  irregular 
fever.  The  stools  were  loose,  very  offensive,  and  contained  small  particles 
of  clotted  blood.     All  the  symptoms  persisted,  vomiting  became  more 


294  Chapter   XX  V. 

frequent,,  and  the  child  died  from  asthenia  in  another  6  weeks.  In  the 
small  intestine  were  multiple  ulcers,  many  of  them  completely  surrounding 
the  »ut ;  and  the  csecum  was  extensivelv  ulcerated.  In  the  colon  were  2  large 
irregular  ulcers,  one  of  which  had  caused  a  stricture  with  a  lumen  onlv 
the  size  of  an  ordinary  penholder.  There  was  no  general  peritonitis,  but  at 
the  bases  of  the  ulcers  were  miliary  tubercles  on  the  peritoneum,  and  some- 
adhesive  peritonitis  matting  together  adjacent  coils  of  intestine.  Neither 
the  mediastinal  nor  mesenteric  glands  were  caseous.  Caseous  nodules  in 
the  upper  lobe  of  the  left  lung  made  it  almost  certain  that  there  was  the 
primary  focus  of  infection.  Another  case  of  very  acute  type,  but  ending 
in  recovery,  was  that  of  a  boy,  aged  5  years,  under  Dr.  Graham  Morris, 
Wallington.  Diarrhoea  and  irregular  pyrexia,  septic  in  type,  often  up  to 
103c  F.,  had  persisted  for  a  month.  The  stools  were  frequent,  loose  and 
offensive,  and  contained  much  mucus.  The  abdomen  was  lax  and  empty, 
the  spleen  not  enlarged,  and  a  small  lump  was  felt  to  the  right  of  and  below 
the  umbilicus.  The  diagnosis  lay  between  tuberculous  enteritis  and  chronic 
ileo-colitis,  probably  the  former,  the  lump  being  an  enlarged  mesenteric 
gland.  One  month  later  there  were  still  frequent  stools,  4  or  5  a  day,  with 
the  occasional  passage  of  blood-stained  pus  :  and  the  temperature  ranged 
between  97"  and  101"  F.  This  went  on  for  another  2  months,  and  under  an 
anaesthetic  nothing  but  enlarged  abdominal  glands  could  be  found.  Under 
careful  diet  and  treatment  the  boy  completely  recovered. 

The  usual  symptoms  in  this  variety  of  ulceration  are  wasting,  diarrhcea, 
with  offensive  stools,  which  contain  mucus  and  probably  pus  and  blood, 
and  variable  pyrexia.  Appetite  is  generally  lost  and  reflex  vomiting  is  not 
uncommon.  Constipation  may  be  present,  although  there  is  extensive 
ulceration.  The  disease  is  often  limited  to  the  small  intestine  and  starts 
in  the  lymph  follicles.  It  is  almost  always  secondary  to  tuberculosis  else- 
where, though  it  is  possibly  occasionally  primary.  The  characteristics  of 
the  ulcers  are  the  same  as  in  adults,  and  the  presence  of  tubercle  bacilli 
in  the  stools  is  conclusive.  The  prognosis  is  not  favourable,  even  under  the 
most  satisfactory  conditions.  Death  results  from  exhaustion,  peritonitis, 
and,  rarely,  perforation  or  haemorrhage. 

Complications  of  Liarrhcea. — Erythema  and  the  excoriation  of  the 
skin  about  the  buttocks,  extending  to  the  scrotum  or  vulva,  are  common 
results  of  the  irritating  discharges.  Superficial  ulceration  is  not  infrequent. 
Pneumonia,  lobular  in  type,  is  apt  to  occur  in  the  infective  varieties,  being 
ushered  in  with  fever,  cough  and  frequent  respiration.  If  the  child  is  very 
ill,  it  may  give  rise  to  no  special  symptoms.  The  bacillus  cola,  has  been 
found  in  the  lung  in  some  of  these  cases.  Pulmonary  collapse  is  common  in 
young  children.  Other  complications  are  thrush,  otitis  media,  thrombosis 
of  cerebral  or  other  vessels,  and  subcutaneous  haemorrhages.  Petechial 
spots  on  the  abdomen  and  back  are  generallv  seen  in  conditions  in  which 
there  is  profound  marasmus,  and  are  signs  of  an  almost  certainly  fatal  issue. 


Diarrhoea!    Affection*.  295 

The  child  may  recover  from  the  attack  but  remain  weak  and  delicate, 
with  impaired  powers  of  absorption  and  assimilation,  and  ultimately  die 
from  marasmus.  Chronic  diarrhoea  results  from  atrophy  of  the  gut,  persistent 
enteritis  or  enteric  catarrh,  or  chronic  colitis.  The  infant  remains  ill,  and 
does  not  gain  weight,  although  food  is  taken  ravenously  and  there  is  no 
vomiting.  It  steadily  emaciates,  the  complexion  is  dull  and  earthy,  the 
skin  harsh  and  dry,  and  there  may  be  profuse  sweating.  Irregular  pyrexia 
is  often  present  and  continues  for  some  weeks,  and  oedema  of  the  extremities 
develops  towards  the  end.  The  abdomen  is  distended  and  perhaps  tender  ; 
colicky  pains  are  not  infrequent.  Peristalsis  may  be  visible  through  the 
thin  parietes.  The  stools  are  abnormal  and  offensive,  varying  in  different 
cases  and  during  the  progress  of  the  same  case.  They  may  be  greyish, 
pultaceous,  and  only  a  little  increased  in  frequency ;  greenish  or  dirty  brown, 
watery,  frequent  and  offensive  ;  or  contain  mucus  and  blood.  On  post 
mortem  examination  the  mucous  membrane  of  the  small  intestine  may  be 
much  thinned  and  the  glandular  cells  atrophied.  In  other  cases  catarrhal 
enteritis  or  follicular  colitis  is  present. 

Diagnosis. — Early  stages  of  infective  diarrhoea  may  be  indistin- 
guishable from  those  due  to  food.  Subsequently  the  more  than  transient 
fever  and  the  character  of  the  stools  are  of  value  in  diagnosis.  Infective 
diarrhoea  with  prolonged  fever  has  to  be  diagnosed  from  enteric  fever. 
This  is  infrequent  under  2  years  of  age  and  in  isolated  cases.  Leucopenia, 
AVidal's  reaction,  and  an  enlarged  spleen  are  present.  Intussusception, 
with  passage  of  frequent  small  stools  containing  mucus  and  blood  and 
frequent  vomiting,  may  be  mistaken  for  acute  ileo-colitis  ;  but  it  is  rare  for 
the  opposite  error  to  be  made.  The  differential  diagnosis  of  the  seat  of  the 
morbid  process  is  often  impossible.  There  is  no  line  of  demarcation  and 
many  cases  are  compound  in  character.  A  simple  infective  diarrhoea,  with- 
out gross  anatomical  changes,  may  develop  into  one  or  other  of  the 
different  forms  of  ileo-colitis  or  colitis.  If  the  catarrhal  process  is  limited 
to  the  duodenum,  there  is  rarely  diarrhoea,  and  jaundice  is  almost  invariable. 
Patches  of  isolated  catarrh  in  the  small  intestines  are  indicated  by  the 
faeces  being  fairly  solid  and  thoroughly  mixed  with  lumps  of  mucus.  If  the 
affection  is  in  the  colon,  the  mucus  covers  or  surrounds  the  faeces,  unless 
they  are  liquid.  Bright  blood  in  the  stools  shows  that  colitis  exists,  and  in 
tenesmus  the  rectum  is  involved. 

Prognosis  depends  primarily  upon  the  cause  of  the  diarrhoea,  and 
secondarily  on  the  severity  of  the  attack.  A  mild  case  may  become  rapidly 
acute  and  medical  assistance  is  often  sought  too  late.  Simple  diarrhoea 
is  rarely  fatal,  except  in  marasmic  infants  and  those  suffering  from  other 
illness.  The  prognosis  of  infective  diarrhoea  depends  upon  the  severity  of 
the  onset  and  the  signs  of  toxaemia.  Bad  signs  are  continued  high  tempera- 
ture, hyperpyrexia,  or  persistently  subnormal  temperature  ;  continued 
vomiting  and  the  passage  of  watery  offensive  stools  ;   loss  of  elasticity  of 


296  Chapter   XX  V. 

the  skin,  oedema,  scanty  urine  ;  and  the  development  of  the  hydrocepha- 
loid  state,  cyanosis,  broncho-pneumonia  and  collapse  of  the  lungs. 
Favourable  indications  are  the  subsidence  of  bad  signs,  and  the  re- 
appearance of  fsecal  matter  in  the  stools.  A  comatose  state  is  rarely 
recovered  from.  The  profuseness  of  the  diarrhoea  has  not  so  much  influence 
on  the  prognosis  as  would  be  expected.  It  is,  however,  a  measure  of  the 
dose  of  the  poison,  and  is  a  grave  sign  when  there  is  much  vomiting  and 
consequent  inability  to  take  sufficient  fluid  to  make  up  for  that  lost.  Of 
the  choleraic  cases  only  about  1  in  4  recover.  No  case  is  hopeless,  but  the 
younger  the  child,  the  worse  is  the  prognosis.  Relapses  are  liable  to  occur 
and  may  be  of  greater  severity. 

If  there  are  gross  anatomical  changes,  the  outlook  depends  upon  the 
severity  of  the  attack  ;  the  health  and  strength  of  the  patient ;  the 
environment  and  the  weather  ;  and  on  the  chances  of  a  chronic  inflam- 
matory state  persisting.  In  symptomatic  diarrhoea  the  probability  of 
recovery  depends  on  the  severity  and  upon  the  associated  disease.  An  acute 
eliminative  diarrhoea  in  uraemia,  or  a  critical  discharge  in  pneumonia, 
erysipelas  and  other  fevers,  may  prove  fatal. 

Treatment. — The  preventive  treatment  consists  in  the  education  of  the 
mother,  or  attendants,  in  general  attention  to  the  child's  health  ;  regulation 
of  the  diet,  the  avoidance  of  stale  food  ;  good  hygiene  and  ventilation  ; 
cool  climates  or  sea-air,  if  the  weather  is  hot,  and  bathing  in  cold,  not 
tepid,  water.  Whenever  a  child  passes  a  watery  green  stool,  it  requires 
medical  treatment.  Once  the  attack  has  commenced  we  have  to  replace 
the  drain  of  fluid,  destroy  or  get  rid  of  infective  germs,  and  keep  the  child 
alive  until  the  attack  is  over.  In  the  adult  gastric  juice  contains  hydro- 
chloric acid  in  sufficient  quantity  to  prevent  development  of  putrefactive 
organisms,  but  in  the  infant  hydrochloric  acid  is  deficient  in  quantity. 
Many  of  the  lower  animals  secrete  a  gastric  juice  which  contains  no  ferment, 
but  is  very  rich  in  acid,  and  they  are  able  to  eat  infected  food  with  impunity. 
Antiseptics  by  the  mouth  may  have  the  very  reverse  effect  to  that  intended. 
Small  doses  of  some  of  them  interfere  with  the  action  or  the  activity  of  the 
enzymes  of  the  digestive  tract ;  and  large  doses  render  them  inert.  Car- 
bohydrate food  is  nutritive  and  antiseptic.  It  is  unsuitable  as  a  medium 
for  the  growth  of  proteolytic  bacteria,  and  it  lessens  the  albuminous 
putrefaction  in  the  intestines  by  producing  lactic  and  other  organic  acids 
which  destroy  or  inhibit  the  growth  of  many  dangerous  organisms. 

Simple  Diarrhoea. — First  get  rid  of  any  irritant  matter  by  means  of  a 
dose  of  castor  oil,  calomel  or  grey  powder,  sodium  or  magnesium  sulphate  ; 
and,  secondarily,  attend  to  the  diet.  In  the  breast-fed  infant,  it  is  usually 
sufficient  to  regulate  the  nursing  according  to  the  principles  of  breast- 
feeding. If  the  child  is  over  6  months  of  age,  weaning  may  be  advisable. 
In  the  bottle-fed  it  may  be  sufficient  to  regulate  the  feeds.  Give  a  smaller 
quantity  of  a  weaker  food  at  longer  intervals,  or  dilute  the  milk  with  a  weak 


Diarrhcoal   Affections.  297 

solution  of  arrowroot  or  rice  water.  Often  it  is  enough  to  stop  the  admin- 
istration of  some  proprietary  food  to  which  the  attack  is  due.  It  may  be 
necessary  to  peptonise  the  milk  for  a  few  days,  or  even  to  get  a  wet  nurse. 
Should  the  attack  be  due  to  febrile  conditions,  as  in  teething,  the  quality 
and  quantity  of  the  food  must  be  reduced.  Attention  must  be  paid  to  the 
milk  supply,  the  mode  of  preparation  and  administration  of  each  feed,  the 
temperature  of  the  food,  and  the  cleanliness  of  all  the  apparatus.  Hot 
foods  increase  the  motility  of  the  stomach,  and  iced  water  diminishes  it. 
Both  are  liable  to  set  up  reflex  intestinal  peristalsis,  so  it  is  advisable  that 
all  food  be  given  lukewarm. 

In  older  children  the  diet  must  be  limited  for  at  least  24  hours.  It 
should  consist  of  equal  parts  of  boiled  milk  and  thin  arrowroot  or  corn- 
flour gruel.  Complete  starvation  is  often  advisable,  or  milk  should  be 
entirely  omitted.  In  every  case  the  patient  must  be  kept  warm,  and  put  to 
bed  if  the  attack  is  severe. 

After  the  preliminary  purge  drugs  are  rarely  required,  but  the  return 
to  the  ordinary  diet  must  be  gradual.  Give  bread  and  milk,  tea  and  toast, 
boiled  egg,  bread  and  butter,  cornflour  and  ground  rice  puddings,  fish  and 
mashed  potato,  and  so  on.  Drugs  are  often  necessary  and  useful.  For  green 
stools  in  infants,  the  addition  of  sod.  bicarb,  or  sod.  citrat.,  grs.  1-5  to  each 
feed,  is  frequently  efficacious.  If  the  stools  contain  curds,  small  doses  of 
castor  oil  m.  3-5  with  mucilage  and  caraway  water,  4  times  a  day,  frequently 
cause  constipation  in  2  or  3  days.  For  catarrhal  or  inflammatory  states  of 
the  alimentary  tract,  especially  if  mucus  and  blood  are  present  in  the  stools, 
give  bismuth  in  large  quantities.  Even  a  drachm  of  the  carbonate  or 
subnitrate  may  be  given  as  an  initial  dose.  More  usually  frequent  doses  of 
grs.  5-10  are  sufficient.  A  suitable  mixture  consists  of  bismuth  carb., 
glycerin.,  pulv.  acacia?,  aa  dr.  1.,  aq.  cinnam.  to  2  oz.  ;  1  dr.  being  given 
every  2-4  hours  for  infants  of  6  months.  In  these  cases  it  is  often  advisable 
to  give  in  addition  grey  powder,  gr.  J- J,  bis  or  ter  in  die.  To  any  of  the  above 
mixtures  tr.  opii.  m.  J-^  may  be  added,  if  there  is  any  pain  or  if  the  diarrhoea 
is  uncontrolled.  It  is  generally  best  given  alone  in  water,  and  repeated 
according  to  the  effect  on  the  child.  It  is  particularly  useful  in  cases  of 
profuse  diarrhoea  and  excessive  peristalsis,  in  which  the  stools  are  shot  out 
as  from  a  pump.  Older  children  may  be  given  bismuth  grs.  10-20,  or 
pulv.  cretse.  aromat.,  with  or  without  opium,  grs.  10-20,  for  a  few  days. 
Astringents  are  very  rarely  required.  As  a  rule  they  are  merely  of  tem- 
porary benefit  and  are  followed  by  recrudescent  signs.  They  may  be  useful 
in  prolonged  chronic  cases. 

The  treatment  of  infective  diarrhoea  consists  of  starvation,  elimination, 
Warmth,  stimulation,  the  administration  of  much  fluid,  good  nursing  and 
cleanliness.  Subsequently  measures  for  the  reduction  of  inflammation  are 
needed.  The  principles  of  treatment  are  the  same  in  all  cases,  requiring 
modification  with  the  severity  of  the  attack.     Except  in  very  bad  attacks, 


298  Chapter   X  X  Y. 

begin  with  an  initial  dose  of  castor  oil  or  calomel  ;  the  latter  if  there  is  much 
vomiting.  Even  in  the  worst  attacks  frequent  doses  of  calomel,  gr.  -^q-^o 
hourly,  are  beneficial.  For  babies  over  9  months  of  age,  sod.  sulphat. 
grs.  10,  every  J-l  hour  for  4-6  doses,  is  better  than  castor  oil  or  calomel. 
It  does  not  cause  vomiting,  and  it  flushes  out  the  bowel,  eliminates  toxins, 
and  reduces  the  temperature.  If  there  is  much  fever,  it  is  very  useful ; 
but  it  is  contra-indicated  by  low  temperature,  great  debility  and  sunken 
fontanelle.  It  can  be  given  even  when  there  is  blood  in  the  stools,  if  used 
early.  If  there  is  much  vomiting,  the  stomach  can  be  washed  out  with 
warm  alkaline  solution.  This  gets  rid  of  food,  mucus,  fermenting  products 
and  toxins,  and  permits  the  introduction  of  a  dose  of  castor  oil  before 
taking  out  the  tube. 

Diet. — In  acute  cases  milk  must  be  discontinued  for  12-48  hours, 
and  nothing  given  by  mouth  except  plain  hot  water  every  hour,  or  in 
quantities  of  dr.  1  every  J  hour.  It  is  of  little  use  giving  food  which  will 
be  at  once  vomited.  Water,  even  if  vomited,  washes  out  the  stomach, 
relieves  thirst,  is  diuretic  and  eliminative.  Hot  weak  tea,  cold 
water,  toast  water,  and  rice  or  barley  water  may  be  given  if  preferred. 
Albuminous  foods,  even  albumin  water,  should  be  avoided,  if  the  stools 
are  putrid  or  contain  mucus  or  blood,  and  when  the  toxaemic  symptoms  are 
marked.  The  attack  is  most  frequently  due  to  organisms  which  grow  best 
in  albuminous  foods.  In  these  cases  cereal  decoctions  are  much  more 
beneficial.  The  value  of  carbohydrate  food  in  the  prevention  of  intestinal 
putrefaction  has  been  already  discussed  (pp.  272-3).  On  the  other  hand 
carbohydrates  are  contra-indicated  when  there  are  flatus  and  abdominal 
distension,  acid  and  frothy  stools,  and  no  constitutional  symptoms.  Un- 
sweetened condensed  milk,  weak  peptonised  milk  and  albumin  water  are 
suitable  in  such  attacks. 

Meat  broths  are  generally  permissible,  for  they  are  little  more  than 
solutions  of  extractives,  almost  devoid  of  protein  and  carbohydrate.  They  are 
stimulants  rather  than  food,  and  can  be  given  in  most  acute  cases  after 
24  hours,  or  before,  if  they  can  be  retained.  Sometimes  they  help  to  main- 
tain the  diarrhoea.  Fresh  meat  juice,  dr.  1  every  £  hour,  can  sometimes  be 
retained  when  everything  else  is  vomited.  In  hot  weather  it  is  constantly 
full  of  microbes  and  may  prove  more  dangerous  than  the  disease.  On  the 
whole  there  is  little  benefit,  and  perhaps  much  risk  in  the  use  of  meat 
preparations.  The  proprietary  foods  containing  albumoses  and  peptones 
actually  cause  diarrhoea.  The  jellies  are  generally  pleasant  and  harmless. 
After  the  acute  stage  or  as  soon  as  food  can  be  retained,  give  whey,  white 
wine  whey,  unsweetened  condensed  milk,  cream  and  water,  or  diluted 
peptonised  milk.  Then  try  Benger's  Food,  milk  and  barley  water,  arrow- 
root gruel,  and  gradually  return  to  the  ordinary  diet.  On  account  of  the 
great  liability  to  relapse  and  to  chronic  inflammatory  mischief  in  infective 
cases,  the  diet  must  only  be  increased  slowly. 


Biarrhceal   Affections.  299 

Elimination  is  assisted  by  subcutaneous  injections  of  normal  saline 
solution,  small  enemata  of  saline,  and  irrigation  of  the  colon  according  to  the 
methods  described  under  rectal  therapeutics.  The  temperature  of  the 
fluid  for  colon  irrigation  should  be  60-70°  F.,  if  there  is  much  fever  ;  100°  F. 
in  cases  of  medium  severity  with  much  mucus  ;  and  110°  F.,  as  a  stimulant, 
if  the  temperature  is  subnormal  or  the  patient  weak.  Irrigation  in  acute 
colitis  washes  away  mucus,  germs  and  irritating  particles  of  undigested 
food,  but  cannot  reach  the  deeper  layers  of  the  inflamed  mucous  membrane. 

Subcutaneous  injections  are  also  useful  in  collapse.  From  50-150  c.c. 
of  normal  saline  solution  should  be  injected  every  6  hours.  It  is  intro- 
duced quite  slowly  into  the  loose  cellular  tissue  of  the  abdomen,  axilla, 
groins  or  thighs.  Marfan  recommends  an  injection  of  1-4  drs.  every  4  hours 
of  a  mixture  of  caffeine  citrate  0-75  gms.,  sod.  chlorid.  2-5  drs.,  sterilised 
water  300  c.c. 

Stimulants  are  best  given  as  small  doses  of  brandy  or  whiskey,  m.  3-10, 
in  hot  water  every  1-3  hours.  In  choleraic  cases  and  collapse  it  can  be 
given  freely  by  mouth  or  rectum.  The  next  most  valuable  stimulant  is 
strychnia  gr.  ¥^  hourly  and  given  subcutaneously.  Or  we  can  make  use 
of  sal  volatile,  m.  3-5  in  water,  or  subcutaneously  in  extreme  stupor  ; 
sulphuric  ether  m.  5-15  by  mouth  or  sub  cutem  ;  musk  gr.  \-1  every  15-30 
minutes  until  grs.  5-10  have  been  taken  ;  camphor  dissolved  in  olive  oil, 
1  in  30,  and  given  sub  cutem,  or  by  mouth  mixed  with  glycerine  in  doses 
cf  gr.  J-2,  or  spirits  of  camphor  m.  5-10,  every  J  hour  by  the  mouth  and 
less  often  subcutaneously. 

The  child  must  be  kept  very  quiet,  the  mouth  cleaned  with  weak 
alkaline  solution,  and  the  room  well  ventilated.  The  nurse  must  carefully 
disinfect  her  hands  after  attending  to  the  child,  wash  before  she  prepares 
the  meals,  and  disinfect  all  napkins. 

Bathing. — Infective  cases  must  be  kept  very  clean  and,  if  there  is 
much  fever,  should  be  sponged  after  the  usual  methods  (p.  75).  Hot 
baths  and  mustard  baths  are  given  as  stimulants  in  collapse  and  prostration. 
A  hot  bath,  for  5-10  minutes  night  and  morning  and  given  very  gently, 
allays  restlessness  and  to  some  extent  relieves  thirst  and  aids  elimination. 
A  tepid  bath  at  80°  F.,  with  the  addition  of  a  handful  of  sea-salt  in  4  gals, 
of  water,  is  useful  in  convalescence  and  as  a  preventive  measure  in  hot 
weather.  It  may  be  followed  by  a  cold  douche  at  60°  F.,  if  the  child  is  old 
enough. 

Drug  Treatment. — Purgatives,  antiseptics,  sedatives  and  astringents 
are  all  used.  Acacia  is  added  for  the  suspension  of  soluble  drugs  and  as  a 
sedative  for  the  gastric  and  intestinal  mucosa.  Glycerine  is  better  than 
syrup  as  a  sweetening  agent,  as  it  does  not  ferment  in  hot  weather.  At 
the  onset  small  doses  of  calomel,  gr.  ^--g,  may  be  combined  with  Dover's 
powder,  gr.  J,  and  given  every  2  or  3  hours  for  5  or  6  doses.  After  the  acute 
stage  it  should  be  given  every  4-6  hours,  with  the  addition  of  bismuth  carb. 


300  Chapter   X  X  V. 

grs.  10.  Bismuth  compounds  are  valuable  sedatives,  mildly  astringent. 
They  are  said  to  be  antiseptic,  to  stop  the  evolution  of  gas,  to  be  alterative, 
and  to  exert  a  tonic  action  on  the  stomach  and  bowels.  The  subcarbonate 
is  the  lightest,  is  most  free  from  grit,  and  most  pleasant  to  take.  A 
suitable  mixture  for  a  baby  6  months  of  age,  consists  of  the  subcarbonate, 
glycerine,  acacia  aa  dr.  1.,  aq.  carui  to  2  oz.,  given  in  doses  of  dr.  1  every 
1-3  hours.  The  salicylate,  subnitrate  or  oxide  can  be  used  in  similar  doses. 
To  the  above  2-oz.  mixture  there  may  be  added  acid  carbol.  gr.  1-2,  paregoric 
m.  15-30,  and  sodii  bicarb,  dr.  1.  Bismuth  preparations  should  be  preceded 
by  a  mild  purge,  kept  cool,  well  shaken  before  using,  and  given  frequently. 
They  are  chiefly  of  value  after  the  acute  stage.  The  bismuth  is  said  to  be 
more  active  when  converted  into  a  sulphide,  and  for  this  purpose  the 
addition  of  sulph.  prgecip.  gr.  1  to  bism.  subnit.  grs.  10  is  sufficient. 

For  excessive  f  cetor  give  the  sulphocarbolates  of  soda,  lime  and  zinc, 
aa  gr.  %-h  ;  or  phenol  m.  1,  tr.  iodi.  m.  1,  glyc.  m.  5.,  aqua  ad.  dr.  1  ;  or 
tr.  iodi.  m.  1,  glyc.  ac.  carbol.  m.  1,  aqua  ad.  dr.  1. 

Innumerable  antiseptics  have  been  used  with  varying  success.  Sodium 
salicylate  is  highly  recommended  by  Jacobi,  but  in  my  experience  it  is  of 
little  value.  Salol  gr.  1  every  1-2  hours,  alone  or  combined  with  bismuth 
and  given  in  sugar-coated  tabloids,  is  of  more  use.  It  breaks  up  into  salicylic- 
acid  and  phenol  in  the  intestines,  and  should  not  be  given  for  more  than 
3  days.  Phenol,  combined  with  bismuth  and  aromatic  chalk  powder,  is 
also  valuable.  Of  the  naphthalin  group  benzo-naphthol  and  beta-naphthol 
give  the  best  results,  but  are  often  useless.  They  are  given  in  doses  of 
gr.  1  for  24  hours,  for  each  month  of  life  under  1  year  of  age,  and  in  doses 
of  grs.  5-10  combined  with  equal  quantity  of  sugar  3  times  a  day  for  older 
children.  The  stools  become  odourless,  the  fever  less,  and  the  general 
condition  improves.  They  can  be  combined  with  bismuth  preparation,  and 
small  doses  of  Dover's  powder.  Naphthalin,  naphthol,  phenocoll,  and  betol 
(b-naphthol  salicylate)  have  a  somewhat  similar  effect.  Creosote  prevents 
fermentation  and  acts  favourably  in  tuberculous  ulceration.  Styracol 
grs.  5-10  is  also  useful  in  this  type  of  ulceration.  It  passes  through  the 
stomach  unchanged,  and  is  converted  into  guiacol  and  cinnamic  acid. 
If  intestinal  antiseptics  are  given  the  most  reliable  are  carbolic  acid, 
calomel,  b-naphthol,  salol,  iodine,  iodoform,  chlorine,  creosote  and  guiacol. 
Turpentine  is  useful  for  haemorrhage  and  prevents  meteorism. 

Astringents  are  injurious,  until  the  alimentary  tract  is  clear  of  poisonous 
products.  They  are  comparatively  of  little  value  and  rarely  advisable, 
especially  in  infants.  Tannin  irritates  the  stomach,  and  sets  up  pain  and 
vomiting.  It  can  be  given,  without  producing  such  effect,  in  the  form  of 
tannigen,  alone  or  combined  with  bismuth  and  other  drugs  ;  or  as  tannalbin, 
a  powder  containing  about  50  per  cent,  of  tannic  acid,  insoluble  in  the 
mouth  and  stomach,  and  resolved  in  the  intestine  into  tannin  and  albumin. 
It  is  given  in  doses  of  grs.  2-10,  and  is  useful  for  chronic  and  tuberculous 


Diarrhceal   Affections.  301 

diarrhoea.  Other  astringents  are  siver  nitrate,  gr.  |-|-,  given  in  water 
with  acid,  nitrici  dil.  m.  1,  3  times  a  day;  zinc  oxide  grs.  1-5  with  bismuth 
grs.  5-20  every  2  hours  ;  and  drugs  such  as  logwood,  coto,  kino  and  catechu. 
A  useful  powder  consists  of  calomel  gr.  |-J,  pulv.  kino  co.  gr.  h,  pulv.  ipecac. 
co.  gr.  |,  1-3  times  daily,  in  chronic  cases  with  restlessness. 

Opium  andi  ts  preparations  must  not  be  given  in  early  stages,  for  they 
interfere  with  elimination  and  may  paralyse  the  intestines.  Opium  is  more 
efficacious  than  codeia.  It  allays  pain  and  restlessness,  reduces  shock, 
and  promotes  sleep.  It  must  not  be  given  if  the  tongue  is  furred,  if  there 
is  much  vomiting,  or  in  the  presence  of  collapse.  In  small  doses  it  is  beneficial 
if  the  stools  are  frequent,  watery  and  accompanied  by  straining  ;  if  the 
tongue  is  clean  and  the  stools  are  offensive  on  account  of  excessive  peristalsis  ; 
and  if  blood  and  mucus  persist.  It  may  be  used  in  late  and  chronic  stages, 
and  is  also  valuable  in  reflex  or  lienteric  diarrhoea.  In  bad  cases  it  is 
best  given  alone,  in  the  required  dose,  and  repeated  according  to  circum- 
stances. In  less  severe  ones  it  may  be  added  in  minute  doses  to  bismuth 
or  castor  oil  mixtures.  The  best  preparations  are  tr.  camph.  co.  m.  3-10, 
tr.  opii.  m.  \-\,  and  pulv.  ipecac,  co.  gr.  J^- 1,  every  2-3  hours.  As  an  enema 
tr.  opii.  m.  2-5  in  1  oz.  of  starch  can  be  given  to  an  infant  over  6  months  of 
age,  for  it  produces  topical  effects  and  is  more  slowly  absorbed.  Morphine 
may  be  given  subcutaneously  in  doses  of  gr.  yi^  under  6  months  of 
age,  and  gr.  ^  over  1  year  of  age.  Opiates  must  be  given  cautiously,  the 
pupils  watched,  and  the  child  never  awakened  for  its  dose.  With  these 
precautions  no  evil  effects  result  from  small  doses. 

Serum  treatment  has  not  proved  of  much  value  up  to  the  present,  except 
in  cases  of  dysentery  and  those  due  to  Shiga's  or  Flexner's  bacillus. 

In  chronic  colitis  treatment  is  carried  out  on  the  same  lines.  Mild  cases 
recover  on  simple  dietetic  measures,  warmth,  bismuth,  and  attention  to 
the  bowels.  Foods  containing  indigestible  residues  must  be  avoided. 
If  due  to  simple  chronic  constipation  a  liberal  fruit  diet  or  a  modified 
cellulose  diet  may  be  beneficial.  A  saline  purge,  such  as  Apenta  water,  is 
given  every  morning.  In  more  severe  attacks  the  child  must  be  kept  in 
bed  and  fed  on  peptonised  milk,  lactose  and  eggs.  Iodoform  pills  or 
creosote  mixtures  are  given  if  the  stools  are  offensive  ;  mild  purgatives  or 
enemata  for  constipation  ;  large  doses  of  salicylate  of  bismuth  and  aromatic 
chalk  powder  in  acute  diarrhoea,  or  some  of  the  drugs  above  recommended. 
A  diet  of  curdled  milk  or  butter  milk  is  sometimes  of  value  for  intestinal 
infection,  proteolytic  organisms  being  crowded  out  or  destroyed  by  the 
lactic  acid  bacilli.  If  there  is  ulceration,  the  bowel  can  be  irrigated  with 
solutions  of  common  salt  or  boric  acid,  tannin  or  tannic  acid  1  per  cent., 
or  silver  nitrate  gr.  J-l  to  the  ounce.  The  silver  nitrate  injection  is  preceded 
by  irrigation  of  the  colon,  and  from  5-20  oz.  are  injected,  according  to  the 
age  of  the  child  (p.  87).  It  can  be  repeated  every  3  days  for  3  or  4  times 
and  is  then  discontinued  for  an  interval  of  10-14  davs.     If  it  causes  much 


302  Chapter  X  X  V. 

pain,  a  small  close  of  opium  may  be  given.  The  other  silver  compounds 
are  not  nearly  as  efficacious.  Should  this  fail,  appendicostomy  will  enable 
the  bowel  to  be  washed  out  daily  with  alkaline,  antiseptic  or  astringent 
lotions.  The  results  of  appendicostomy  have  been  fairly  satisfactory  in 
dysentery  in  adults,  but  less  so  in  ulcerative  colitis.  One  great  drawback 
to  it  is  that  it  leads  to  secondary  contraction  of  the  colon,  rendering  it 
impossible  to  close  the  opening.  Even  in  these  cases  the  patient  is  not 
certainly  cured,  and  may  have  more  or  less  haemorrhage  from  time  to  time. 

Symptomatic  treatment  must  be  adopted  in  many  cases  with  a  view 
to  the  relief  of  the  most  urgent  symptoms.  For  hyperpyrexia  the  cold 
pack  with  ice  to  the  head  is  the  best  remedy,  though  too  vigorous  for  most 
children.  In  mild  cases  ice  suppositories,  cold  rectal  injections,  tepid  or 
cold  sponging,  and  cradling  may  be  sufficient.  In  the  worst  ones  the  cold  bath 
may  be  essential.  The  temperature  must  be  taken  in  the  rectum,  or  it  may 
not  be  realised  that  the  blue,  cold,  apparently  collapsed  child  is  in  a  state  of 
hyperpyrexia. 

Vomiting  must  be  stopped,  for  it  is  exhausting  and  neither  aperient.? 
nor  stimulants  can  be  retained.  The  usual  methods  recommended  for  the 
treatment  of  vomiting  (p.  252)  must  be  adopted.  Collapse  is  treated  by 
alcohol  and  strychnia;  mustard  applications  and  heat  in  various  forms, 
e.g.  rectal  irrigations  ;  and  the  subcutaneous  injection  of  salines  and 
stimulants.  It  is  probably  due  to  the  action  of  the  poison  on  the  splanchnic 
area,  and  is  very  analogous  to  shock.  The  subcutaneous  injection  of  m.  3 
of  a  10  per  cent,  solution  of  chloral  hydrate  ;  atropin.  sulph.  gr.  g-Jo'ToVo 
hourly,  as  an  antidote  to  the  toxaemia,  until  the  pupils  dilate  ;  or  glonoin 
gr.  gio  ;  or  atropine  gr.  j^,  morphine  gr.  ^  hourly  are  all 
recommended. 

For  cerebral  symptoms  give  a  hot  bath,  or  apply  hot  bottles  to  the  feet 
and  ice  to  the  head.  Tenesmus  is  relieved  by  a  warm  injection  of  starch 
and  opium,  oil  or  gelatine  ;  the  local  application  to  the  anus  of  cocaine 
ointment  5  per  cent,  or  ichthyol  1  in  8  ;  and  the  administration  of  Dover's 
powder. 

Every  case  must  be  treated  on  its  merits  ;  bearing  in  mind  that  some 
attacks  of  diarrhoea  are  simple  and  harmless,  others  infective  and  virulent, 
and  a  few  chronic  and  persistent.  The  bulk  of  the  cases  are  due  to  errors 
in  diet,  and  on  a  suitable  diet  the  patient  may  rapidly  recover.  There  are 
no  hard-and-fast  rules  of  treatment  appropriate  for  rich  and  poor,  for  the 
intelligent  and  the  stupid,  for  the  well-nourished  and  the  marasmic,  in 
the  heat  of  a  tropical  climate  and  the  cold  of  more  northern  regions.  With 
care  and  patience  investigate  every  case,  ascertain  its  causation  and  the 
nature  of  the  pathological  process.  Attend  to  the  minutest  detail  in 
symptoms  and  treatment,  giving  the  most  careful  directions  to  the  atten- 
dant, for  it  is  on  these  minutiae  that  success  in  the  treatment,  of  infantile 
diarrhoea  in  particular,  especially  depends. 


CHAPTER    XXVI. 

CONSTIPATION. 

Simple  Constipation  —  Dilatation  of  the    Colon  —  Hirschsprung'' s   Disease. 

Constipation  means  infrequent  action  of  the  bowels  or  the  passage  of 
hard,  dry  faeces  at  an  age  when  they  should  be  semi-solid  or  almost  liquid. 
The  tendency  to  regular  daily  evacuations  is  inherited  and  varies  in 
different  families.  The  habit  can  be  cultivated  by  careful  training.  It 
is  advisable  that  the  bowels  should  act  once  or  twice  a  day  in  the  first 
year  of  life,  as  otherwise  the  consistence  of  the  faeces  becomes  hard.  For 
older  children  daily  evacuation  is  advantageous,  though  not  absolutely 
necessary. 

Constipation  in  Infants. — Complete  obstipation  in  the  newborn  depends 
on  atresia  or  stenosis  of  some  part  of  the  alimentary  tract.  Later  on  it 
may  be  due  to  hypertrophic  stenosis  of  the  pylorus,  dilatation  of  the  colon, 
the  pain  and  spasm  caused  by  anal  fissure,  or  some  of  the  mechanical 
forms  of  obstruction  more  common  in  older  children.  The  infant  is 
normally  predisposed  to  constipation,  because  the  sigmoid  flexure  is  tor- 
tuous and  up  to  2  years  of  age  is  relatively  much  longer  than  in  later  life. 
Apart  from  these  causes  it  is  generally  functional  or  dietetic  in  origin. 
It  occurs  in  both  the  breast-fed  and  the  bottle-fed,  more  frequently  in  the 
latter.  The  dietetic  causes  include  lack  of  food,  profuse  vomiting,  defective 
quality  of  food  and  unsuitable  composition.  If  the  milk  is  too  watery, 
it  may  be  fully  digested  and  assimilated,  but  the  stools  are  small  and 
infrequent,  the  urine  excessive  in  amount,  and  the  child  wastes.  If  the 
quantity  is  deficient,  constipation  is  accompanied  by  scanty  secretion  of 
urine.  Deficiency  of  fat  in  the  milk  is  a  common  cause ;  so,  too,  sterilised 
milk  and  starchy  foods,  unless  they  set  up  fermentation.  The  functional 
causes  are  those  dependent  upon  deficient  intestinal  secretion,  weak 
muscles,  and  defective  nerve  impulses.  Deficient  peristalsis  may  depend 
on  atony  of  the  gut,  impaired  reflex  excitability  or  a  mental  defect,  such 
as  the  cretinoid  state.  It  may  be  produced  by  some  of  the  popular  remedies 
for  colic  and  the  various  soothing  mixtures.  The  intestinal  secretions  are 
deficient  in  fever  and  malnutrition,  and  the  stools  become  dry,  friable, 
and  chalk-like. 

Symptoms. — The  baby  may  be  brought  for  treatment  because  of  colic, 
constant    screaming,    flatulence,    restlessness,    insomnia,    and    muscular 


304  Chapter   XXVI. 

twitehings.  Wasting  is  often  present  in  cases  due  to  an  insufficient  food 
supply,  as  well  as  in  others  in  which  the  food  does  not  appear  defective. 
Toxic  symptoms  are  rare  because  of  the  simple  character  of  the  food. 
Anorexia,  flatulent  eructations,  vomiting  after  each  feed,  fever,  and  even 
convulsions  may  occur.  Vomiting,  associated  with  constipation,  generally 
indicates  that  the  food  is  excessive  in  quantity  or  too  rich  in  quality.  On 
physical  examination  there  may  be  nothing  abnormal  except  a  little 
abdominal  distension.  In  severe  and  prolonged  cases  the  abdomen  becomes 
tense,  drum-like  and  tender.  The  increasing  tympanites  pushes  up  the 
liver,  and  the  splenic  dulness  becomes  obliterated.  Secondary  effects,  such 
as  umbilical  or  inguinal  hernia,  prolapse  of  the  rectum,  haemorrhage,  piles, 
and  dilatation  of  the  colon  may  be  found.  The  stools  are  scanty  and  dry. 
Hard,  whitish,  scybalous  masses  are  voided  with  much  pain  and  straining. 
Wasting  is  consequent  on  imperfect  digestion,  insufficient  absorption  of 
nutriment,  and  the  effects  of  colic  and  restlessness. 

In  older  children  the  condition  may  be  due  to  persistence  of  the 
infantile  habit,  atony  of  the  intestines,  deficient  innervation,  faulty  diet, 
or  defective  intestinal  secretions.  The  intestinal  atony  may  be  hereditary, 
muscular  or  nervous  in  origin.  Frequently  it  is  acquired  as  a  result  of 
recurrent  constipation,  inattention  to  the  calls  of  nature,  or  the  continued 
use  of  large  enemata  and  cathartic  drugs.  Sometimes  it  depends  on 
mechanical  obstruction,  such  as  intussusception,  hernia,  peritoneal  ad- 
hesions or  inflammation,  and  stenosis  of  the  gut.  Deficient  innervation 
leads  to  deficient  peristalsis  and  may  be  hereditary  or  secondary  to  nervous 
affections,  such  as  imbecility  and  meningitis,  or  to  atrophy  of  the  gut  aided 
by  deficient  secretion.  The  dietetic  causes  are  chiefly  an  insufficient 
supplv  of  fluid,  fat  or  indigestible  residue  ;  the  excessive  or  too  early  use  of 
starchy  foods  (this  may  cause  diarrhoea)  ;  astringent  wines,  tea,  and 
vegetables  containing  tannin.  Bolting  food  and  imperfect  mastication  are 
additional  factors.  Most  of  these  causes,  and  fever  also,  lead  to  deficiency 
of  intestinal  secretions.  Constipation  occurs  in  rickets  and  other  con- 
stitutional diseases  which  give  rise  to  anEemia  and  general  debility. 

Symptoms  are  not  uncommon,  except  in  trivial  cases,  and  are  generally 
toxemic  in  character.  The  child  is  dull,  languid,  easily  tired,  depressed 
and  irritable ;  of  a  sallow,  muddy,  yellowish  complexion,  with  dark 
rings  under  the  eyes ;  and  suffers  from  headache,  bad  or  capricious  appetite, 
flatulence,  nausea,  and  disturbed  sleep.  The  tongue  is  coated,  breath  foul, 
abdomen  often  distended,  abdominal  pain  common,  and  the  child  wastes. 
The  stools  are  hard,  lumpy,  dark  coloured,  and  covered  with  mucus.  A 
scanty  evacuation  takes  place  daily  or  much  less  frequently.  Hard  masses 
may  be  felt  in  the  descending  colon,  and  the  irritation  gives  rise  to  rectal 
discomfort  and  useless  straining  efforts,  catarrh,  and  the  exudation  of 
mucus  in  which  thread  worms  readily  live.  Intermittent  attacks  of  fever 
are  sometimes  entirely  due  to  constipation.     The  chief  secondary  results 


Constipation.  305 

are  proctitis,  anal  fissure,  prolapsus  recti  and  piles.      A  less  frequent  but 
more  important  sequel  is  dilatation  of  the  colon. 

Treatment  in  Early  Infancy. — First  relieve  the  retention  of  fasces, 
and  then  try  to  cure  the  habit.  In  the  simplest  cases  in  breast-fed  infants 
attend  to  the  diet  and  habits  of  the  mother,  with  the  object  of  reducing  the 
percentage  of  protein  and  increasing  the  percentage  of  fat  in  the  milk  and 
the  total  quantity.  In  order  to  accomplish  this,  prescribe  a  liberal  nitro- 
genous diet,  a  moderate  amount  of  alcohol,  tonics,  plenty  of  exercise,  and 
prolong  the  intervals  between  each  nursing.  The  administration  of  a  tea- 
spoonful  of  cream  in  warm  water,  twice  a  day  before  nursing,  is  sometimes 
a  sufficient  remedy.  For  a  bottle-fed  child  give  a  mixture  containing  a  high 
proportion  of  fat  and  sugar,  and  at  a  suitable  age  give  malted  food  or  oatmeal. 
Brown  sugar  and  treacle  are  somewhat  laxative.  Water  should  be  given 
freely  in  hot  weather.  The  habit  of  evacuation  at  the  same  hour  daily  must 
be  taught.  At  first  it  may  be  necessary  to  stimulate  the  action  of  the 
bowels  by  the  introduction  of  the  oiled  tip  of  the  finger,  the  nozzle  of  a 
syringe  or  a  soap  suppository.  If  these  simple  measures  are  insufficient, 
give  a  lump  of  manna  the  size  of  a  piece  of  sugar  once  or  twice  a  day  ; 
or  in  each  bottle-feed  sulphur  gr.  1,  or  sodium  phosphate  or  citrate 
grs.  5-10  ;  or  one  dose  daily  of  fluid  magnesia,  cream  of  magnesia,  or  mag. 
carb.  levis  grs.  2-5.  If  the  stools  are  chalky  and  white,  tr.  podophyllin 
m.  1-2  may  be  given  2  or  3  times  daily.  Peristalsis  is  encouraged  by 
abdominal  massage  along  the  colon,  in  a  circle  round  the  umbilicus,  for 
5-10  minutes  3  times  a  day.  The  skin  is  rubbed  first  with  oil  to  prevent 
excoriation.  After  the  first  year  of  life  the  tips  of  the  fingers  may  be  applied 
and  no  oil  used.  Treat  the  colon  as  if  you  were  trying  to  empty  a  long 
sausage.  Begin  over  the  sigmoid,  then  direct  the  movements  from  the 
splenic  flexure  to  the  sigmoid,  and  next  from  the  hepatic  flexure  onwards, 
and  finally  from  the  csecum.  Soap  suppositories  consist  of  gr.  1  of  soap  to 
m.  5  of  oil  of  theobroma,  and  are  comparatively  harmless.  Small  glycerine 
suppositories,  gluten  suppositories,  and  a  simple  cone  of  oiled  paper  are  of 
similar  value.  They  should  be  well  oiled  before  insertion,  and  used  once 
or  twice  a  day.  To  obtain  immediate  relief  inject  glycerine  dr.  J-l,  in 
water  oz.  \.  Other  useful  injections  are  oz.  J-l  of  cold  water,  soap  and 
water,  salt  solution  or  olive  oil.  Medicated  suppositories  containing  aloin, 
ext.  belladonnas,  ext.  nuc.  vomicae  aa  gr.  aViV?  can  be  used  after 
the  age  of  2  years,  but  are  of  little  more  value  than  the  simple  suppositories. 
The  prolonged  use  of  suppositories  or  injections,  whether  of  soap  or 
glycerine,  may  set  up  catarrh  of  the  rectum. 

Internal  medication  is  often  needed  for  chronic  and  severe  cases.  The 
doses  should  be  given  regularly,  1-3  times  daily,  in  sufficient  quantity  to 
keep  the  bowels  open  without  purging,  and  continued  for  weeks  or  months, 
being  gradually  omitted.  Manna,  aloes,  sulphate  of  soda  ;  the  syrups  of 
senna,  rhubarb  and  figs  ;   hyd.  c.  cret.,  alone  or  with  pulv.  rhei  co.  ;    and 


306  Chapter   XXVI. 

fluid  magnesia  or  cream  of  magnesia,  are  generally  used.  At  6  months  of 
age  a  mixture  containing  tr.  aloes  or  tr.  aloes  et  myrrh,  m.  3-5,  tr.  bella- 
donnas m.  1,  tr.  nuc.  vomicae  m.  ^,  syr.  zingiberis  m.  15,  and  water  to  a 
drachm,  3-4  times  a  day,  is  generally  efficacious.  It  can  be  given  more 
frequently  and  the  dose  of  aloes  increased.  It  is  reduced  as  soon  as  a  loose 
stool  is  passed.  Sometimes  maltine,  alone  or  with  cod  liver  oil,  is  sufficient. 
Drastic  purges  should  be  avoided.  The  usual  dose  of  castor  oil  is  followed 
by  recurrence  of  constipation.  For  hard  fsecal  masses  give  an  injection  of 
warm  olive  oil,  dr.  1-4,  followed  in  a  few  hours  by  an  injection  of  soap  and 
water  or  salt  solution,  oz.  1-4.  At  2  years  of  age  an  injection  of  ol.  terebinth 
dr.  1,  ol.  olivee  drs.  2,  and  the  yolk  of  1  egg,  well  mixed  with  4  oz.  of  warm 
water  can  be  used.  Injections  must  be  given  gently  and  slowly,  and 
stopped  at  once  if  pain  is  produced.  Mechanical  aids,  such  as  a  bent 
hairpin,  a  scoop  or  a  teaspoon,  are  rarely  needed. 

Treatment  in  Older  Children. — In  mild  cases  rely  on  hygienic  measures, 
diet,  habit  cultivation,  posture  at  stool,  massage,  and  general  and  abdominal 
exercises.  The  diet  should  contain  plenty  of  fatty  foods  and  waste  matter. 
If  it  fails,  it  does  harm  by  causing  dyspepsia  and  increasing  the  amount  of 
residue  to  be  got  rid  of.  A  liberal  supply  of  water  is  necessary.  On  waking 
give  fruit,  such  as  an  orange  or  apple,  and  half  a  tumblerful  of  hot  water ;  and 
a  full  tumbler  at  night.  Reduce  the  amount  of  cow's  milk,  which  alone  is 
a  frequent  cause  of  constipation,  and  give  a  liberal  supply  of  fruit,  porridge, 
wholemeal  stale  bread,  and  green  vegetables.  Olive  oil,  cod-liver  oil, 
petroleum  emulsion,  terrol  and  paroleine  are  useful,  and  act  mainly  as 
lubricants.  The  squatting  posture  should  be  adopted  at  stool.  If  the 
prdinary  closet  is  used,  the  seat  should  be  small  and  the  feet  raised  on  a 
high  stool.  Massage  should  be  carried  out  at  bedtime  with  the  child  on 
a  hard  mattress,  the  head  and  shoulders  raised,  the  legs  flexed  and  a  little 
rotated  outwards.  It  should  be  done  for  5-10  minutes,  while  standing  on 
the  left  side  of  the  patient  and  using  the  tips  of  the  fingers  in  the  manner 
above  described.  It  can  be  applied  by  the  child,  using  a  rubber  ball 
filled  with  2  or  3  lbs.  of  No.  10  shot  and  rolling  it  over  the  abdomen  for 
10  minutes  night  and  morning.  It  can  be  supplemented  by  an  injection  of 
olive  oil,  oz.  J,  and  by  galvanism  or  faradism  of  the  abdomen. 

Of  all  drugs  the  various  preparations  of  aloes  and  cascara  are  the 
most  valuable.  They  exert  a  stimulating  and  tonic  effect  on  the  lower 
bowel.  The  ordinary  aloes  pill  and  the  mixture  of  aloes,  belladonna,  nux 
vomica  and  ginger,  recommended  for  babies  but  in  larger  doses,  are  most 
satisfactory.  Sodium  sulphate  can  be  added  if  necessary.  Nux  vomica  or 
strychnia  is  generally  essential  in  order  to  increase  muscular  activity  and 
peristalsis.  Cascara  is  best  given  in  the  form  of  the  aromatic  syrup  or  as 
cascara  and  malt.  If  there  is  evidence  of  deficient  hepatic  activity  and 
defective  intestinal  secretion,  add  tr.  podophyllin,  or  give  small  doses  of 
calomel  or  grey  powder  and  rhubarb.     Other  mild  preparations  are  the 


Constipation.  307 

syrups  of  senna,  rhubarb  and  figs  ;  confections  of  sulphur  and  senna  ; 
sulphur  lozenges ;  tamarind  pulp,  tamar  indiens,  and  laxative  fruit 
pastilles  containing  senna.  The  recent  synthetic  drugs,  such  as  purgen 
or  phenolphthalein,  laxoin,  and  exodin  in  doses  of  gr.  J-2  are  tasteless, 
efficacious,  and  harmless,  and  act  in  much  the  same  way  as  salines.  Continued 
enernata  are  liable  to  cause  ballooning  and  irritation  of  the  rectum,  and 
render  it  atonic.  Glycerine  is  unsuitable  for  prolonged  use  ;  it  is  too 
stimulating  and  makes  the  rectum  tolerant  of  lesser  stimuli.  If  enemata  are 
used,  give  olive  oil  oz.  \,  soap  and  water  or  plain  cold  water  2-3  oz. 

The  most  useful  purges  for  children  are  castor  oil,  rhubarb,  sulphate 
of  magnesia  or  jalap,  calomel,  grey  powder  or  blue  pill,  and  aloes. 
Liquorice  powder,  calcined  magnesia  with  or  without  rhubarb,  and  mineral 
waters,  such  as  Apenta,  are  also  valuable.  Castor  oil  is  the  most  harmless. 
Rhubarb,  especially  in  the  form  of  Gregory  powder,  is  particularly  useful 
if  there  are  stomachic  conditions.  Salines  are  preferable,  if  a  watery 
■evacuation  is  desired  ;  mercurials,  if  the  function  of  the  liver  is  at  fault ; 
and  aloes,  if  the  defect  is  in  the  muscular  activity  of  the  lower  bowel.  In 
purgative  doses  they  do  not  cure  constipation.  If  they  are  given  for  this 
purpose,  they  must  be  given  systematically,  and  the  dose  reduced  as  soon 
as  a  single  loose  stool  is  passed.  For  severe  cases  aloes  and  sodium  sulphate 
•combined  are  given  in  increasing  doses  until  2  liquid  stools  are  passed  daily. 
The  full  dose  is  continued  for  2  or  3  weeks,  and  then  reduced  slowly.  The 
aloes  or  aloes  and  iron  pill  is  used  in  a  similar  way. 

To  relieve  chronic  accumulation  give  a  full  dose  of  castor  oil  and  a 
warm  olive  oil  enema,  followed  by  soap  and  water  enema  in  a  few  hours 
time.  If  this  fail,  give  extract  belladonna  gr.  \  every  2  hours  until  the 
pupils  are  widely  dilated.  Complete  impaction  is  treated  by  calomel  gr. 
1-5,  followed  by  castor  oil  and  large  injections  of  thin  warm  gruel  con- 
taining ol.  ric.  oz.  1,  ol.  terebinth  oz.  \  ;  or  pure  olive  oil ;  or  ox  gall  and 
water  p. a.  This  may  be  combined  with  the  belladonna  treatment  and 
mechanical   assistance. 

Dilatation  of  the  Colon. — The  persistence  of  chronic  constipation, 
faecal  obstruction,  foreign  bodies,  and  stricture  may  cause  considerable 
dilatation  of  the  colon.  In  the  so-called  idiopathic  variety,  or  Hirchsprung's 
Disease,  there  is  no  evidence  of  any  obstruction.  In  other  instances  there 
may  be  marked  narrowing,  to  the  size  of  a  lead  pencil,  of  the  rectum  and 
■colon  (Atkin)  ;  the  sigmoid  flexure  and  rectum  (Treves)  ;  the  ascending 
and  transverse  colon  (Dodd).  These  cases  of  congenital  narrowing  of  a 
portion  of  the  gut  must  be  distinguished  from  those  of  idiopathic  dilatation. 
The  symptoms  date  from  birth  or  shortly  after,  and  may  be  delayed  for  a 
few  years  if  the  narrowing  is  not  sufficient  to  cause  definite  constipation. 
The  ordinary  sequence  is  constipation,  abdominal  distension  and  intestinal 
■obstruction. 

Hirschsprung    (1887)    reported    2    cases    of    the    idiopathic    variety. 


308  Chapter   XXVI. 

Tuffier  (1907)  collected  88  cases,  of  which  one  was  in  a  7  months  foetus, 
21  in  the  first  year  of  life,  and  61  over  19  years  of  age.  These  are  cases  which 
are  not  due  to  faulty  habits,  chronic  constipation,  or  the  abuse  of  drugs 
or  enemata. 

The  Etiology  of  the  condition  is  uncertain.  There  is  evidence  that 
dilatation  may  depend  on  the  nerve  and  blood  supply.  Thus  "  ballooning  " 
of  the  rectum  is  due  to  defect  in  the  muscles,  and  is  often  associated  with 
conditions  affecting  its  innervation  and  blood  supply.  Excessive  tym- 
panites of  the  small  intestine  results  from  thrombosis  of  the  superior  mesen- 
teric vein,  and  has  been  produced  by  ligature  of  the  main  mesenteric  vein 
in  animals.  Probably  there  is  a  neuro-muscular  defect  of  congenital 
origin,  leading  to  inertia  of  a  portion  of  the  colon.  Hawkins  reported  a 
case  in  a  baby,  aged  6  months,  whose  grandfather  had  been  under  his  care 
for  a  similar  condition  and  had  died  from  it  at  40  years  of  age. 

Morbid  Anatomy. — The  sigmoid  flexure  is  divisible  into  the  iliac  colon, 
occupying  the  left  iliac  fossa  ;  and  the  pelvic  colon,  which  extends  from  the 
inner  edge  of  the  psoas  into  the  pelvis,  there  forms  a  loop  and  turns  back 
along  the  posterior  wall  of  the  pelvis  to  the  third  piece  of  the  sacrum, 
where  it  joins  the  rectum.  The  loop  has  a  mesentery  and  is  entirely  free. 
In  the  child  it  varies  much  in  length,  is  relatively  longer  than  in  the  adult, 
and  lies  in  the  abdomen.  At  the  junction  of  the  pelvic  colon  with  the- 
rectum  is  an  increased  amount  of  circular  muscle  fibres,  forming  a  kind  of 
sphincter.  Possibly  a  similar  kind  of  sphincter  is  present  at  the  junction  of 
the  colon  and  sigmoid,  a  colo-sigmoid  pylorus,  and  the  faeces  are  stopped 
and  moulded  in  the  sigmoid.  Dilatation  almost  invariably  begins  in  the- 
lower  3  ins.  of  the  pelvic  colon,  not  in  the  rectum.  This  suggests  a 
predisposing  anatomical  factor.  Sometimes  it  is  extreme,  at  the  time  of 
death,  and  there  is  no  hypertrophy.  More  commonly  there  is  secondary 
hypertrophy  of  the  circular  muscle  fibres  and  the  muscularis  mucosa?.. 
The  wall  may  reach  J  in.  in  thickness,  the  bowel  forming  a  rigid  tube.. 
Other  changes  are  probably  secondary.  Concetti  has  noted  cases  in  which 
areas  of  hypertrophy  of  the  large  intestine  alternated  with  atrophic- 
portions. 

No  definite  organic  stricture  is  found.  The  anus  is  normal  ;  and. 
anal  spasm  can  be  excluded,  for  the  rectum  is  not  funnel-shaped,  though 
sometimes  decidedly  roomy.  The  pelvic  colon  usually  shows  funnel-shaped 
dilatation,  but  the  lower  2  or  3  ins.  may  be  unaffected.  The  enlargement 
is  rapid,  but  not  abrupt,  somewhat  resembling  the  sloping  neck  of  a  bottle,, 
reaching  a  diameter  up  to  8  ins.  The  loop  shape  of  the  pelvic  colon  is 
generally  preserved.  It  rises  out  of  the  pelvis,  and  the  butt  end  of  the  loop- 
may  reach  the  right  costal  margin.  If  the  mesentery  is  short,  it  may 
become  stomach-shaped.  The  rest  of  the  colon  may  be  normal,  or  more  or 
less  dilated  for  a  variable  distance,  rarely  as  far  as  the  caecum.  The  small 
intestine,  is  collapsed  and  empty.     The  contents  of  the  colon  are  nearly- 


Constipation.   ,  309 

always  semi-solid,  greenish -yellow,  somewhat  like  wet  sand,  inoffensive 
and  deficient  in  fpecal  smell  ;  sometimes  there  are  scybala.  There  is  almost 
invariably  much  gas  and  this  must  be  regarded  as  the  dilating  force. 

Symptoms. — Constipation  is  present  from  birth,  or  an  early  age,  and 
may  alternate  with  diarrhoea.  There  may  be  no  spontaneous  evacuation 
of  meconium.  Usually  constipation  is  incomplete  and  flatus  is  passed. 
Sometimes  the  bowels  only  act  once  in  3-6  weeks,  and  complete  obstipation 
of  2  or  3  months'  duration  has  been  reported.  Gradually  the  abdomen 
enlarges  and  is  often  asymmetrical,  with  prominence  in  the  left  iliac 
region.  It  is  surprisingly  flaccid  and  rarely  dull,  the  resonance  being  due 
to  the  formation  of  gas  in  the  colon,  which,  becomes  enormously  dilated, 
tympanitic  and  distended.  The  pelvic  loop,  extending  up  to  the  umbilicus 
or  costal  margin,  may  be  visible  through  the  thin  parietes  ;  and  peristalsis 
may  be  obvious  and  excessive,  though  it  is  absent  in  great  distension.  The 
abdomen  becomes  hugely  distended,  forming  the  "  balloon  belly,"  but  still 
remains  flaccid  and  doughy.  The  splenic  and  liver  dulness  are  obliterated. 
The  superficial  veins  are  dilated,  and  the  skin  may  be  cedematous.  The  lower 
part  of  the  thorax  is  so  distended  that  the  costal  margin  forms  almost  a 
straight  line.  The  mechanical  pressure  produces  shortness  of  breath, 
displacement  of  the  heart  upward,  palpitations,  intermittent  pulse,  oedema 
of  the  legs  and  scrotum,  and  possibly  albuminuria.  The  dyspnoea  may  be 
so  great  as  to  cause  lividity  and  inability  to  move.  Vomiting  and  pain  are 
rare  ;  diarrhoea  may  result  from  passive  overflow,  secondary  catarrh  and 
ulceration,  with  possibly  the  passage  of  bloody  stools.  Indicanuria  may  be 
present.  In  the  terminal  stages  there  may  be  abdominal  pain,  hiccough, 
constant  vomiting,  increased  micturition,  cyanosis,  coldness,  collapse  and 
syncopal  attacks,  or  pyrexia  due  to  toxaemia.  The  general  health  remains 
remarkably  good  for  a  long  time,  and  the  final  stage  begins  with  dyspeptic 
symptoms  and  loss  of  weight.  Death  is  due  to  chronic  obstruction  and 
stercorsemia,  acute  obstruction,  or  ulceration,  perforation  and  peritonitis. 

Prognosis. — Many  cases  die  in  infancy.  Thus,  a  girl,  8  weeks  old, 
under  my  care,  died  from  collapse  due  to  the  perforation  of  one  of  three 
stercoral  ulcers  8  ins.  from  the  anus.  She  had  been  costive  since  birth. 
The  large  intestine  was  greatly  distended  from  the  caecum  to  the  sigmoid, 
especially  in  the  transverse  colon,  and  its  contents  were  like  wet  sand. 
There  were  neither  scybala  nor  stenosis.  Few  cases  live  to  be  over  40 
years  of  age.  The  affection  is  rarely  thought  serious  until  purgatives,  and 
then  enemata  fail  to  give  relief.  Attacks  of  obstruction  occur  at  intervals. 
Untreated  cases  steadily  get  worse  and  develop  failure  of  compensation, 
stagnation,  obstruction,  toxoemia,  and  the  effects  of  mechanical  pressure. 
Death  may  be  sudden  and  unexpected.  Ulceration  is  found  in  about  one- 
third  of  the  cases  after  death. 

Treatment  is  unsatisfactory,  unless  the  dilatation  is  due  to  chronic 
constipation,  or  depends  on  more  or  less  stenosis  of  the  gut.    Constricted  gut 


310  Chapter   XXVI. 

has  been  removed  with  satisfactory  results.  In  the  idiopathic  cases  acute 
obstruction  must  be  treated  by  immediate  colotomy,  unless  the  bowels 
can  be  quickly  emptied  by  the  persistent  use  of  castor  oil  and  olive  oil 
enemata,  and  mechanical  means.  In  the  chronic  cases  similar  methods  are 
adopted,  in  conjunction  with  careful  dieting,  small  and  concentrated  meals, 
saline  purgatives,  strychnia,  tight  bandaging,  abdominal  massage  and 
faradism  of  the  gut.  Massage  is  dangerous  in  bad  cases.  Surgical  measures 
are  generally  advisable  for  idiopathic  cases.  Colotomy  may  prolong  life 
but  is  not  curative.  Excision  of  the  dilated  portion  of  the  colon  has  given 
good  results,  but  the  part  that  is  left  is  liable  to  undergo  subsequent 
dilatation.  Anastomosis  of  the  iliac  and  pelvic  colon  and  fixation  of  the 
dilated  pelvic  loop,  with  subsequent  excision  of  the  loop,  has  also  been 
tried.  On  the  whole  it  is  justifiable  to  explore  and  empty  the  bowel  by 
manual  pressure,  before  trying  further  measures.  If  this  is  unsuccessful, 
appendicostomy  and  systematic  lavage  of  the  colon  may  be  tried.  So 
far  I  am  unaware  of  any  case  having  been  treated  by  this  method,  but 
it  seems  justifiable,  seeing  that  it  leads  to  contraction  of  the  colon  in  cases 
of  colitis. 


CHAPTER    XXVII. 

INTESTINAL  PARASITES. 

Tapeworms —  Roundworms —  Threadivorms —  Trichince — Myiasis. 

Tapeworms  (Cestoda)  are  flat  compound  worms  with  no  mouth  or 
alimentary  canal,  multiplying  by  gemmation  from  a  pyriform  head  or 
nurse.  Each  segment,  or  proglottis,  contains  ova,  which  are  set  free  when  the 
segment  is  discharged  from  the  human  body.  The  ova  are  then  swallowed 
and  pass  an  intermediate  stage  of  existence  in  another  host,  in  which  the 
embryo  comes  to  rest  in  some  part  of  the  body,  being  transformed  into  a 
bladder-like  structure,  called  a  cysticercus,  bladder  worm,  or  measle.  It  is 
swallowed  in  this  form  by  the  child.  In  the  stomach  the  wall  of  the  cysti- 
cercus is  dissolved  and  the  head,  or  scolex,  is  set  free.  This  attaches 
itself  to  the  mucous  membrane  of  the  intestine  and  develops  into  the 
mature  worm.  It  attains  full  maturity  in  about  3  months,  and  may  live 
20-30  years  or  longer. 

Tapeworms  occur  at  any  age,  but  are  rare  under  5  years.  It  is 
exceptional  for  more  than  one  to  be  present  in  the  same  child.  The 
Tcenia  Solium  or  pork  worm,  "ver  solitaire,''''  is  acquired  by  eating  in- 
sufficiently cooked  sausages,  pork,  etc.  It  attains  the  length  of  6-10  feet. 
The  head  is  the  size  of  that  of  a  pin,  and  provided  with  4  suckers,  a  ros- 
tellum  and  a  circlet  of  hooklets.  The  fully  developed  segments  are  almost 
square,  a  little  longer  than  broad. 

The  Tcenia  Mediocanellata  vel  Saginata,  or  beef  worm,  is  acquired  by 
eating  insufficiently  cooked  infected  beef.  There  may  be  more  than  one. 
It  attains  the  length  of  12-20  feet.  The  head  is  provided  with  4  suckers, 
but  no  rostellum  or  hooklets.  The  segments  are  larger  than  those  of  T. 
solium,  and  longer  than  they  are  wide.  It  is  the  most  common  tapeworm 
in  children. 

The  Bothriocephalus  Latus  is  rare  in  this  country,  and  acquired  from 
fresh-water  fish.  It  attains  the  length  of  24-60  feet.  The  head  is  small, 
ovoid,  with  two  lateral  suckers.    The  segments  are  much  wider  than  long. 

The  Taznia  Elliptica  vel  Cucumerina  (dipylidium  caninum)  passes 
its  intermediate  existence  in  lice  and  fleas  of  cats  and  dogs.  It  is  the 
common  tapeworm  found  in  cats  and  dogs,  and  rare  in  human  beings.  It 
has  been  found  at  the  age  of  6  weeks,  and  possibly  many  tapeworms  in 
infants  are  of  this  kind.    Its  length  is  6-12  ins.     The  head  has  a  rostellum, 


312  Chapter   XXVII. 

circlet  of  hooklets  and  sucking  discs.  The  segments  are  long,  narrow  and 
somewhat  ovoid. 

The  Taenia  Nana,  or  dwarf  tapeworm,  is  found  in  Central  and  South 
Europe,  America  and  Egypt.  It  consists  of  150-200  segments,  which  are 
small,  oval,  reddish- white,  like  minute  gherkins.  The  head  has  a  rostellum, 
circlet  of  hooklets  and  sucking  discs.  The  taenia  flava  punctata  has  been 
occasionally  found. 

The  Tcenia  Echinococcus  lives  in  the  dog  and  such-like  animals.  The 
ova  are  swallowed  in  watercress,  etc.,  and  the  embryos  develop  and  pass 
into  the  tissues,  especially  the  liver,  and  form  hydatids. 

Symptoms  may  be  absent ;  or  may  be  due  to  the  worm,  catarrh  of  the 
intestine,  or  drugs  given  for  treatment.  The  growth  of  the  worm  at  the 
expense  of  the  host  withdraws  food  supplies,  notably  albumin,  and  leads 
to  malnutrition.  Mechanically  it  may  give  rise  to  obstruction,  or  by 
migration  may  set  up  myositis,  meningitis,  liver  abscess  or  asphyxia. 
Such  results  are  rare,  except  from  hydatids.  Some  of  the  symptoms  are 
due  to  reflex  irritation,  and  others  are  toxaemic  in  origin.  The  common 
abdominal  symptoms  are  variable  appetite,  nausea,  vomiting,  discomfort 
or  colic,  tympanites,  and  constipation  or  diarrhoea.  Karely  a  tapeworm 
gets  into  the  stomach  and  is  vomited.  Constitutionally,  it  may  produce 
irritability,  uncertain  temper,  restless  nights  and  malnutrition.  Erythe- 
matous rashes  may  be  due  to  toxaemia  or  secondary  digestive  disturbance. 
The  nervous  symptoms  include  cough,  itching  of  the  nose  and  anus,  giddi- 
ness, tinnitus,  pavor  nocturnus,  hallucinations,  hysterical  symptoms, 
habit  spasm,  chorea,  convulsions  and  epilepsy.  It  is  difficult  to  believe  that 
some  of  these  affections  are  more  than  coincident ;  the  symptoms  having 
been  perhaps  exaggerated  by  intestinal  catarrh  and  toxaemia.  Severe 
cough  and  serious  loss  of  weight  may  be  due  to  worms.  The  cough  is  dry, 
noisy,  incessant  or  occurring  in  fits  of  alarming  intensity,  and  lasting  for 
hours  but  without  rales  or  fever.  In  a  boy,  33  months  old,  the  symptoms 
were  strongly  suggestive  of  meningitis,  and  cleared  up  on  the  evacuation 
of  a  tapeworm.  The  diagnosis  depends  on  the  appearance  of  segments  in 
the  stools,  and  from  these  the  variety  of  worm  can  be  determined. 

The  prognosis  is  good  as  regards  life,  but  uncertain  as  regards  the 
evacuation  of  the  worm.  The  drawback  to  drugs  is  that  the  most  efficacious 
ones  are  unpleasant  to  take.  They  are  liable  to  affect  the  stomach,  may  not 
be  retained,  and  may  cause  severe  enteritis,  toxic  symptoms  and  death. 
No  such  drugs  should  be  given,  unless  the  diagnosis  is  certain.  Their  use 
is  contra-indicated  by  early  age  of  the  patient,  recent  abdominal  disease, 
and  uncompensated  heart  lesions. 

Treatment. — For  taenia  elliptica  give  calomel  and  santonin.  For  the 
common  tapeworm  the  extract  of  male  fern  is  the  best  drug,  but  it  may 
have  to  be  given  in  large  doses.  Care  must  be  taken  that  the  drug  is  soon 
evacuated,  for  even  small  doses  may  give  rise  to  toxic  symptoms  and  an 


Intestinal  Parasites.  313 

■erythematous  rash.  In  the  case  of  a  child  of  4  years  or  more  of  age,  it  is 
advisable  to  have  the  bowels  opened  freely  by  mag.  sulph.  dr.  1  and  tr. 
jalap  m.  15,  or  such  a  dose  as  may  be  necessary,  for  4  or  5  days  before 
giving  the  male  fern.  No  food  should  be  given  after  1  p.m.,  except  possibly 
a  little  weak  tea  at  bedtime.  The  child  is  kept  in  bed  during  the  course 
of  treatment  on  the  following  day.  At  7  a.m.,  it  is  given  a  mixture  of  ext. 
filic.  maris,  liq.,  ext.  glycyrrhizse  liq.,  syr.  zingib.,  aa.  dr.  1,  in  1-1J  oz. 
of  water.  If  it  is  not  retained  a  second  full  or  half  dose  is  given  in  an  hour's 
time.  Two  hours  later  castor  oil  oz.  \,  or  a  full  dose  of  the  mag.  sulph  and 
jalap  mixture,  which  has  been  found  to  act  quickly  and  efficaciously,  is 
given.  Tincture  of  jalap  can  be  given  with  the  castor  oil.  If  the  bowels 
do  not  act  in  3  hours,  an  enema  should  be  given.  For  the  next  day  or  two 
the  diet  must  be  a  light  one.  If  the  head  of  the  worm  is  not  found,  careful 
watch  must  be  kept  for  the  reappearance  of  segments  in  the  stools,  and 
the  treatment  repeated  in  about  3  months,  when  the  worm  is  well  developed. 
It  dies  if  separation  takes  places  shortly  behind  the  head.  Male  fern 
can  be  given  in  doses  of  m.  15  of  the  liquid  extract  or  oleoresin  in  capsules 
every  quarter  of  an  hour  for  4  doses,  instead  of  the  mixture  recommended 
above  ;  the  other  treatment  being  the  same.  The  oil  of  filmaron  is  more 
pleasant  to  take  and  has  been  recently  recommended.  In  the  case  of  dogs 
it  is  given  in  castor  oil,  without  previous  starvation,  and  an  efficient  purge 
given  an  hour  later.    But  it  must  not  be  given  on  successive  days. 

It  is  hardly  necessary  to  mention  other  drugs,  seeing  that  they  are  not 
nearly  as  efficacious,  but  sometimes  it  is  advisable  to  adopt  less  severe 
treatment.  Black  oxide  of  copper  has  been  recommended  by  Hager  (1888) 
and  Sass  (1898).  A  mixture  of  black  oxide  of  copper  gms.  5,  prepared  chalk 
gm.  1,  mag.  carb.  gm.  1,  tragacanth  gms.  10,  glycerine  gms.  5,  and  white  sugar 
gms.  40,  is  made  up  with  water  into  50  pastilles.  Two  or  three  are  given  daily 
for  a  fortnight.  Nothing  acid  must  be  taken  and  rest  in  bed  is  not  required. 
Debris  appears  in  2  or  3  days. 

Fresh  pomegranate  bark,  macerated  in  an  equal  quantity  of  hot  water 
and  boiled  down  to  half  its  bulk,  is  given  in  doses  of  drs.  6-12  on  two  successive 
mornings,  and  followed  by  a  purgative.  Other  remedies  are  pumpkin  seeds 
in  doses  of  oz.  1,  pounded  up  with  sugar  and  honey  into  a  paste  ;  cucumerin, 
a  concentrated  extract  of  the  seeds  which  tastes  like  beef  juice  ;  kousso, 
an  infusion  of  1  dr.  for  half  an  hour  in  3  oz.  of  boiling  water,  and  given  in 
■3  doses  at  intervals  of  2  hours,  preceded  by  castor  oil  the  night  before  ; 
pelleterine  ;   and  turpentine. 

Roundworms. — The  Ascaris  Lumbricoides  is  acquired  through  the 
ingestion  of  the  ova  or  embryos  in  drinking  water  or  contaminated 
vegetables.  An  intermediate  host  is  unnecessary.  These  worms  are  very 
•common  in  children  from  1-10  years  of  age,  especially  in  Cornwall,  and 
almost  universal  in  the  natives  of  India  and  the  West  Indies.  They  are 
.more  frequent  in  girls  than  boys,  usually  multiple,  and  inhabit  the  small 


314  Chapter   XXVII. 

intestine.  Although  generally  harmless,  they  are  dangerous  on  account 
of  their  migratory  habits.  Thus,  they  have  passed  into  the  trachea  and 
caused  fatal  asphyxia,  atelectasis  or  pneumonia  ;  into  the  pancreatic  duct, 
setting  up  interstitial  pancreatitis  ;  into  the  bile  duct,  appendix,  and 
through  a  typhoid  ulcer  ;  into  the  Eustachian  tube,  through  the  external 
ear  or  nose  ;  and  through  an  umbilical  fistula.  It  is  even  said  that  the  worm 
may  perforate  a  healthy  intestine.  They  have  also  given  rise  to  intussus- 
ception, intestinal  obstruction,  and  peritonitis. 

The  symptoms  are  mainly  those  of  indigestion,  viz.,  anorexia,  variable 
appetite,  nausea,  vomiting,  abdominal  pain,  tympanites,  diarrhoea  and 
offensive  stools.  The  pain  may  be  vague  and  about  the  navel ;  occasionally 
acute,  causing  moaning  and  crying.  In  other  cases  the  symptoms  are 
limited  to  headache,  constipation,  wasting,  pallor,  debility  and  syncopal 
attacks.  The  chief  nervous  symptoms  are  picking  the  nose,  grinding  the 
teeth,  restlessness,  sleeplessness,  somniloquence  and  pavor.  Occasionally 
there  are  found  irregular  pulse,  unequal  pupils,  contracted  fields  of  vision, 
transient  squint,  hemiplegia,  aphasia,  vertigo,  hallucinations,  tetany, 
chorea,  laryngeal  spasm,  meningitic  symptoms,  jaundice,  enuresis,  pal- 
pitations, crying  fits,  hysterical  symptoms,  unconsciousness,  convulsions, 
and  fever. 

Worm  fever,  "  fievre  vermineuse"  or  "  lumbricose  a  forme  typhoide," 
may  closely  resemble  typhoid  fever  or  the  cerebral  type  of  meningitis. 
The  temperature  rises  to  104°  F.,  with  malaise,  anorexia,  headache,  thirst, 
and  occasionally  rigors,  delirium,  and  epileptiform  convulsions.  The 
symptoms  are  due  to  reflex  irritation  and  toxins,  excreted  by  the  worm 
or  from  decomposition  of  dead  worms  in  the  duct.  The  presence  of  normal 
stools  enables  many  other  causes  of  the  child's  illness  to  be  excluded.  Usually 
a  large  number  of  worms  are  present  in  these  cases,  rarely  one  only. 

These  worms  are  readily  evacuated  by  giving  santonin  on  an  empty 
stomach,  preceded  by  a  laxative  and  followed  by  castor  oil  or  calomel. 
A  suitable  powder  consists  of  santonin  gr.  ^,  calomel  gr.  J,  pulv.  scamm.  co. 
gr.  \,  for  each  year  of  age,  and  given  at  bedtime  for  3  or  4  nights. 
Santonin  should  never  be  given  in  large  doses.  The  urine  becomes 
very  yellow  and  turns  red  on  the  addition  of  alkali.  An  excessive 
dose  produces  headache,  vertigo,  vomiting,  dilated  pupils,  yellow  vision  and 
convulsions.  It  may  be  fatal.  Groosefoot  oil,  ol.  chenopodii  anthelmin- 
tic! aethereum,  is  said  to  be  almost  a  specific  for  roundworms.  It  is  given 
in  drop  doses  with  sugar  and  water,  or  as  an  emulsion.  It  is  not  difficult 
to  take,  acts  promptly,  and  has  no  unpleasant  effects. 

Threadworms. — The  Oxyuris  Vermicularis  chiefly  inhabits  the  rectum 
and  lower  part  of  the  colon  ;  is  common  in  the  csecum  and  appendix  ; 
and  has  even  been  seen  in  the  stomach  and  mouth.  No  intermediate  host 
is  needed,  and  apparently  they  breed  in  the  intestines.  They  are  found 
in  large  numbers,   embedded  in  the   mucus  resulting  from  the   catarrh 


Intestinal  Parasites.  315 

to  which  they  give  rise,  and  lodged  in  folds  of  the  swollen  mucosa.  Catarrhal 
states  predispose  to  their  development.  It  is  doubtful  whether  they  can 
live  in  a  healthy  mucous  membrane. 

They  give  rise  to  itching  of  the  anus  and  genitals,  soon  after  going  to 
bed,  due  to  migration  of  the  worms  from  the  rectum.  This  may  induce 
local  sores,  enuresis,  balanitis,  vulvitis  and  masturbation.  Constipation 
is  usually  present,  but  catarrhal  colitis,  proctitis  and  diarrhoea  are  not 
infrequent.  Possibly  they  set  up  appendicitis.  The  nervous  symptoms 
include  itching  of  the  nose,  restlessness,  irritability,  nervous  twitchings, 
convulsions  and  chorea.  Eosinophilia  is  present  in  less  than  half  the  cases 
of  threadworms  and  tapeworms,  and  often  absent  in  roundworms.  It  may 
occur  in  children  without  apparent  cause.  A  diagnosis  is  made  by  inspec- 
tion of  the  anal  region  and  stools.  Wash  out  the  rectum  with  cold  water, 
and  examine  the  fluid  against  a  dark  background.  Seek  for  eggs  under  the 
microscope. 

Treatment  is  directed  to  curing  the  catarrh  and  evacuating  the 
worms.  Reduce  the  starches,  sweets,  vegetables  and  fruits  in  the  diet  ; 
and  give  a  daily  dose  of  hyd.  cum.  cret.  gr.  1,  pulv.  rhei.  grs.  5,  sod.  bicarb, 
grs.  5.  Small  doses  of  perchloride  of  iron  with  a  saline  laxative  ;  alkalies 
with  gentian  and  rhubarb  ;  gentian  and  quassia  ;  sulphur  lozenges  ; 
garlic;  naphthalin  gr.  -|-5  t.d.s.,  omitting  fat  from  the  diet;  and  petroleum 
emulsion  are  also  useful.  Powders  of  santonin,  calomel,  and  scammony 
are  as  valuable  as  in  its  treatment  of  roundworms. 

Rectal  injections  of  common  salt,  5  per  cent,  solution,  and  infusions  of 
quassia,  garlic,  asafoetida  or  weak  perchloride  of  iron  are  given  in  order 
to  get  rid  of  the  worms  in  the  lower  part  of  the  bowel.  The  salt  solution 
is  the  simplest,  cheapest,  most  harmless  and,  in  my  experience,  is  effi- 
cacious as  well.  It  washes  away  the  mucus  in  which  the  parasite  lives. 
Strict  cleanliness  is  necessary,  for  patients  re-infect  themselves  by  scratch- 
ing and  getting  the  ova  under  the  nails.  The  nails  must  be  kept  short  ; 
and  gloves  and  tights  worn,  if  necessary.  The  anus  must  be  washed  after 
each  stool,  and  freely  anointed  with  ung.  hydrarg.  nit.,  diluted  if  necessary, 
every  night  for  6  weeks,  to  destroy  the  parasite  as  it  emerges  or  prevent 
its  emergence.  If  these  measures  are  insufficient,  all  drinking  water  must 
be  boiled,  for  it  is  sometimes  a  source  of  infection.  Uncooked  fruit  and 
vegetables  should  be  washed  before  being  eaten. 

The  TricJiocephalus  Dispar  is  very  common  in  the  caecum,  but  rarely 
gives  rise  to  ill  effects.  It  is  an  occasional  cause  of  enteritis,  appendicitis, 
reflex  colic  and  nervous  symptoms.  The  ova  are  found  on  microscopical 
examination  of  the  stools.  The  treatment  consists  in  attention  to  the 
intestinal  tract,  and  drugs  such  as  thymol,  benzine  and  male  fern. 

The  Anchtjlostoma  or  Dochmius  Duodenalis  is  a  dangerous  inhabitant 
of  the  alimentary  tract,  but  unknown  in  this  country  in  children.    It  causes 


316  Chapter   XXVII. 

great  anaemia,  from  the  abstraction  of  blood  by  the  parasite  and  bleeding 
from  the  local  punctures.     It  is  treated  by  thymol  and  male  fern. 

Trichinosis.— -Trichinae  are  rare  in  this  country.  The  embryos  are 
swallowed  in  imperfectly  cooked  measly  pork.  In  the  stomach  they  are 
set  free  and,  passing  into  the  intestine,  multiply  with  great  rapidity  and 
cause  gastro-enteritis,  sometimes  profuse  diarrhoea,  and  even  superficial 
ulceration  in  the  upper  part  of  the  small  intestine.  The  young  worms  then 
penetrate  the  intestinal  walls,  and  reaching  the  muscles  set  up  myositis 
with  local  tenderness  and  swelling.  There  they  become  encapsuled  and 
finally  calcified.  The  constitutional  symptoms  of  the  intestinal  stage 
and  the  muscular  invasion  may  be  severe  and  simulate  typhoid  fever. 
The  disease  is  often  fatal,  if  the  number  of  trichinae  SAvallowed  is  at  all 
large.  Calomel,  anthelmintics,  and  intestinal  antiseptics,  followed  by 
castor  oil,  are  indicated  in  the  treatment  of  the  intestinal  stage,  but  it  is 
rarely  diagnosed  and  generally  is  assumed  to  be  simple  ileo-colitis.  The 
muscular  stage  is  treated  on  general  principles. 

Myiasis. — Accidental  parasitism  of  dipterous  larvae,  the  maggots  of 
flies,  is  occasionally  seen.  Ambrose  Pare  (1582)  reported  a  case  in  which 
a  maggot  was  passed  per  urethram,  and  similar  cases  are  on  record.  Maggots 
are  not  infrequent  in  cutaneous  wounds,  the  nose  and  the  external  auditory 
meatus.  They  are  readily  cured  by  blowing  in  calomel,  and  then  syringing 
with  warm  boric  acid  lotion  ;  by  warm  oil,  carbolic  acid  lotion  2  per  cent., 
chloroform  vapour  or  tobacco  juice.  In  rare  instances  subcutaneous 
swellings  have  developed,  broken  down,  and  extruded  maggots.  These  are 
due  to  some  fly  depositing  its  eggs  under  the  skin. 

Myiasis  interna,  or  gastro-intestinal  myiasis,  is  occasionally  seen. 
Usually  the  eggs  of  a  fly,  or  the  larva?,  are  swallowed,  and  perish  in  the 
intestinal  tract.  If  they  effect  a  lodgment,  they  may  give  rise  to  enteritis 
and  colitis  from  mechanical  irritation  or  toxins.  Vomiting,  fits  of  screaming, 
and  attacks  of  colic  have  also  been  noted.  The  larvae  may  be  vomited  or 
passed  in  the  stools.  In  many  supposed  cases  they  are  due  to  subsequent 
infection  of  the  excreta.  Calomel,  thymol  and  naphthalin  are  the  most 
useful  drugs. 

Protozoa. — The  chief  protozoa  are  the  amoeba  coli,  cercomomas  intes- 
tinalis,  trichomomas  intestinalis,  megastomum  entericum,  and  balantidium 
coli.  They  are  usually  taken  as  encysted  forms  in  water,  raw  fruit,  vege- 
tables and  salad.  For  treatment  give  a  slightly  constipating  diet,  cure  the 
intestinal  catarrh,  and  prescribe  drugs,  such  as  calomel,  thymol,  tannalbin, 
and  quinine  tannate.  Irrigate  the  bowel  with  quinine  or  thymol  solution 
0"2  per  cent,  or  tannin  0*5  per  cent,  strength. 


CHAPTER    XXVIII. 

INTESTINAL    OBSTRUCTION. 

Malformations —  Volvulus — Intussusception —  Hernia —  Congenital 

Hydrocele. 

Intestinal  obstruction  occasionally  follows  abdominal  operations,  as 
the  result  of  adhesions.  Sometimes  it  is  caused  by  the  adhesions  of  tuber- 
culous peritonitis,  but  there  is  the  danger  of  mistaking  the  constipation 
and  vomiting  at  the  onset  of  meningitis  for  that  due  to  obstruction. 
Anatomical  defects,  except  Meckel's  diverticulum,  are  rare.  The  mesentery 
has  been  found  attached  to  the  spinal  column  only,  and  the  colon  behind 
instead  of  in  front  of  the  small  intestine  (Thursfield's  case).  Obstruction, 
from  abnormalities  in  connection  with  Meckel's  diverticulum,  causes  localised 
meteorism  and  bulging  above  or  below  the  umbilicus,  tenderness  to  the 
right  of  the  umbilicus,  and  early  faecal  vomiting.  The  navel  may  be 
indrawn  or  scarred.    Sometimes  there  is  a  past  history  of  minor  attacks. 

Congenital  Intestinal  Atresia  and  Stenosis. — Intestinal  atresia  is  much 
more  common  than  stenosis,  and,  apart  from  the  rectum,  is  decidedly 
infrequent.  Silbermann  (1882)  collected  24  cases  of  duodenal  atresia  and 
30  of  atresia,  but  only  3  of  stenosis  in  the  jejuno-ileum.  Gartner's  (1883) 
statistics  of  the  site  of  atresia  were  duodenum  16,  jejuno-ileum  20,  large 
intestine  2.  Schlegel's  statistics  (quoted  by  Braun,  1902)  were  duodenum 
29,  jejuno-ileum  54,  large  intestine  6.  Atresia  is  most  common  in  the 
lower  portion  of  the  jejuno-ileum,  generally  in  the  ileum  near  the  caecum, 
usually  with  a  cord  connecting  the  two  ends.  It  is  rare  in  the  colon  and, 
when  present,  generally  in  the  first  part. 

The  Duodenum. — Cordes  (1901)  collected  56  cases  and  added  one  of 
his  own.  Of  these,  48  were  cases  of  atresia  and  9  stenosis.  The  close 
relation  to  the  bile  duct  is  important.  The  defect  may  be  above  or  below, 
and  rarely  on  a  level  with  the  entrance  of  the  duct.  Bland  Sutton  states 
that  the  bile  duct  almost  always  enters  the  distal  extremity  of  an  imper- 
forate duodenum.  The  duodenum  may  be  completely  occluded,  ending  in 
a  blind  pouch  or  converted  into  an  impervious  cord.  D'Arcy  Power  has 
reported  a  case  in  which  the  obstruction  was  due  to  a  complete  transverse 
septum,  composed  of  mucous  membrane  and  circular  muscle  fibres,  in  the 
second  part  of  the  duodenum.     The  child  lived  5  days. 

The   Jejuno-ileum  may  contain  single  or  multiple  occlusions.     As  a 


318  Chapter   XXVIII. 

rule  there  is  complete  atresia,  the  ends  of  the  gut  ending  blindly  but 
united  by  a  band  continuous  with  the  mesentery.  A  narrow  lumen  may  be 
found  sometimes  in  the  band,  and  occasionally  muscular  tissue  and  intes- 
tinal glands.  The  band  may  be  absent,  and  the  ends  of  the  gut  in  close 
apposition  or  widely  separated  and  in  different  parts  of  the  abdomen. 
Sometimes  the  occlusion  is  due  to  a  diaphragm,  with  a  central  perforation, 
formed  by  mucous  membrane,  and  the  intestine  is  surrounded  externally 
by  a  furrow.  Congenital  multiple  occlusions  of  the  small  intestine  have 
been  repeatedly  described.  Stenosis  and  atresia  may  co-exist  in  the  same 
patient.  In  stenosis  the  lumen  may  be  so  small  as  to  prevent  the  passage 
of  the  contents  of  the  bowel.  The  gut  is  distended  above,  often  much 
thickened,  and  collapsed  below  the  stenosis.  In  the  cases  of  multiple 
occlusions  normal  meconium  has  been  found  in  the  gutr  even  in  portions 
which  are  completely  shut  off. 

The  Colon  is  rarely  occluded.  In  intestinal  atresia  the  small  and  large 
intestine  below  the  obstruction  are  very  contracted  and  empty,  the  bowel 
being  about  the  thickness  of  a  lead  pencil.  An  absence  of  continuity 
between  the  small  and  large  intestine  has  been  reported  (Souter),  and  other 
rare  developmental  anomalies,  e.g.,  absence  of  the  caecum  and  ascending 
colon  (Clogg)  ;  absence  of  the  whole  colon,  except  the  caecum,  and 
sigmoid  (Nash)  ;  absence  of  the  descending  colon  and  sigmoid 
(Westwood  Fyfe).  In  Nash's  case,  a  girl  of  5  years,  a  foreign  body 
was  successfully  removed  from  the  small  intestine  by  operation.  The 
large  intestine  was  represented  by  a  short  tube,  passing  from  the  caecum 
to  the  brim  of  the  pelvis  on  the  left  side  and  continued  as  the  rectum. 

Etiology. — Usually  there  are  no  other  malformations,  but  there  are 
anomalies  in  position  and  length  of  the  gut.  There  is  no  common  cause. 
Most  cases  are  due  to  developmental  errors  in  early  foetal  life,  for  it  is 
unusual  to  find  bile  in  the  distal  segment.  Possibly  it  is  a  failure  of  the 
lumen  to  become  patent.  Duodenal  atresia  is  associated  with  the  develop- 
ment of  the  liver  and  pancreas.  The  development  of  the  liver,  as  an  out- 
growth from  the  duodenum,  and  of  the  pancreas  may  be  irregular.  Other 
malformations  have  been  described  in  connection  with  the  development  of 
the  liver,  viz.,  diverticula  of  the  duodenum  near  the  orifice  of  the  bile  duct, 
anomalies  in  the  bile  and  pancreatic  ducts,  and  an  accessory  liver  or 
pancreas.  Intestinal  atresia  is  associated  with  Meckel's  diverticulum, 
which  may  cause  atresia  by  producing  strangulation.  This  will  not  explain 
the  cases  in  which  the  occlusions  are  multiple.  Cases  have  been  ascribed 
to  intussusception,  volvulus,  constriction  in  the  umbilical  ring,  compression 
by  tumours,  and  obliterating  arteritis.  Braum  and  Chiari  found  the 
remains  of  intussusceptions.  There  is  no  satisfactory  evidence  in  favour  of 
fcetal  peritonitis,  though  traces  of  it  have  been  found.  The  occlusion  takes 
place  too  early  in  fcetal  life  to  render  it  probable.  Nor  is  there  evidence 
of  embolism  or  thrombosis  of  mesenteric  vessels,  nor  of  intestinal  ulceration. 


Intestinal   Obstruction.  319 

In  one  instance  (Pearce  Gould,  1882)  the  obstruction  was  due  to  plugs 
of  inspissated  mucus  in  the  lower  ileum  and  colon.  The  plugs  contained  no 
bile,  so  must  have  been  formed  before  the  third  month  of  foetal  life. 

Symptoms  depend  on  the  situation  of  the  obstruction.  The  higher  up 
it  is  in  the  intestinal  tract,  the  earlier  the  vomiting  begins.  In  Souter's 
case  it  began  as  soon  as  the  head  was  born.  Usually  it  starts  on  the  first 
or  second  day.  If  the  occlusion  is  above  the  entrance  of  the  bile  duct,  no 
bile  is  found  in  the  vomit,  and  the  case  may  be  mistaken  for  one  of  stenosis 
of  the  pylorus  ;  but  the  symptoms  are  earlier  in  onset  and  more  urgent. 
If  the  obstruction  is  low  down,  the  vomit  contains  food  given  ;  bloody 
matter  from  the  gastric  mucosa,  the  result  of  straining  ;  and  perhaps 
meconium.  These  cases  also  show  abdominal  distension,  visible  and 
violent  peristalsis,  and  gurgling.  Practically  nothing  is  passed  per  anum, 
though  the  anus  and  rectum  are  normal.  If  the  obstruction  is  above 
the  entrance  of  the  bile  duct,  meconium  is  passed.  The  symptoms  are 
those  of  starvation — pinched  and  drawn  face,  dry  tongue,  subnormal 
temperature,  feeble  pulse,  scanty  or  suppressed  urine,  rapid  wasting, 
collapse,  and  both  tonic  and  clonic  spasms.  Emaciation  and  exhaustion 
terminate  the  scene  in  4-7  days,  rarely  longer.  Abdominal  distension  may 
be  so  great  as  to  cause  dyspnoea  and  cyanosis.  Treatment  has  so  far  proved 
useless. 

Volvulus. — A  congenital  twist  of  the  third  part  of  the  duodenum  was 
found  by  J.  F.  Gordon  (1906)  in  a  girl  of  6  years,  who  died  from  asthenia 
after  15  weeks  of  intermittent  vomiting.  Volvulus  of  the  ordinary  type 
is  rare  in  children.  It  affects  the  sigmoid,  is  very  uncommon  in  the  small 
intestine,  and  is  said  not  to  occur  in  normal  bowel.  Complete  volvulus 
includes  the  entire  small  intestine,  csecum  and  ascending  colon.  It  is  due 
to  a  congenital  arrest  of  development,  and  is  more  common  in  boys  than 
girls.  Volvulus  causes  severe  abdominal  pain,  early  and  persistent  vomiting, 
constipation,  and  other  signs  as  in  adults. 

Intussusception. — An  intussusception  is  an  invagination  of  one  portion 
of  the  bowel  into  an  adjacent  part.  A  constricted  portion  is  "  swallowed  " 
by  the  segment  below.  Sometimes  more  than  one  is  present.  It  accounts 
for  three-fourths  of  the  cases  of  acute  intestinal  obstruction  in  infancy,  but 
is,  nevertheless,  of  quite  infrequent  occurrence.  Prompt  recognition  and 
suitable  treatment  of  acute  cases  are  essential,  if  life  is  to  be  saved.  Chronic 
cases  are  rare. 

Etiology. — It  is  most  common  in  England  and  America.  A  family 
predisposition,  if  present,  is  associated  with  careless  feeding.  Males  are 
more  often  affected  than  females,  in  the  proportion  of  2-1  under  12  years 
of  age,  and  3-1  under  12  months  of  age.  Two-thirds  of  the  cases  occur  during 
the  first  year  of  life,  and  three-fourths  during  the  first  2  years.  It  is  most 
frequent  at  3-6  months  of  age,  and  in  only  10  per  cent,  is  the  child  over 
10  years.    It  has  occurred  as  early  as  the  second  day  of  life  (E.  H.  Tweedy, 


320 


Chapter   XXVIII. 


1906),  but  very  few  cases  come  on  before  the  third  month.  The  number 
then  rises  rapidly  to  a  maximum  in  the  sixth  month,  and  falls  rapidly 
after  the  seventh. 

Age — Incidence  of  466  cases  under  1  year.     Fitzwilliams  (1908). 


Month  of  Life 

1 

2 

3       4       5 

6 

7 

8 

9     10 

11 

12 

No.  of  Cases 

2 

2 

35 

63  i  74 

i 

84     77 
1 

35 

36 

25 

25 

8 

The  seasonal  incidence  shows  a  sudden  rise  to  a  maximum  in  March 
and  December,  i.e.,  at  Easter  and  Christmas,  and  is  well  brought  out  by 
Fitzwilliams'  figures  : — 


January  .  . 

37 

May 

.     44 

September 

18 

February 

35 

June 

.     41 

October    . . 

25 

March 

58 

July 

.     37 

November 

29 

April 

45 

August     . 

.     33 

December 

51 

The  rapidly  increasing  disproportion  between  the  transverse  diameters 
of  the  large  and  small  intestine  during  early  life  is  a  possible  predisposing 
cause.  The  colon  grows  in  width  and  length.  Too  rapid  growth  is  associated 
with  perversion  of  function  ;  and  irregular  localised  contraction  of  the 
small  intestine  is  liable  to  be  set  up  by  simple  spasm.  There  is  little  evidence 
of  an  exciting  cause.  Violent  cough,  exertion  and  injury  are  infrequent 
at  the  common  age.  It  is  rarely  due  to  foreign  bodies,  roundworm,  polypus, 
sarcoma,  tuberculous  ulcer,  or  an  invaginated  Meckel's  diverticulum 
or  appendix.  In  quite  50  per  cent,  no  cause  can  be  found.  Strong,  healthy, 
well-nourished  infants  seem  more  predisposed  than  weakly  ones,  perhaps 
by  reason  of  more  vigorous  peristalsis  and  more  liberal  diet.  Diet  has  a 
definite  influence.  In  a  few  instances  there  is  gastro-enteric  disorder  or 
evidence  that  indigestible  food  has  been  given.  This  is  probably  the 
explanation  of  the  increased  frequency  at  Easter,  Christmas  and  the  New 
Year.  Diarrhoea  is  the  most  common  cause  to  which  it  can  be  assigned.  Yet 
it  does  not  appear  less  frequent  in  the  breast-fed  than  in  the  bottle-fed, 
except  that  it  is  less  frequent  in  those  countries  where  breast-feeding  is  most 
constant.  Of  46  cases  under  1  year  85  per  cent,  were  entirely  breast-fed 
(Hirschsprung).    It  may  occur  during  sleep. 

Pathologtj. — For  some  reason  or  other,  probably  on  account  of  spasm, 
a  wave  of  peristalsis  stops  suddenly  short  at  a  ring-like  constriction  of  the 
gut.  Perhaps  this  is  due  to  the  lack  of  co-ordination  so  characteristic  of 
infancy.  Next,  in  consequence  of  the  contraction  of  the  longitudinal 
muscles,  the  portion  of  gut  below  the  constriction  passes  upwards  over  the 
constricted  portion.     Subsequently,  violent  peristaltic  movements,  in  an 


Intestinal  Obstruction.  321 

effort  to  get  rid  of  what  has  become  a  foreign  body,  force  the  intussuscep- 
tion downwards.  More  probably  the  descent  is  due  to  the  paralysis  of  the 
circular  fibres  below  and  the  continued  contraction  of  the  longitudinal 
fibres  which  pull  up  the  sheath  over  the  intussusception.  The  mesentery 
is  included  between  the  sheath  and  the  inner  layer.  It  is  either  unduly 
long,  or  becomes  stretched  and  perhaps  torn  as  the  tumour  gets  larger. 
Being  attached  to  the  spine,  the  tumour  forms  the  arc  of  a  circle  with  its 
concavity  towards  the  spine.  The  stoppage  of  the  peristaltic  wave  may  be 
due  to  temporary  obstruction  by  indigestible  food,  or  to  local  paralysis 
or  atony  of  a  portion  of  the  gut.  If  the  paralysis  is  limited,  a  simple  descend- 
ing intussusception  is  formed,  but  if  it  involves  a  considerable  portion 
of  the  gut,  there  may  be  both  ascending  and  descending  intussusceptions. 
The  apex  of  the  invagination  may  remain  constant,  for  the  increase  in  size 
takes  place  by  the  outer  sheath  rolling  over  and  being  drawn  up  at  the  neck. 
Spontaneous  reduction  is  brought  about  by  anti-peristalsis  ;  the  circular 
fibres  contracting  beyond  the  apex  and  driving  it  up. 

The  stretching  of  the  mesentery  and  pressure  cause  obstruction  to  the 
circulation  in  the  vessels  and  strangulation  leading  to  congestion,  oedema, 
haemorrhage  and  gangrene.  The  intestinal  obstruction  is  partly  due  to 
mechanical  interference  and  partly  to  the  oedema.  After  a  time  the  in- 
vagination becomes  irreducible,  at  first  on  account  of  the  swelling,  later 
because  of  local  peritonitis  and  adhesions  between  the  peritoneal  sur- 
faces. These  adhesions  are  the  main  cause  of  irreducibility  in  chronic  cases. 
Occasionally  the  tumour  as  a  whole  becomes  twisted  or  the  prolapsed 
portion  is  nipped,  increasing  the  difficulty  of  reduction. 

Gangrene  and  sloughing  of  the  invagination  may  occur  in  acute  cases, 
the  slough  being  passed  per  anum  about  the  end  of  the  second  week.  The 
slough  varies  in  length  from  a  few  inches  to  several  feet  of  intestine.  Even 
the  whole  colon  has  been  sloughed  off,  and  the  child  has  recovered  with  an 
ileum  attached  to  the  lower  end  of  the  rectum.  Recovery  by  sloughing 
is  rare  in  infants,  and  more  likely  to  occur  in  older  children.  It  is  liable 
to  be  followed  by  annular  stricture. 

Varieties. — The  common  type  is  the  descending  variety,  the  upper 
portion  of  the  gut  being  invaginated  into  the  lower.  In  the  ascending  or 
"  retrograde  "  kind  the  upper  portion  passes  over  the  lower.  Both  types 
may  be  present  in  the  same  patient,  and  even  overlap  each  other,  though 
generally  there  is  an  intervening  portion  of  unaffected  gut.  An  enteric 
intussusception  may  be  jejunal  or  ileic.  It  is  called  ileo-colic  if  the  ileum 
passes  through  the  ileo-coecal  valve,  and  ileo-ccecal  if  the  invagination 
passes  onward  and  involves  the  caecum.  These  two  latter  types  are 
differentiated  with  difficulty,  and  it  is  better  to  include  them  both  under 
the  name  of  ileo-colic  or  ileo-caecal.  The  ileo-caecal  type  is  by  far  the 
most  common.  The  percentage  varies  from  44  (Treves,  Leichtenstein) 
to  89  (Wiggin).     The  least  frequent  variety  is  the  colic  intussusception 

Y 


322  Chapter  XXVIII. 

in  the  colon.  Intussusception  of  the  appendix  may  be  secondary  to  attempts 
of  the  appendix  to  expel  abnormal  contents  ;  of  17  recorded  cases  16  were 
under  9  years.  It  is  a  chronic  condition,  and  may  lead  to  invagination  of 
the  large  intestine  and  an  acute  attack. 

Agonal  intussusceptions  are  often  found  in  infants  under  2  years  of 
age  after  death.  They  are  generally  multiple,  small,  descending,  in  the 
small  intestine,  free  from  any  sign  of  congestion,  and  due  to  the  act  of 
dying. 

Symptoms  are  due  to  local  obstruction,  but  are  not  always  typical. 
A  characteristic  case  is  that  of  a  breast-fed  infant,  3-9  months  of  age,  well- 
nourished  and  apparently  healthy,  who  is  suddenly  seized  with  severe 
paroxysmal  abdominal  pain,  nausea  and  vomiting,  the  passage  of  blood 
and   mucus  per  anum,  marked  prostration  and  a  subnormal  temperature. 

The  onset  is  almost  invariably  sudden  in  babies,  and  almost  as  con- 
stantly so  in  older  children.  Violent  colicky  pains  and  vomiting  are  the 
initial  symptoms.  Food  is  refused  and  the  legs  are  drawn  up.  Occasionally 
diarrhoea,  with  blood  and  mucus  in  the  stools,  is  the  first  indication.  Slight 
fever  is  sometimes  present.  In  sub-acute  cases  there  may  be  merely  obscure 
symptoms  of  intestinal  obstruction,  or  less  marked  pain,  vomiting  and 
constipation.  In  chronic  cases  all  the  characteristic  symptoms  may  be 
absent,  and  the  diagnosis  is  based  on  progressive  wasting,  diarrhoea  and 
an  abdominal  tumour. 

The  pain  is  severe,  paroxysmal,  causing  agonising  cries,  and  usually 
referred  to  the  umbilicus  or  the  site  of  invagination.  Between  the  paroxysms 
the  child  may  seem  quite  well.  It  is  most  marked  during  the  first  2  days, 
perhaps  only  present  on  the  first  day.  It  is  not  always  severe,  rarely 
continuous,  and  only  occasionally  absent.  In  colic  intussusception  pain 
and  collapse  are  marked,  but  the  pain  is  less  paroxysmal  and  more  constant. 

Vomiting  is  present  in  80-90  per  cent.  ;  most  marked  at  the  onset ; 
and  usually  not  repeated  until  later  stages  of  obstruction,  but  it  may 
continue  throughout.  It  is  persistent,  uncontrollable,  immediately  after 
feeding,  and  often  projectile.  At  first  the  contents  of  the  stomach  are 
brought  up,  then  bile,  and  finally,  in  about  20  per  cent.,  fsecal  matter, 
Blood  may  be  present  from  straining.  Stercoraceous  vomiting  is  uncommon 
in  infants,  rarely  occurs  before  the  third  day,  is  indicative  of  complete 
obstruction  rather  than  of  strangulation,  and  is  not  necessarily  a  fatal 
omen. 

The  stools  are  very  characteristic.  At  first,  intestinal  contents  below 
the  obstruction  are  passed  in  the  shape  of  one  or  more  normal  stools. 
More  often  there  is  diarrhoea.  Sometimes  blood  is  passed  at  the  onset,  but 
usually  not  for  6-12  hours.  Clubbe  found  blood  in  all  but  6  out  of  144 
cases,  and  in  99  per  cent,  of  them  within  2-10  hours.  The  stools  then 
consist  of  blood  and  mucus  or  pure  blood,  without  a  trace  of  faeces,  faecal 
odour  or  gas  ;    the  constipation  is  complete.     Often  there  are  frequent 


Intestinal   Obstruction.  323 

stools  of  this  nature,  perhaps  several  in  an  hour,  following  attacks  of  pain. 
They  are  liable  to  be  ascribed  to  diarrhoea,  if  not  properly  examined.  The 
haemorrhage  varies  from  a  mere  trace  up  to  an  ounce  or  more  of  pure 
blood,  and  occasionally  is  so  severe  as  to  prove  fatal.  Mucus  is  generally 
present.  Sometimes  the  discharge  resembles  red  paint.  On  rectal  examina- 
tion a  polypoid  tumour  may  be  felt,  and  the  finger  is  covered  with  blood 
and  mucus. 

A  tumour  is  found  in  80-90  per  cent,  of  all  cases,  if  the  child  is  examined 
rectally  and  bimanually  under  an  anaesthetic.  In  quite  50  per  cent,  of 
babies  it  cannot  be  felt,  or  only  very  indefinitely,  in  early  stages.  In  a 
relaxed  abdomen  it  may  feel  like  an  undefined  thickening  in  the  region  of 
the  caecum  and  ascending  colon.  A  small  enteric  tumour  cannot  always  be 
felt.  The  characteristic  lump  is  present  within  a  few  hours,  rather  movable, 
somewhat  sausage-shaped,  and  perhaps  a  little  curved.  It  is  found  most 
often  in  the  right  half  of  the  abdomen,  the  umbilical  region  or  left  iliac 
fossa.  It  becomes  harder  and  more  prominent  during  paroxysms  of  pain, 
and  from  contraction  under  examination.  It  reaches  the  rectum  very 
quickly,  and  can  be  felt  per  anum  in  about  one-third  of  the  cases.  It  may 
even  protrude  for  an  inch  or  two  as  a  deep  purplish  or  gangrenous  lump, 
liable  to  be  mistaken  for  rectal  prolapse,  piles,  or  polypus  ;  and  shows 
superficial  ulceration  and  exudation.  Per  rectum  the  end  of  the  invagina- 
tion feels  rather  like  the  os  uteri. 

Prostration  or  Collapse  is  a  marked  feature,  sudden  in  development 
and  out  of  proportion  to  the  symptoms.  The  child  looks  ill,  pale,  with 
-anxious  expression,  sunken  eyes,  cold  sweat  on  the  forehead  and  cold 
extremities.  The  "  abdominal  facies  "  develops  in  a  few  hours.  Occasionally 
there  is  a  remarkable  limpness  without  any  special  facial  indication  of 
illness.  The  pulse  is  small,  frequent  and  feeble  ;  and  the  temperature 
normal  or  subnormal. 

The  abdomen  is  relaxed  at  first,  but  the  muscles  become  contracted 
and  rigid  during  the  paroxysms.  A  little  local  tenderness  may  be  found 
over  the  site  of  the  mischief  ;  generally  on  the  right  side  and  associated 
with  rigidity  of  the  right  rectus.  Absence  of  tympanites  in  the  early  stages 
is  of  value.  Later,  the  degree  of  tympanites  and  the  contour  of  the 
abdomen  depend  upon  the  site  of  the  obstruction  and  on  peritonitis.  Tenes- 
mus is  present,  if  the  tumour  reaches  the  sigmoid  flexure  or  the  rectum, 
and  is  due  to  attempts  to  expel  what  is  practically  a  foreign  body.  The  urine 
is  diminished  in  amount  and  micturition  often  painful. 

At  first  the  child  is  restless.  Gradually  it  passes  into  an  apathetic  or 
stuporous  condition  with  increasing  prostration,  continued  pain  and 
vomiting,  and  towards  the  end  a  rapidly  rising  temperature.  If  the  case 
is  prolonged,  the  usual  signs  of  peritonitis  develop.  Tonic  contractures  of 
the  limbs  and  convulsions  may  occur  at  any  period  and  terminate  the 
attack,  but  death  generally  results  from  exhaustion. 


324  Chapter   XXVIII. 

Chronic  cases  may  be  ushered  in  by  an  attack  of  diarrhoea,  and 
followed  by  paroxysmal  abdominal  pain  for  24  hours  or  more.  Sometimes 
the  attacks  of  pain  come  on  daily  or  at  rather  long  intervals.  Vomiting 
may  be  late  and  inconstant.  The  stools  are  constipated  or  loose,  mixed 
with  mucus,  and  passed  with  tenesmus.  The  abdomen  is  soft ;  the  tempera- 
ture subnormal ;  and  a  tumour  rarely  felt.  Occasionally  a  tumour  may 
prolapse  from  the  rectum,  for  even  2  weeks.  Thirst  and  wasting  are  often 
present.    Some  of  these  cases  are  due  to  invagination  of  the  appendix. 

Diagnosis. — There  is  little  probability  of  erroneous  diagnosis,  if  an 
examination  is  made  under  an  anaesthetic  in  all  cases  of  acute  vomiting, 
with  pain  and  the  passage  of  blood-stained  mucus.  It  is  rare  for  the 
three  cardinal  signs,  tumour,  blood  and  collapse,  to  be  all  absent.  In  early 
cases,  within  18  hours  of  the  onset,  the  state  of  the  child  is  often  so  good  that 
the  mischief  is  unsuspected.  In  others,  the  child  is  collapsed  from  the 
onset.  An  attack  may  be  ascribed  to  gastritis  because  of  the  vomiting  ; 
or  to  ileo-colitis  because  of  the  stools,  but  in  this  there  is  no  severe  and 
paroxysmal  pain.  The  Signe  de  Dance,  absence  of  the  caecum  from  its 
normal  position,  is  of  a  little  value.  After  infancy  the  diagnosis  is  more 
difficult,  for  the  bowels  may  act  daily  and  appear  normal,  and  examination 
per  rectum  may  be  negative,  but  vomiting  is  frequent  and  a  tumour  is 
found  on  abdominal  examination.  In  chronic  cases  the  diagnosis  is  based 
chiefly  on  the  presence  of  a  tumour.  Incomplete  cases  are  rare,  and  give 
rise  to  colic,  blood  and  mucus  in  the  stools,  wasting,  little  or  no  vomiting, 
and  an  indefinite  variable  tumour.  Usually  there  is  little  blood.  They 
may  last  for  weeks  or  years.  Cases  have  to  be  diagnosed  from  enteritis, 
appendicitis,  undescended  testicle,  thrombosis  of  the  mesenteric  artery, 
tumours,  glands,  polypus,  and  rectal  prolapse.  Henoch's  purpura  gives 
rise  to  abdominal  pain,  the  passage  of  blood  and  mucus,  and  persistent 
severe  vomiting.  The  vomit  never  becomes  faecal,  and  faecal  matter  is 
generally  found  in  the  stools.  Other  evidence  of  purpura  may  be  present. 
An  intussusception  may  occur  with  purpura  but  be  independent.  Exten- 
sive rectal  prolapse,  cured  by  sloughing,  may  be  mistaken  for  a  cured 
intussusception. 

The  passage  of  blood  is  a  most  valuable  sign  of  intussusception,  but 
it  is  of  the  utmost  importance  not  to  think  it  necessary  to  wait  for  this 
before  making  a  diagnosis.  Profuse  bleeding  indicates  considerable  des- 
truction, oedema,  and  paralysis  of  the  gut.  Gangrene  and  ulceration  give 
rise  to  subnormal  temperature,  severe  collapse  and  profound  toxaemia. 

Prognosis. — Spontaneous  reduction  is  possible  in  early  cases,  and  has 
even  occurred  after  6  days  duration.  Some  cases  of  severe  colic  are  due  to 
temporary  intussusception.  Operation  in  these  has  shown  that  the  intes- 
tine involved  was  thick  and  tensely  congested,  oedematous,  and  covered 
with  flakes  of  lymph.  Spontaneous  recovery  by  sloughing  is  rare  at  all  ages, 
and  almost  unknown  in  infancy.     It  is  most  likely  to  occur  in  the  colic 


Intestinal   Obstruction.  325 

variety.  According  to  Treves,  elimination  of  a  gangrenous  intussusception 
takes  place  in  about  42  per  cent,  of  irreducible  cases  ;  and  the  death  rate, 
among  those  in  whom  it  does  occur,  is  over  40  per  cent.  Such  cases  rarely 
recover  completely  and  may  develop  stenosis.  In  infancy  the  affection  is 
almost  invariably  fatal,  if  untreated  within  24  hours  or  even  within 
12  hours.  Two-thirds  of  the  untreated  die  within  a  week,  usually  on  the 
third  to  the  sixth  day.  Older  children  die  in  the  second  week.  Occasionally 
the  duration  is  prolonged  for  3  weeks.  Death  in  acute  cases  is  due  to  shock. 
In  more  prolonged  ones  there  is  general  or  local  peritonitis  or  perforation. 
Chronic  cases  die  from  wasting,  exhaustion  or  complications,  but  may 
live  for  years.    The  younger  the  patient,  the  worse  is  the  prognosis. 

The  prognosis  of  operative  treatment  depends  on  the  age  of  the  child, 
the  duration  of  the  intussusception,  and  the  duration  and  nature  of  the 
operation.  The  results  are  good,  if  reduction  is  effected  on  the  first  or 
second  day.  The  mortality  of  cases  treated  by  laparotomy  on  the  first 
day  is  extremely  small,  less  than  5  per  cent.  After  48  hours  the  outlook 
is  much  less  hopeful,  about  30-40  per  cent.  die.  Statistics  of  operation  are 
valueless,  unless  they  are  based  on  the  age  of  the  patient  and  the  duration 
of  the  illness. 

Treatment. — The  proper  treatment  is  by  laparotomy.  All  other 
methods  are  extremely  uncertain  and  very  likely  to  involve  a  fatal  waste 
of  time.  If  a  case  is  seen  within  a  few  hours  of  its  onset,  attempts  to 
encourage  spontaneous  reduction  may  be  made  by  gentle  manipulation 
abdominally  and  rectally,  in  a  hot  bath  or  after  the  application  of  heat 
to  the  abdomen  to  encourage  faintness  and  cause  relaxation.  Irrigation 
with  warm  water  may  be  tried.  In  the  meantime  all  necessary  preparations 
for  operation  must  be  made.  No  food  is  given  by  the  mouth,  and  purges 
are  injurious.  If  the  diagnosis  has  been  made,  a  small  dose  of  tincture 
of  opium  may  be  given  to  relieve  pain,  relax  spasm  and  lessen  peristalsis. 
It  must  be  used  with  great  caution,  as  it  is  liable  to  cause  paralytic  disten- 
sion of  the  gut,  and  it  masks  symptoms. 

If  operation  is  postponed  until  reduction  is  impossible  from  swelling, 
adhesions  or  gangrene,  it  is  almost  invariably  fatal.  It  should  be  done 
as  early  as  possible  in  every  case,  no  matter  the  age  of  the  child.  Such  a 
line  of  action  may  lead  to  unnecessary  operation  in  the  rare  cases  which 
might  undergo  spontaneous  reduction  or  be  reduced  by  an  injection. 
Even  so,  such  a  result  is  amply  compensated  by  the  number  of  lives  saved, 
for  a  fatal  issue  is  constantly  due  to  the  delay  involved  in  carrying  out 
other  treatment  and  waiting  to  see  if  it  has  proved  successful.  Preliminary 
irrigation  is  justifiable  to  reduce  the  size  of  the  tumour  and  render  mani- 
pulation more  easy.  The  usual  precautions  must  be  adopted  to  minimise 
shock  and  prevent  extrusion  of  the  bowels.  The  room  and  table  must  be 
warm  ;  the  limbs  wrapped  in  cotton  wool  and  the  body  exposed  as  little 
as  possible  ;   a  minimum  dose  of  anaesthetic  given  ;   and  the  operation  done 


326  Chapter   XXVIII. 

as  quickly  as  possible.  A  small  incision  through  the  rectus  muscle,  in 
the  right  semilunar  line,  or  in  the  median  line  may  enable  the  intussus- 
ception to  be  reduced  in  situ.  To  save  time  it  is  generally  advisable  to  make 
a  larger  incision  and  effect  the  reduction  outside  the  abdomen,  A  certain 
amount  of  force  is  justifiable  under  the  age  of  2  years,  because  of  the 
enormous  mortality  of  resection.  After  the  operation  the  child  can  be 
given  a  rectal  feed,  and  should  be  fed  by  the  mouth  as  soon  as  it  recovers 
from  the  anaesthetic.  Opiates  must  be  used  with  great  caution.  Give 
castor  oil  in  48  hours  if  the  bowels  have  not  acted,  and  strychnia  if  necessary. 
There  is  generally  some  rise  of  temperature  for  a  few  days,  and  the  child 
recovers  if  it  survives  48  hours.  Death  may  result  from  shock,  the  effect 
of  the  anaesthetic,  toxaemia,  or  persistent  paralysis  of  the  gut.  Recurrence 
is  rare.  Occasionally  the  temperature  rises  considerably,  even  to  107°  F., 
from  intestinal  toxaemia,  and  may  be  fatal.  A  rare  occurrence  is  the 
passage  of  blood  and  mucus  without  faecal  matter  in  the  second  week  after 
operation,  with  anorexia,  perhaps  slight  vomiting,  and  no  fever.  Possibly 
this  condition  is  allied  to  Henoch's  purpura.  No  recurrence  is  found  at 
operation.  Expectant  treatment  must  be  adopted.  Rupture  of  the 
wound  and  prolapse  of  the  gut  is  a  rare  sequel. 

If  the  intussusception  is  irreducible,  or  if  the  bowel  shows  signs  of 
gangrene,  or  its  moribund  condition  is  indicated  by  the  loss  of  gloss,  absence 
of  bleeding  when  pricked  and  inability  to  reduce  the  congestion  by  massage, 
other  methods  must  be  adopted.  In  irreducible  cases  the  best  results  have 
been  obtained  by  resection  and  end-to-end  anastomosis  of  the  gut,  but  the 
operation  is  generally  fatal  from  shock  or  exhaustion.  It  is  hardly  ever 
successful  under  2  years  of  age,  though  recovery  has  taken  place  even  at 
3  months.  Similar  treatment  is  necessary  for  gangrene  or  rupture  during 
manipulation.  Other  methods  include  incision  of  the  sheath  and  removal 
of  the  invagination,  short  circuiting,  and  the  formation  of  an  artificial 
anus.     A  second  operation  to  close  the  anus  may  be  fatal. 

Apart  from  operation  recourse  must  be  had  to  inflation,  injection  and 
irrigation.  It  is  extremely  improbable  that  any  variety  of  intussusception, 
except  the  colic  one,  can  be  reduced  by  this  means.  The  great  majority 
are  of  the  ileo-caecal  kind.  The  bulk  of  the  intussusception  may  be  reduced, 
but  an  inch  or  more  remains,  and  its  existence  cannot  be  diagnosed  until 
the  child  has  been  allowed  to  come  round  from  the  anaesthetic  and  the 
general  symptoms  watched  for  a  further  period.  Even  if  reduction  is 
complete,  an  engorged  and  cedematous  gut  may  still  suggest  its  presence. 
The  treatment  creates  uncertainty  and  serious  waste  of  time.  It  rarely 
causes  complete  reduction,  and  if  the  slightest  invagination  is  left,  recur- 
rence occurs.  This  is  by  no  means  uncommon  within  24  hours,  and  multiple 
recurrence  of  colic  intussusceptions  has  been  reported.  If  the  treatment 
fails,  as  it  generally  does,  the  child  has  to  undergo  further  anaesthesia.  There 
is  a  small  risk  of  rupture  of  the  gut,  for  it  is  impossible  to  gauge  the  amount 


Intestinal   Obstruction.  327 

of  pressure  and  to  exclude  the  presence  of  serious  changes  leading  to 
softening  of  the  gut.  It  is  useless  if  there  are  adhesions,  and  if  there  is 
much  bleeding  or  severe  collapse.  Symptoms  may  persist  afterwards 
from  failure  or  from  intestinal  palsy.  There  are  few  recoveries  under  this 
treatment,  even  in  the  early  stages,  at  any  rate  after  12  hours  duration. 

For  injection  or  inflation  the  child  is  ansesthetised,  placed  on  the 
back  with  the  pelvis  well  raised  and  the  thighs  flexed,  and  is  inverted 
from  time  to  time,  to  get  the  assistance  of  traction.  A  hand-bellows  or 
Higginson's  syringe  attached  to  a  catheter  is  used  to  inject  air,  and  a  funnel 
and  tube  held  not  more  than  2  feet  above  the  buttocks  for  the  injection  of 
fluids,  such  as  salt  solution,  barley  water,  milk  and  water  or  oil,  at  a 
temperature  of  100-105°  F.  The  process  must  be  done  slowly,  in  15-20 
minutes,  and  be  assisted  by  manipulation.  Keduction  is  indicated  by 
the  escape  of  faeces  and  gas,  disappearance  of  the  tumour,  and  return  of 
the  abdomen  to  its  normal  contour.  Afterwards,  the  child  is  given  a  small 
dose  of  opium,  light  diet,  no  purgative,  kept  quiet,  and  carefully  watched 
for  signs  of  recurrence. 

Hernia. — Hernia  occurs  at  one  or  other  of  those  parts  of  the  abdominal 
wall  which  are  structurally  weak  or  incomplete,  especially  the  umbilicus, 
and  the  inguinal  and  crural  canals.  Some  surgeons  hold  that  in  every  case 
there  is  a  precedent  congenital  peritoneal  pouch.  This  is  probably  true 
of  inguinal  hernia,  but  it  hardly  explains  those  cases  in  which  there  is  no 
peritoneal  pouch,  e.g.,  hernia  of  the  caecum  and  ventral  hernia  secondary 
to  operation.  Direct  inguinal  hernia  is  also  a  protrusion  in  the  lower  part 
of  the  semilunar  line,  through  Hesselbach's  triangle,  and  has  no  sac.  It 
is  very  rare  in  children.  Frequently  the  divaricated  recti  permit  the 
linea  alba  to  be  stretched  and  thinned  ;  it  will  then  protrude  as  a  ventral 
hernia.  This  common  condition,  peculiar  to  children,  is  congenital  or 
acquired,  and  the  hernia  has  no  neck.  The  multiplicity  of  hernise  and  the 
frequency  of  the  ventral  protrusion  suggest  a  common  origin  in  intestinal 
fermentation  and  distension,  rather  than  a  congenital  sac.  The  chief 
predisposing  factors  in  inguinal  hernia  are  the  large  internal  abdominal 
ring  and  the  weakened  muscles  guarding  it.  The  chief  exciting  factor, 
probably,  of  more  importance  than  the  predisposing  congenital  factor,  is 
the  increased  intra-abdominal  pressure  so  frequently  seen  in  rickets, 
consequent  on  abdominal  distension  due  to  the  intestinal  fermentation  and 
weakened  muscles. 

One-third  of  all  cases  occur  under  14  years  of  age  (Coley).  In  children 
two-thirds  are  multiple  and  one-third  single  (Corner).  It  occurs  in  from 
5-10  per  cent,  of  all  children,  and  is  much  more  common  in  males,  especially 
in  the  first  year  of  life. 

Inguinal  Hernia  is  a  common  variety  in  early  life  and  almost  invari- 
ably oblique.  It  is  often  bilateral.  Nine-tenths  occur  in  males.  In  males 
it  is  3  or  4  times,  and  in  females  twice  as  frequent  on  the  right  side  as  on 


328  Chapter   XXVIII. 

the  left.  The  vaginal  process  closes  later  on  the  right  side.  It  depends  on 
total  or  partial  patency  of  the  peritoneal  prolongation  known  as  the  pro- 
cessus vaginalis  or  funicular  process.  The  walls  of  the  inguinal  canal  are 
not  primarily  at  fault.  Under  normal  conditions  of  development  the  testis 
descends  into  the  scrotum,  carrying  with  it  the  funicular  process.  From 
this  process  the  tunica  vaginalis  is  cut  off  by  obliteration  of  the  narrow  neck 
of  the  sac.  In  the  common  form  of  inguinal  hernia  the  funicular  process 
remains  open,  continuous  with  the  peritoneal  cavity,  and  forms  a  sac  into 
which  the  abdominal  viscera  can  descend.  In  10-20  per  cent,  it  communi- 
cates with  the  tunica  vaginalis.  The  true  congenital  inguinal  hernia  is 
spoken  of  as  total  or  partial  funicular,  according  to  the  degree  of  patency 
of  the  process.  "  Congenital  "  means  that  the  sac  exists  at  birth,  not  that 
the  hernia  does.  The  sac  is  congenital,  the  hernia  may  be  acquired.  The 
sac  may  be  present  throughout  life  without  any  hernia  forming,  but  the 
predisposition  to  it  remains.  Obliteration  of  this  funicular  process  may  be 
merely  delayed  and  may  take  place  subsequent  to  birth.  The  partial 
congenital  or  acquired  variety  is  similar  to  the  acquired  hernia  of  adults, 
in  that  its  sac  is  cut  off  and  separated  from  the  testicle  and  tunica 
vaginalis.  It  is  a  common  type  in  infants,  and  is  spoken  of  as  Incomplete, 
as  opposed  to  the  Complete  or  total  variety  when  the  tunica  vaginalis  is 
also  patent.  Possibly  it  is  always  due  to  a  congenital  defect,  namely,  the 
persistence  of  a  diverticulum,  a  portion  of  the  processus  vaginalis,  which 
has  not  been  retracted  into  the  abdominal  cavity.  If  truly  acquired,  it 
must  be  ascribed  to  abdominal  distension  and  weakening  of  the  wall,  and 
greater  importance  attached  to  these  factors  than  to  patency  of  the 
processus. 

Congenital  Hydrocele  is  also  due  to  patency  of  the  processus,  though 
it  may  be  narrowed  at  its  neck  like  the  neck  of  a  bottle.  Through  the 
•channel  fluid  passes  into  and  out  of  the  abdominal  cavity.  It  flows  back 
slowly  into  the  abdomen  while  in  the  recumbent  posture,  and  returns  when 
the  erect  posture  is  assumed.  The  swelling  is  translucent,  dull  on  per- 
cussion, empties  slowly  without  the  gurgle  produced  on  reduction  of  the 
hernia,  and  on  its  return  fills  up  from  the  bottom.  If  it  is  shut  off,  it  forms 
an  encysted  hydrocele  of  the  cord.  Infantile  hernia  shows  a  certain  degree 
of  translucency  and  carelessly  may  be  mistaken  for  hydrocele.  From  its 
pathology  it  is  obvious  that  local  treatment  of  the  hydrocele  by  painting, 
tapping,  etc.,  is  futile.  Many  get  well  without  treatment,  for  the  obliteration 
of  the  sac  may  be  merely  delayed.  Others  can  be  cured  by  truss  ;  or  by 
operation,  if  the  condition  is  still  present  at  4-5  years  of  age. 

Hernia  and  Phimosis. — Undue  importance  has  been  attached  to 
phimosis  as  a  factor  in  the  causation  and  maintenance  of  hernia  ;  partly 
because  hernia  is  more  common  in  boys,  but  this  is  due  to  the  descent 
of  the  testicles.  Severe  phimosis  is  frequent  without  hernia  and  cir- 
cumcision alone  will  not  cure  hernia  ;   nor  is  hernia  less  frequent  among  the 


Intestinal   Obstruction.  329 

circumcised  than  the  uncircumcised.  Straining  on  micturition  is  rarely 
due  to  a  minute  orifice  in  the  foreskin  and,  unless  there  are  extensive 
adhesions,  ballooning  of  the  foreskin  quickly  attracts  attention  long 
before  hernia  can  be  produced.  If  there  are  straining  and  pain,  they  are 
more  often  due  to  a  narrow  meatus  than  to  phimosis.  Crying  and  straining 
rather  tend  to  strengthen  the  fibres  of  the  internal  oblique  and  transversalis 
muscles,  approximate  the  anterior  and  posterior  walls  of  the  inguinal  canal, 
and  reduce  the  tendency  to  hernia.  Such  straining  may  encourage  hernia, 
if  there  is  abdominal  distension  and  a  patent  processus  vaginalis  keeping 
open  the  inguinal  canal. 

Malnutrition  and  Bad  Feeding. — The  majority  of  cases  are  seen  in 
badly  nourished,  unsuitably-fed  children.  It  is  quite  common  to  find  a 
hernia  in  severe  cases  of  marasmus. 

The  Contents  of  the  Sac  in  order  of  frequency  are  small  intestine, 
cgecum  and  vermiform  appendix,  bladder,  omentum,  sigmoid  flexure, 
and  rarely  a  Meckel's  diverticulum  (Littre's  Hernia).  The  hernia  is  often 
associated  with  encysted  hydrocele  of  the  cord.  In  females  an  ovary 
and  fallopian  tube  may  be  present,  sometimes  in  conjunction  with  con- 
genital malformation.     Occasionally  the  sac  is  tuberculous. 

Diagnosis. — An  inguinal  hernia  is  higher  in  the  abdominal  wall  than 
in  adults.  It  is  more  inguinal  than  scrotal,  and  not  always  obvious  or 
induced  by  straining.  It  forms  a  swelling  in  the  groin,  tense  on  straining, 
reducible,  disappearing  during  sleep,  and  often  translucent.  Irreducible 
hernia  is  rare.  Hernia  of  the  caecum  on  the  right  side  is  frequently  incar- 
cerated. The  testicle  may  be  undescended.  An  appendix  in  a  hernial 
sac  may  simulate  encysted  hydrocele  of  the  cord. 

Treatment. — Remember  the  tendency  to  spontaneous  cure.  Medicinal 
treatment  is  directed  to  careful  dieting,  so  as  to  cure  abdominal  distension 
and  improve  nutrition.  Grey  powder  and  rhubarb  with  soda  are  of  great 
use.  If  the  hernia  keeps  coming  down,  the  child  should  be  kept  in. bed 
with  the  legs  and  pelvis  well  raised  for  a  week  or  two.  The  value  of  truss 
treatment  consists  in  keeping  the  sac  empty,  preventing  distension  of  the 
surrounding  structures,  and  perhaps  setting  up  adhesive  inflammation 
about  the  neck  of  the  sac  and  thus  causing  obliteration.  Unless  it  sets  up 
inflammation,  a  truss  does  not  cure,  but  it  prevents  prolapse  and  dilatation 
of  the  neck  of  the  sac,  and  gives  better  opportunity  for  the  normal  processes 
of  obliteration.  The  canal  becomes  more  oblique  as  the  child  grows  older. 
All  benefit  is  lost  if  once  the  hernia  comes  down,  so  the  truss  must  be  kept 
on  day  and  night.  The  ordinary  soft  worsted  or  wool  truss  is  of  little  value. 
A  rather  better  one  consists  of  a  2-in.  flannel  bandage,  with  a  pad  of 
boracic  lint  over  the  inguinal  canal  and  external  ring.  These  trusses  can 
be  used  temporarily  for  slight  hernia  in  private  practice,  but  never  for  more 
than  6  months.  The  spring  truss,  with  a  pad  distended  with  air  or  water 
and  covered  with  indiarubber,  is  better.     The  skin  must  be  bathed  with 


330  Chapter  XXVIII. 

weak  alcohol  and  water  to  prevent  chafing.  It  is  harmless  in  girls,  but  it 
may  do  injury  to  boys  by  pressure  on  the  spermatic  cord,  setting  up 
orchitis,  atrophy  and  fibrosis.  These  results  are  most  liable  to  happen  if 
the  hernia  is  of  the  complete  congenital  variety.  In  the  incomplete  or 
acquired  variety  the  treatment  is  more  satisfactory.  It  is,  therefore,  of 
great  importance  to  recognise  the  difference  between  the  two  types.  The 
former  is  often  associated  with  congenital  hydrocele  or  imperfectly  descended 
testicle.  Objections  to  the  truss  treatment  are  numerous  and  its  manage- 
ment troublesome.  A  truss  never  fits  for  long  on  account  of  the  rapid 
growth,  and  if  it  does  not  fit  it  is  useless  and  dangerous.  It  has  to  be 
continued  for  several  years  and,  even  then,  the  sac  remains  and  is  a 
potential  danger  in  later  life.  In  mild  cases  truss  treatment  must  be 
continued  for  2  years.  Operative  treatment  is  far  more  satisfactory  for  boys. 
If  it  is  done  early  in  life  there  is  no  malformation  of  the  ring,  and  it  is 
sufficient  to  ligature  the  sac  at  the  level  of  the  internal  ring  and  remove  it. 
Higher  up  there  is  a  risk  of  injuring  the  bladder.  The  early  operation  is 
done  at  any  age  previous  to  the  onset  of  the  first  dentition,  preferably  after 
the  third  month  and  before  weaning.  It  is  a  complete  cure,  if  the  sac  is 
removed.  A  radical  operation  is  not  necessarily  a  radical  cure,  but  recur- 
rence is  rare.  The  chief  objection  to  it  is  that  many  cases  are  cured  by 
truss  treatment  continued  for  1-2  years,  though  a  potential  sac  remains. 
For  this  reason  many  surgeons  refuse  to  operate  before  the  age  of  4  years  ; 
but  the  early  operation  is  steadily  becoming  more  popular.  The  objection 
that  it  is  difficult  to  obtain  asepsis  is  absurd  and  untrue.  The  mortality 
is  extremely  small,  and  a  cure  is  effected  in  2  weeks.  It  is  very  suitable 
if  there  is  difficulty  in  applying  the  truss  properly  or  inability  to  afford 
prolonged  treatment.  Operation  is  necessary  for  a  large  hernia,  which  can- 
not be  controlled  by  truss  ;  for  femoral,  irreducible,  or  strangulated  hernia 
at  any  age  ;  for  hernia  with  reducible  hydrocele,  if  a  truss  is  painful ;  for 
incomplete  hernia  with  imperfectly  descended  testicle  ;  and  if  the  hernia 
is  persistent. 

Strangulated  Inguinal  Hernia. — More  than  100  cases  have  been 
recorded  under  1  year  of  age  ;  a  small  number  in  comparison  with  the  great 
frequency  of  hernia.  Fifty  per  cent,  of  those  in  the  first  year  of  life  are 
under  3  months  of  age  ;  and  of  these  one-fourth  occur  in  the  first,  one- 
fourth  in  the  second,  and  one-half  in  the  third  month.  In  a  case  of 
Kellock's  (1902),  a  boy  aged  10  weeks  had  bilateral  strangulation,  with  an 
interval  of  15  days  between  the  two  operations.  The  symptoms  are  more 
gradual  in  development  than  in  adults,  because  of  the  greater  elasticity 
of  the  inguinal  canal  and  the  absence  of  chronic  thickening  of  the  neck  of 
the  sac.  There  is  the  usual  history  of  a  hernia,  perhaps  treated  by  truss  ; 
of  the  rupture  coming  down  and  staying  down  ;  and  the  development  of 
vomiting,  constipation  or  the  passage  of  bloody  mucus,  and  frequently 
suppression  of  urine.     There  is  a  tense,  painful,  tender,  irreducible  local 


Intestinal  Obstruction.  331 

swelling,  perhaps  resonant  and  with  no  impulse  on  cough.  It  may  be  so 
transparent  as  to  simulate  hydrocele.  In  later  stages  there  are  redness  and 
oedema  of  the  skin,  general  malaise,  lividity  and  collapse.  The  mortality 
of  operation  is  very  small,  if  operation  is  done  in  reasonable  time,  for  the 
diagnosis  is  usually  made  before  gangrene  has  set  in.  Stiles  had  no  death 
in  15  cases.  The  baby  will  take  the  breast  a  few  hours  after  operation. 
In  the  treatment  of  irreducible  hernia  a  gentle  attempt  at  reduction  by 
taxis  should  be  made,  with  the  child  in  a  hot  bath  or  suspended  so  that 
it  almost  stands  on  its  head.  This  is  by  no  means  uncomfortable,  and  the 
steady  drag  of  the  intestine  may  disengage  an  irreducible  and  even 
strangulated  hernia. 

Femoral  Hernia  is  much  more  rare.  Bull  and  Coley  (1905)  had  only 
35  in  1,424  cases  of  hernia  in  children,  1,366  being  inguinal.  It  may  be 
bilateral.    Stiles  had  only  one  in  a  series  of  360  cases  (1904). 

The  Appendix  and  Hernia. — It  is  not  very  uncommon  to  find  the 
appendix  and  sometimes  portions  of  the  caecum  in  a  hernial  sac,  and  not 
infrequently  such  a  hernia  becomes  strangulated.  The  appendix  may  be 
attacked  by  acute  inflammation  while  in  its  abnormal  position. 


CHAPTER    XXIX. 


THE    RECTUM    AND    ANUS. 

Malformations  —  Fwcal    Incontinence  —  Fissure  —  Spasm  — Polypus — Pro- 
lapse— Proctitis —  Haemorrhoids — Fistula —  Abscess. 

Examination  of  the  rectum  and  anus  often  affords  valuable  and 
essential  evidence  of  local  mischief,  and  sometimes  of  affections  of  other 
organs.  The  rectum  of  the  infant  admits  the  little  finger.  The  sigmoid 
flexure  is  loosely  attached,  and  it  may  be  possible  to  palpate  the  kidneys 
and  under  the  surface  of  the  liver.  Examine  for  polypus  or  foreign  body  in 
cases  of  diarrhoea  and  haemorrhage.  Other  affections  which  may  be  recog- 
nised by  rectal  examination  are  faecal  accumulation,  intussusception, 
enlarged  glands,  an  appendix  abscess  or  inflamed  appendix,  the  matting 
of  tuberculous  peritonitis,  localised  gonorrhceal  peritonitis,  salpingitis, 
ovarian  cysts  and  tumours,  and  enlarged  spleen.  It  is  sometimes  of  value 
in  the  differential  diagnosis  of  renal  and  other  tumours.  It  is  almost  needless 
to  add  that  the  examination  must  be  carried  out  with  extreme  gentleness, 
bimanually,  and  frequently  under  anaesthesia. 

Malformations. — In  the  consideration  of  malformations  of  the  rectum 
and  anus  it  is  necessary  to  investigate  the  development  of  the  hind  end 
of  the  body,  including  the  urethra  and  vagina,  i.e.,  of  the  rectum  and 
urogenital  passages.  Three  demonstrations  on  the  subject  by  Keith  (1908) 
contain  the  most  recent  observations  on  the  subject.  Keith  found  37 
specimens  of  malformation  of  the  rectum  in  the  museum  of  the  Royal 
College  of  Surgeons  and  77  in  other  London  hospital  museums.  These 
may  be  contrasted  with  Curling's  100  cases  (1876)  in  the  following  table, 
showing  the  frequency  of  the  different  varieties. 

Malformations  of  the  Rectum. 


GROUPS. 

KEITH. 

CURLING. 

TOTAL. 

A.  Males— 

1.  Rectum  opening  in  urethra . . 

33 

26 

59 

2.  Rectum  ending  as  cord  at  or  above 

base  of  prostrate 

7] 

3.  Rectum  ending  as  cord  at  site  of 

proctodaeum 

7 

~ 

38 

59 

4.  Rectum  ending  blindly  at  procto- 

dseum 

7 
j 

The  Rectum  and   Anus. 
Malformations  of  the  Rectum — continued. 


333 


GROUPS. 

KEITH. 

CURLING. 

TOTAL. 

B.  Females — 

1.  Rectum  ending  in  vulva  or  vagina . . 

2.  Rectum  ending  as  cord  above  upper 

fornix  of  vagina 

3.  Rectum  ending  as   cord  at   upper 

fornix  of  vagina     . . 

4.  Rectum  ending  as  cord  on  vagina 

below  upper  fornix 

5.  Rectum  ending  blindly  or  as  cord 

at  proctodeum 

6 

5^ 

3 

2 

10, 

■ 

11 

19 

17 
39 

C.  Miscellaneous — 

1.  Imperfect 

2.  Imperforate  rectum  in  females  with 

male  form  of  ext.  genitals 

3.  Rectum  opening  abnormally 

4.  Rare  malformations 

5.  Abnormalities  in  domestic  animals 

6 

6 

1 

5 

16 

6 

7 

In  the  process  of  development  the  hind-gut  grows  backward  and 
loses  its  connection  with  the  cloaca,  but  the  other  cloacal  orifice,  the 
allantoic  opening,  persists  and  forms  the  urogenital  sinus  and  finally 
the  urethra.  Into  this  sinus  there  open  the  bladder  in  front  and  the 
Miillerian  ducts  behind. 

Apparently  the  orifice  of  these  ducts  is  lost  in  early  foetal  life  and 
develops  again  later.  The  vagina  appears  as  a  solid  rod-like  structure 
in  the  tissues  between  the  urethra  and  the  hind-gut,  now  the  rectum. 
It  is  formed  by  an  active  tubular  downgrowth  from  a  portion  of  the  wall 
of  the  allantois,  and  the  hymen  is  due  to  incomplete  absorption  of  the 
terminal  portion.  Atresia  is  the  result  of  failure  of  this  downgrowth 
to  develop. 

The  male  urethra,  as  far  as  the  bulb,  is  equivalent  to  the  female  urethra, 
which  for  a  time  is  obliterated  as  a  tube  and  is  subsequently  regenerated. 
The  penile  urethra  is  formed  by  the  desquamation  of  a  plug  of  cells  invading 
the  penis.  Hence  the  urethra  in  foetal  life  is  for  a  time  imperforate,  and 
if  the  condition  persists  the  bladder  bursts  from  internal  pressure,  urine 
being  secreted  in  utero,  and  ectopia  vesicae  results.  Thus,  there  is  a  stage 
of  imperforation  in  all  the  posterior  orifices,  and  this  stage  may  be  per- 
sistent and  give  rise  to  various  defects,  more  especially  in  the  rectum. 


334  Chapter   XXIX. 

An  imperforate  urethra  is  the  least  common,  for  foetal  use  is  made  of  the 
channel.  It  causes  great  distension  of  the  bladder,  ectopia  vesicas,  umbilical 
fistula  and  epispadias,  provided  the  kidneys  develop.  Atresia  vagina?, 
ectopia  vesicae  and  imperforate  anus  may  be  combined.  The  hymen  is 
almost  invariably  present  and  may  be  persistent. 

According  to  this  theory,  that  of  Wood  Jones,  the  urethral  orifice  of 
the  rectum  is  the  original  anus,  and  the  portion  of  the  rectum  between 
that  and  the  perineal  anus  is  a  post-allantoic  prolongation  of  the  original 
rectum,  or  hind-gut.  Keith  brings  forward  evidence  (British  Medical 
Journal,  1908)  which  makes  this  hypothesis  unsatisfying.  Keference  to 
his  papers  must  be  made  for  further  details  of  what  is  a  very  complicated 
process  of  development.  According  to  this  writer  it  depends  on  modifi- 
cations of  the  cloaca  for  sexual  purposes.  Mall  (1908)  found,  from  the 
results  of  the  examination  of  163  malformed  embryos,  that  the  chorion 
invariably  showed  evidence  of  uterine  inflammation  ;  and  he  regards  this 
as  the  cause  of  fcetal  malformation. 

The  anus  is  formed  from  the  proctodseum  by  the  absorption  of  a 
definite  cellular  mass,  the  "  bouchon  cloacal  "  of  Tourneux,  a  specialised 
part  of  the  "  anal  membrane,"  forming  the  anterior  wall  of  an  internal 
cloaca  at  the  junction  of  the  allantoic  stalk  with  the  hind-gut.  The  anal 
canal,  and  both  the  internal  and  external  sphincters,  arise  in  this  way, 
independently  of  the  bowel,  and  the  rectum  terminates  at  the  entrance 
into  the  anal  canal.  Certain  malformations  arise  from  imperfect  absorp- 
tion. Occasionally  a  membrane  closes  the  external  orifice  of  the  anus. 
Sometimes  a  thick  tail-like  fold  of  skin  extends  from  the  median  raphe 
of  the  scrotum  to  just  behind  the  anal  opening  or  the  tip  of  the  coccyx. 
In  some  cases  faeces  pass  freely,  or  with  pain,  on  either  side  of  the  fold. 
It  can  be  dissected  off  and  the  anus  dilated.  In  other  instances  there 
is  no  anus  or  evidence  of  one,  perhaps  a  puckered  depression  lined  with 
normal  skin.  Or  there  is  a  well-marked  median  raphe  and  the  rectum 
bulges  down  as  a  blind  pouch  to  within  a  variable  distance  of  the  surface. 
Or  the  anus  may  open  into  a  definite  cul-de-sac,  and  the  rectum  bulges 
down  the  apex  of  the  pouch,  thus  leaving  a  definite  thick  separating 
membrane  about  §  in.  from  the  anus.  In  one  child  under  my  notice 
this  cul-de-sac  was  divided  by  a  median  fold  of  skin.  Congenital  stricture 
of  the  anus  may  be  due  to  a  membranous  septum,  with  a  small  central 
orifice,  or  to  a  fold  of  mucous  membrane. 

In  rare  instances  the  sigmoid  and  rectum  are  absent,  the  colon  ending 
in  a  blind  pouch  in  the  left  iliac  fossa  ;  or  the  first  and  second  portions  of 
the  rectum  are  absent,  and  the  sigmoid  and  descending  colon  dilated. 
The  former  malformation  supports  the  view  that  there  is  a  normal  extension 
of  growth  of  the  hind-gut  backwards,  and  that  it  is  due  to  failure  in  the 
development  of  this  prolongation. 


The  Rectum  and   Anus.  335 

The  symptoms  of  imperforate  anus  or  rectum  are  those  of  increasing 
intestinal  obstruction.  The  state  of  the  anus  is  easily  ascertained  by 
examination ;  and  rectal  examination  will  elucidate  the  condition  of 
affairs  in  obstruction  higher  up.  In  some  malformations  there  is  partial 
obstruction  and  passage  of  faeces  by  other  routes.  Should  the  rectum 
communicate  with  the  urethra,  bladder  or  vagina,  meconium  may  be 
passed  in  sufficient  amount  to  enable  the  child  to  live.  The  bladder  becomes 
infected  and  severe  cystitis  ensues.  Faeces  may  be  found  in  the  urine  or 
vagina. 

Treatment  is  essentially  surgical,  but  operation  is  not  urgent  in  the 
incomplete  cases.  Frequently  an  incision  in  the  median  line  will  enable 
the  surgeon  to  find  the  blind  end  of  the  rectum,  to  free  it  for  about  an 
inch,  open  it  and  sew  its  margins  to  those  of  the  artficial  anus.  The 
incision  may  pass  through  the  peritoneal  cavity,  for  the  peritoneum  may 
lie  between  the  rectum  and  the  perineum,  and  between  the  bladder  and 
the  perineum.  Hence  the  incision  may  expose  the  peritoneum,  and  it 
may  be  necessary  to  cut  through  a  parietal  and  visceral  layer  in  order  to 
reach  the  rectum.  The  trocar  is  a  particularly  dangerous  instrument 
to  use  in  attempting  to  afford  relief.  The  prognosis  of  operative  treatment 
is  very  good  as  regards  finding  the  rectum,  but  the  child  often  dies,  even 
if  the  rectum  is  opened  early.  If  the  proctodaeum  is  present  competent 
sphincters  develop.  Unrelieved  cases  die  in  less  than  a  week  from  gangrene 
and  rupture  of  the  colon. 

Faecal  Incontinence  may  occur  as  a  symptom  in  any  serious  illness, 
such  as  meningitis,  fevers  and  prolonged  wasting  diseases  ;  in  affections 
of  the  nervous  system,  viz.,  spina  bifida,  epilepsy,  myelitis  and  injury 
of  the  lumbar  cord  ;  from  local  stretching  of  the  sphincter  ani,  the  result 
of  prolapsus  recti,  chronic  constipation,  impacted  faeces,  the  insertion  of 
foreign  bodies,  sodomy  and  operations  ;  or  from  purgative  drugs.  Few 
of  these  causes  are  operative  in  the  first  three  years  of  life.  Some  cases 
are  analogous  in  many  respects  to  enuresis,  showing  the  same  nervous 
instability  ;  and  apparently  due  to  persistence  of  the  infantile  condition 
or  weakness  of  the  sphincter,  whereby  it  yields  to  a  very  slight  stimulus. 
Others  are  of  congenital  origin,  dependent  on  lack  of  co-ordination,  or  on 
mental  defect. 

Incontinence  is  more  common  in  boys  than  girls.  It  may  be  nocturnal 
and  diurnal,  and  is  more  frequently  diurnal  than  nocturnal  only.  The 
stools  may  be  constipated,  but  are  more  commonly  loose,  offensive  and 
slimy.     Occasionally  there  is  lienteric  diarrhoea. 

Cases  analogous  to  enuresis  are  easily  curable,  generally  in  a  few 
days.  Those  associated  with  diarrhoea  soon  yield  to  bismuth.  Some  con- 
genital cases  have  persisted  beyond  puberty.  The  treatment  consists  in 
attention  to  the  general  health,  diet,  exercise,  fresh  air,  cold  baths,  etc. 
Many  yield  to  treatment  by  gentian  and  rhubarb,  strychnia  or  nux  vomica, 


336  Chapter   XXIX. 

belladonna  and  bromide,  or  small  doses  of  Dover's  powder,  gr.  1-3,  t.d.s. 
Ice  suppositories,  galvanism,  and  local  injections  of  strychnia  are  un- 
necessary. Food  and  drink  should  be  tepid,  not  cold  ;  and  no  irritant 
foods  or  fruits  are  permissible.  Eelapses  are  not  uncommon,  but  the  general 
prognosis  is  excellent. 

Anal  or  Rectal  Spasm. — Anal  spasm  is  usually  due  to  fissure ;  occasion- 
ally to  other  local  irritation  of  the  rectal  mucosa,  such  as  simple  congestion. 
Sometimes  in  highly  neurotic  children  no  cause  can  be  found,  and  the 
nervous  state  must  be  treated.  It  may  be  associated  with  tenesmus.  The 
pain  is  severe.  The  infant  assumes  a  fully  extended  position,  with  the 
head  thrown  back  and  the  thighs  strongly  adducted.  The  duration  of  the 
attack  is  variable.  It  is  treated  by  hot  baths,  injection  of  hot  oil  and, 
if  very  severe,  by  the  injection  of  a  few  drops  of  laudanum.  The  local 
cause  must  be  cured. 

Fissure  of  the  Anus  is  produced  by  scratching,  set  up  by  the  local 
irritation  of  threadworms,  eczema,  etc,  ;  by  constipation,  or  injury  by 
suppositories  or  the  nozzle  of  a  syringe.  It  is  most  frequent  in  the  breast- 
fed. The  common  site  is  the  posterior  wall  of  the  rectum,  near  the  coccyx. 
The  minute  tear  readily  heals  but,  if  the  cause  is  persistent,  it  is  con- 
stantly torn  open  and  a  small  linear  ulcer  results.  The  ulcer  has  thickened 
edges,  a  greyish  base,  and  exudes  a  little  pus  and  perhaps  a  drop  of  blood 
when  the  bowels  act.  The  ano-rectal  mucosa  is  red  and  swollen,  covered 
with  muco-pus  in  bad  cases.  The  child  should  be  examined  in  the  gynae- 
cological position,  with  the  legs  elevated.  Separate  the  gluteal  folds 
and  press  the  fingers  on  either  side  of  the  anus  in  order  to  evert  the  mucous 
membrane.  Occasionally  a  small  bivalve  speculum  is  needed.  Examination 
causes  painful  constriction  of  the  sphincter. 

Fissure  gives  rise  to  pruritus,  sickening  pain  on  defalcation  and  for 
some  time  after,  constipation  due  to  anal  spasm  for  the  child  fears  to 
defalcate,  screaming  attacks  in  babies,  a  haggard  look,  irritability,  sleep- 
lessness, and  even  pavor  and  convulsions.  Streaks  of  blood  may  be  found 
on  the  faeces.  Sometimes  there  is  spasmodic  retention  of  urine  or  reflex 
enuresis,  and  reflex  priapism.  The  pain  may  be  referred  to  adjacent  parts  ; 
such  as  the  foot  and  hip,  causing  dragging  of  the  leg,  inability  to  walk 
or  stand  upright,  and  simulation  of  early  hip  disease.  The  gait  and 
attitude  are  protective,  to  prevent  the  rubbing  together  of  the  nates. 

The  constipation  is  treated  by  diet,  massage,  mild  laxatives  of  senna, 
figs,  etc.  Apply  oil  or  vaseline  before  defeecation,  or  a  suppository  of 
cocaine  gr.  \,  ext.  belladon.  gr.  J.  Keep  the  parts  clean  with  vaseline 
and  cotton  wool,  and  touch  the  base  of  the  ulcer  with  the  solid  stick  of 
nitrate  of  silver,  followed  by  salt  solution,  every  2  or  3  days  until  cured. 
Thomson  recommends  an  ointment  of  ichthyo]  and  tannic  acid  aa  dr.  1 
to  vaseline  oz.  1.  Stretching  the  sphincter  is  rarely  needed.  It  must  be 
done  under  deep  narcosis. 


The  Rectum  and   Anus.  337 

Rectal  Polypus  is  not  uncommon.  The  tumour  is  attached  to  the 
rectal  wall  by  a  pedicle.  It  causes  bleeding  after  defsecation,  and  appears 
when  the  bowels  act  as  a  smooth,  dark  red  or  dusky  purple  swelling,  like 
a  small  cherry.  Blood  and  slime  are  passed  after  the  stool.  It  is  usually 
single,  myxomatous  or  myxo-adenomatous  in  structure,  and  is  sometimes 
mistaken  for  piles,  intussusception  or  prolapsed  rectum.  It  is  easily  twisted 
off  by  a  wire  snare  or  forceps. 

Prolapsus  Ani  and  Recti. — The  mucous  membrane  of  the  anus  may 
be  everted  in  the  form  of  a  dusky  red,  irregular  ring  round  the  orifice.  It 
appears  on  the  passage  of  a  constipated  stool,  and  is  readily  replaced  by 
gentle  pressure  with  an  oily  rag.  No  treatment  is  necessary  beyond  regula- 
tion of  the  bowels.  An  Ano-rectal  Prolapse  is  one  of  the  lowest  part  of  the 
rectum,  with  and  involving  the  anus.  Prolapsus  Recti  is  a  prolapse  of  the 
whole  rectal  wall  for  a  distance  of  2-3  ins.,  projecting  through  the  anus, 
but  not  involving  the  anal  mucosa.  It  is  uncommon  before  the  age  of 
6  months,  for  the  child  is  not  sufficiently  wasted  and  the  pelvic  padding  of 
fat,  which  supports  the  bowel,  is  still  present.  From  this  age  up  to  the 
end  of  the  third  year  it  is  quite  common,  because  of  the  frequency  of 
marasmus,  attacks  of  diarrhoea,  and  weakness  of  the  supporting  pelvic 
muscles  during  early  life.  It  may  be  due  to  the  straining  set  up  by  a  faecal 
concretion,  constipation,  threadworms,  rectal  polypi,  and  vesical  calculus. 
Constipation  is,  in  my  opinion,  an  uncommon  cause.  Sometimes  it  comes 
down  in  the  paroxysms  of  whooping  cough. 

The  prolapse  comes  down  when  the  bowels  act,  and  is  easily  reduced. 
In  bad  cases  it  will  return  in  the  intervals  between  defalcation,  on 
crying  or  coughing.  In  the  worst  ones  it  remains  persistently  down.  Thus, 
it  may  come  down  daily  and  be  returned  for  several  weeks,  and  the  child 
is  not  brought  for  treatment  until  it  has  been  down  persistently  for  a 
week  or  more.  It  projects  from  the  anus  as  a  more  or  less  cone-shaped  or 
cylindrical  protrusion,  dark  red  or  reddish  purple,  corrugated  with  trans- 
verse folds,  and  a  round  central  orifice.  In  advanced  cases  it  tends  to  bend 
forward.  It  often  becomes  inflamed,  covered  with  mucus,  ulcerates  super- 
ficially, and  bleeds  readily.  If  it  has  been  down  for  long  and  cannot  be 
replaced,  constriction  and  necrosis  of  the  mucosa  take  place  at  the  base. 
It  may  be  mistaken  for  polypus  or  intussusception. 

Treatment. — Place  the  child  on  the  side  or  back.  Wash  the  tumour 
with  cold  water  and  reduce  it  by  gentle  pressure  with  the  tips  of  the 
fingers,  well  oiled  or  covered  with  a  soft  oily  rag.  If  it  does  not  go  back 
readily,  apply  ice  or  iced  water  for  a  short  time  and  then  try  again.  Should 
there  be  constipation  give  an  enema  after  reduction  and  put  the  child  on 
a  suitable  diet  and  laxatives.  In  bad  cases  it  may  be  necessary  to  give 
chloroform  or  to  paint  the  prolapse  with  cocaine,  5  per  cent,  solution,  and 
then  to  dilate  the  sphincter  by  inserting  the  little  finger  through  the  central 
orifice  of  the  tumour.    After  reduction  insert  a  cocaine  suppository,  gr.  a, 

z 


338  Chapter   XXIX. 

into  the  rectum  ;   apply  a  pad  to  the  anus  and  strap  the  buttocks  together 
with  adhesive  plaster,  or  put  on  a  T-shaped  bandage. 

To  prevent  recurrence  improve  the  child's  nutrition,  cure  diarrhoea, 
keep  the  bowels  gently  open  without  straining,  and  make  the  child  def aecate 
while  on  the  back  or  side,  with  the  buttocks  supported  by  the  hands  of  the 
nurse.  The  squatting  position,  on  a  small  seat  with  the  legs  off  the  ground, 
is  the  best  position  for  older  children,  and  prevents  undue  straining.  After 
defaecation  inject  ice  cold  water,  insert  a  cone-shaped  ice  suppository,  or 
give  an  astringent  injection  of  sulphate  of  iron  grs.  2  ad.  oz.  1,  to  reduce 
the  venous  congestion  and  brace  up  the  relaxed  tissues.  If  there  is  tenesmus 
or  diarrhoea,  a  suppository  of  cocaine,  belladonna  or  opium  may  be  needed. 
Let  the  child  lie  down  afterwards. 

Recurrence  can  be  prevented  by  keeping  the  child  in  bed  with  the 
legs  suspended,  as  in  the  treatment  of  fractured  thigh,  strapping  the 
nates  together  with  plaster. 

Should  these  simple  measures  fail  recourse  must  be  had  to  dusting 
with  astringents,  such  as  alum ;  the  local  injection  of  strychnine 
gr.  -juo-tIjo,  twice  daily,  to  tone  up  the  levator  ani ;  Pacquelin's  cautery, 
lunar  caustic  or  fuming  nitric  acid,  3  or  4  vertical  lines  being  drawn 
down  the  exposed  mucous  membrane  at  intervals  of  about  an  inch  ; 
injection  of  2-4  oz.  of  2  per  cent,  saline  solution  into  the  superior  pelvic 
Tectal  space,  the  needle  being  inserted  midway  between  the  anus  and 
coccyx  through  the  sacro-coccygeal  ligament  ( it  acts  as  an  irritant,  and 
causes  induration  of  the  cellular  tissues)  ;  injections  of  hard  paraffin, 
melting  point  56-58°  C,  in  the  form  of  a  ring  above  the  anus,  between  the 
skin  and  mucous  membrane.  The  bowels  should  be  opened  freely  for 
2  days  before  the  operation,  and  a  bismuth  mixture  given  the  day  before. 
The  anus  must  be  rendered  aseptic.  An  irreducible  prolapse  is  so  rare 
that  resection  of  the  mass  need  only  be  mentioned. 

Proctitis  is  an  inflammation  limited  to  the  rectum  and  not  part  of  a 
general  affection  of  the  large  intestine.  In  infants  it  is  set  up  by  the  prolonged 
use  of  glycerine  and  irritating  suppositories,  injury  or  infection  by  enema 
syringes,  and  threadworms.  Occasionally  it  is  due  to  gonococcal,  pneu- 
mococcal, streptococcal  or  diphtheritic  infection.  It  may  be  a  sequel 
of  measles  or  scarlatina,  and  very  rarely  occur  in  syphilis  or  tuberculosis. 
A  speculum  is  required  for  accurate  diagnosis.  The  inflammation  is  catar- 
rhal, membranous  or  ulcerative  in  type.  In  simple  catarrh  the  mucosa 
is  redder  than  normal,  swollen,  and  bleeds  easily.  It  secretes  mucus  freely, 
and  discharges  it  in  jelly-like  masses  or  casts,  unmixed  with  faeces.  Pain  and 
tenesmus  are  present  on  defalcation.  The  stools  are  discharged  in  jerks, 
like  water  from  a  squirt,  and  contain  mucus  and  blood.  Prolapse  of  the 
rectum  and  irritation  of  the  skin  of  the  buttocks  and  adjacent  parts  com- 
plicate the  case. 

In  the  membranous  form  the  membrane  may  be  seen  on  the  wall  of 


The  Rectum  and   Anus.  339 

the  rectum,  on  examination  with  the  speculum  ;  on  the  gut  if  it  is  prolapsed  ; 
or  in  the  stools. 

Ulceration  is  usually  superficial,  secondary  to  catarrh,  and  heals 
readily.  Deep  follicular  ulcers  are  sometimes  found  as  part  of  a  follicular 
■colitis.  Tuberculous  and  syphilitic  ulcers  are  rare.  Ulceration  causes 
greater  bleeding,  a  variable  amount  of  pain,  tenesmus  if  it  is  near  the  anus, 
and  pus  in  the  stools  in  chronic  cases. 

Treatment. — Attend  to  any  local  cause  which  may  be  present.  Get 
rid  of  worms.  Give  injections  of  warm  bland  fluids,  such  as  starch  and 
water,  saline  solution,  olive  oil  and  lime  water,  or  boric  acid  lotion.  Later, 
give  astringent  injections,  e.g.  2  per  cent,  solution  of  hamamelis  or  tannic 
acid.  If  there  is  ulceration,  insert  a  speculum  and  apply  nitrate  of  silver 
solution,  0-5  per  cent,  strength.  Give  cocaine  or  opium  suppositories 
ior  pain  and  tenesmus  ;  alkalies  by  the  mouth,  if  the  stools  are  acid  ;  mild 
-purgatives,  a  milk  diet,  and  rest  in  bed. 

Haemorrhoids  are  not  often  seen,  partly  because  they  are  not  looked 
for.  They  may  be  found  in  the  first  few  months  of  life,  but  are  rare  before 
the  fourth  year.  External  piles  are  due  to  constipation.  They  are  generally 
;small,  may  cause  pain  on  defaecation  and  slight  bleeding.  Internal  piles 
are  sometimes  present  without  pain  or  other  signs.  In  a  few  cases  I  have 
•seen  a  single  purple  soft  pile,  which  would  come  down  on  the  child  straining, 
b»ut  not  causing  any  discomfort  or  bleeding.  Such  piles  disappear  in  time 
;and  give  rise  to  no  trouble.  Treatment  is  rarely  necessary.  A  mild  astrin- 
gent ointment  can  be  used,  and  it  is  important  to  keep  the  bowels  gently 
•open.  The  Congenital  Pile  is  a  fibro-fatty  structure  ;  a  malformation  and 
not  a  true  pile.  It  is  a  small  pile-like  tumour,  the  size  of  a  large  pea,  in  the 
middle  line  at  the  anterior  margin  of  the  anus,  on  the  perineum. 

lschio-rectal  Abscess  is  not  uncommon,  even  in  infancy.  It  is  due  to 
lymphadenitis,  secondary  to  proctitis  or  local  infection.  The  abscess  heals 
quickly  after  incision.  I  have  known  it  take  over  a  fortnight  to  get  well. 
It  rarely  burrows,  sloughs  or  ends  in  fistula. 

Fistula  in  Ano  is  rare  in  infants  and  children,  and  usually  tuberculous  ; 
'Occasionally  secondary  to  fish  bones,  infections,  and  ischio-rectal  abscess. 
Ware  (1906)  has  described  a  variety  in  infants,  apparently  of  develop- 
mental origin,  due  to  inclusion  of  skin.  It  is  lined  with  stratified  squamous 
epithelium.  A  probe  can  be  passed  through  it  into  the  rectum.  It  gives 
rise  to  a  constant  discharge  of  moisture  and  f  seces  through  the  small  external 
orifice  near  the  anus.  Cure  is  effected  by  excision  of  the  tract  of  the 
fistula. 


Chapter  XXX. 

APPENDICITIS. 

The  appendix  is  either  a  vestigial  remnant  or  a  highly  differentiated 
and  specialised  lymphoid  structure.  It  is  directly  continuous  with  the 
caecum  in  the  foetus,  and  later  is  provided  with  a  valvular  fold  of  mucous 
membrane  at  the  orifice,  the  valve  of  Gerlach.  Appendicitis  is  by  no  means 
common  in  children,  but  has  become  more  frequent  in  later  years.  Not 
more  than  10  per  cent,  of  all  cases  are  under  10  years  of  age.  It  is  more 
frequent  in  Paris  than  in  London;  and  according  to  Selter,  of  Solingen,. 
Germany,  it  is  7  times  more  common  than  in  adults.  Diagnosis  is  often 
difficult,  for  the  early  signs  are  apt  to  be  unnoticed  or  thought  unimportant. 
Cases  may  be  acute,  chronic,  recurrent  or  relapsing,  latent,  or  fulminating ; 
circiimscribed  or  diffuse  ;  catarrhal,  ulcerative,  gangrenous,  or  perforative,, 
with  or  without  abscess  formation. 

Etiology. — It  is  more  common  in  boys  than  in  girls  in  the  proportion 
of  about  2-1,  and  for  this  there  is  no  satisfactory  explanation.  Neuberg 
(1907)  found  the  sexes  equal  in  82  cases.  It  is  rare  during  infancy.  Death 
has  been  reported  (Porak  and  Durante,  1902)  at  21  days  of  age  from  acute 
peritonitis  and  sloughing  appendix,  due  to  a  suppurating  cord  and  urachus.. 
Kermisson  and  Guimbellot  (1906)  collected  9  cases  under  1  year,  all  fatal- 
One  such  case  has  come  under  my  care.  The  causes  of  the  recent  increase 
in  frequency  have  been  stated  to  be  influenza,  the  habitual  use  of  pur- 
gatives, enamelled  pans,  iron  fragments  in  roller  flour,  and  chilled  meat. 
Preserved  foods  and  chilled  meats  are  particularly  liable  to  bacterial 
contamination.  Any  cause  of  catarrhal  inflammation  or  congestion  of  the 
caecum  and  the  appendix,  e.g.  enteritis,  is  liable  to  set  up  an  attack. 
The  appendix  becomes  swollen,  perhaps  as  large  as  the  little  finger,  filled, 
with  mucus  or  muco-pus,  and  shut  off  from  the  caecum.  A  mild  attack 
subsides,  or  perhaps  leads  to  the  formation  of  a  concretion  ;  or  the  con- 
cretion may  be  the  primary  cause  of  the  catarrh.  In  a  few  cases  foreign 
bodies  have  been  found  present,  e.g.,  small  seeds,  pins  and  threadworms.. 
Santorini,  in  1724,  noted  that  the  appendix  was  often  the  resort  of  intestinal 
worms. 

Usually  the  nucleus  of  the  concretion  is  a  small  mass  of  degenerated 
cells,  bacteria  and  inspissated  mucus.  Probably  most  of  the  cases  ascribed 
to  cold,  rheumatism  and  injury  are  those  in  which  a  concretion  already 
exists  and  fresh  catarrh  has  been  set  up.    The  recovery  of  such  cases  under 


Appendicitis.  3-11 

treatment  by  salicylates  does  not  prove  that  they  are  rheumatic.  The 
threadworms  are  the  most  common  variety  of  worm  found.  Whether 
primary  or  secondary,  they  are  liable  to  prolong  or  increase  local  mischief. 
Tuberculous  and  typhoid  ulceration  may  occasionally  spread  to  the  appen- 
dix. Infection  may  take  place  from  the  female  genitals.  Malignant  disease 
is  exceptional.    Injury  has  caused  perforation. 

Pathology. — The  bacillus  coli  is  constantly  present ;  occasionally 
associated  with  the  staphylococcus  aureus,  and  less  often  with  other 
organisms.  The  normal  appendix  is  never  sterile,  and  microbial  infection 
is  the  main  cause  of  inflammation.  In  the  catarrhal  state  the  inflammation 
may  spread  to  the  peritoneal  surface  and  set  up  local  or  general  peritonitis, 
apart  from  actual  perforation.  Inflammation  of  a  pseudo-membranous 
type  may  lead  to  necrosis  of  the  mucous  membrane  and  gangrene.  The 
catarrhal  process  often  terminates  in  resolution.  This  may  be  complete  ; 
or  may  leave  behind  it  adhesions,  scarred  tissue,  strictures,  or  sclerosis 
and  obliteration  of  the  lumen.  The  inflammation  may  become  chronic, 
in  consequence  of  stricture  and  retention  of  secretions,  forming  a  cyst, 
mucocele,  empyema  or  concretion.  Or  it  may  end  in  abscess  formation,  the 
abscess  being  shut  off  from  the  general  peritoneal  cavity  or  setting  up 
septic  peritonitis.  An  abscess  may  form,  with  or  without  perforation  of  the 
appendix.  It  may  be  localised  in  the  peritoneal  sac,  or  outside  the  peri- 
toneal sac  and  spread  up  behind  the  colon.  Suppuration  may  extend 
upwards  to  form  a  subphrenic  abscess,  or  down  into  the  pelvis.  In  a  girl, 
aged  4  years,  an  abscess  formed  below  and  to  the  left  of  the  umbilicus. 
Perforation  is  secondary  to  concretion,  abscess,  ulceration  or  gangrene. 
It  causes  local  abscess  formation  or  general  peritonitis.  Gangrene  is  due 
to  the  virulence  of  the  inflammation,  or  obstruction  to  the  blood  supply  by 
twisting  or  kinking  of  the  inflamed  appendix.  The  most  striking  features 
of  the  disease  in  children  are  that  obliteration  does  not  occur,  and  that  a 
diffuse  inflammation  is  more  common  than  a  local  one.  The  local  plastic 
type  of  peritonitis,  in  which  adhesions  are  formed  and  the  abscess  cut  off 
from  the  general  peritoneal  character,  is  uncommon.  When  an  abscess  is 
formed  it  is  generally,  but  not  invariably,  situated  in  the  right  iliac  fossa  ; 
for  the  appendix  may  be  situated  in  the  pelvis,  in  the  depression  between 
the  psoas  muscle  and  the  spine,  in  the  region  of  the  kidney,  under  the 
liver,  near  the  umbilicus,  and  even  in  the  left  iliac  fossa  or  a  hernial  sac. 
It  may  discharge  through  the  abdominal  wall,  below  Poupart's  ligament, 
into  the  rectum,  bowel,  bladder,  vagina  or  into  the  peritoneal  cavity. 
Possibly  pus  can  be  located  in  the  appendix  for  a  time  and  discharge  into 
the  caecum. 

Symptoms. — Appendicitis  in  nurslings  is  of  2  types.  It  may  be  insidious 
in  onset  with  foetid  diarrhoea  or  constipation,  vomiting,  slight  fever  and 
wasting.  This  gradually  passes  on  into  a  stage  of  increased  vomiting, 
higher  temperature,  increased  pulse  rate.,  distension  and  peritonitis.     In 


342  Chapter   XXX. 

the  second  type  the  onset  is  sudden,  with  pain  and  vomiting,  high  tempera- 
ture, rapid  pulse,  severe  constipation,  a  swollen  tender  belly,  and  general 
peritonitis  in  a  few  days.  Cases  under  18  months  of  age  are  almost 
invariably  fatal. 

The  classical  signs  are  vomiting,  abdominal  pain,  fever,  increased  pulse- 
rate,  local  tenderness,  rigidity  and  constipation.  In  a  mild  catarrhal 
attack  symptoms  may  be  entirely  absent,  or  ascribed  to  another  cause. 
There  may  be  merely  a  little  fever,  nausea,  slight  colicky  and  paroxysmal 
pain,  dyspepsia  and  constipation.  In  more  severe  attacks  there  may 
be  found  local  tenderness  at  McBurney's  spot  or  Clado's  point,  rigidity  of 
the  right  rectus,  absence  of  the  abdominal  reflex  on  the  right  side,  flatulence, 
nausea,  vomiting,  tenesmus  and  diarrhoea.  McBurney's  spot  is  at  the 
junction  of  a  line  drawn  from  the  umbilicus  to  the  anterior  superior  spine 
with  the  outer  border  of  the  rectus.  Clado's  point  is  at  the  junction  of 
a  line  joining  the  two  anterior  superior  spines,  and  the  outer  border  of  the 
rectus. 

Pain  is  generally  the  first  symptom.  It  varies  greatly  in  severity. 
It  may  be  severe  and  localised  in  the  right  iliac  region.  Sometimes  it  is 
referred  to  the  right  hypochondrium  or  diaphragm,  but  more  usually  to  the 
umbilicus  or  epigastrium,  and  later  to  the  right  iliac  region  and  the  whole 
of  the  abdomen.  There  may  be  merely  a  sense  of  pressure  in  the  region 
of  the  appendix.  Tenderness  is  always  present,  and  varies  with  the  severity 
of  the  disease  ;  it  is  not  always  localised  at  the  same  spot.  Sherren  states 
that  it  is  over  the  skin  supplied  by  the  eleventh  dorsal  nerve,  unless  the 
appendix  is  perforated.  Bigidity  is  limited  to  the  lower  quadrant  of  the 
abdomen  in  simple  cases. 

Vomiting  usually  subsides  in  a  few  hours,  except  in  fulminating  cases. 
Diarrhoea  is  more  frequent  in  children  than  constipation.  Bladder 
troubles  are  common  ;  micturition  is  often  painful  and  frequent ;  reten- 
tion, pain  over  the  bladder  at  the  end  of  micturition  and  vesical  tenesmus 
also  occur,  especially  if  the  appendix  is  in  the  pelvis. 

The  temperature  is  raised,  except  in  appendicular  colic  and  bad 
fulminating  cases.  A  high  temperature  indicates  gravity,  but  a  low  one  is 
no  sign  of  safety.  The  amount  of  fever  often  varies  inversely  as  the  shock 
and  severity  of  infection.  The  temperature  may  rise  because  the  shock  of 
perforation  has  passed  off. 

The  blood  is  of  no  diagnostic  importance  in  catarrhal  cases.  When 
suppuration  occurs  there  is  a  reduction  in  haemoglobin,  of  about  30  per 
cent.,  and  a  leucocytosis  of  polymorphs.  Leucocytosis  is  also  found  in 
gangrene,  perforation  and  peritonitis.  In  perforation  there  may  be  a 
sudden  rise  in  the  number  of  leucocytes.  If  the  patient  is  very  weak,  there 
may  be  a  fall.  Leucopenia  is  present  in  grave  sepsis,  and  is  a  bad  sign  if  the 
symptoms  are  severe. 


Appendicitis.  343 

The  local  signs  are  swelling,  pain  and  rigidity  in  the  right  iliac  region, 
and  a  palpable  tumour  or  diffused  sense  of  resistance.  Sometimes  the 
appendix  can  be  felt  as  a  tender,  cord-like  swelling.  A  bimanual  examina- 
tion must  be  made.  Rectal  examination  affords  indications  of  pelvic 
peritonitis  or  suppuration,  and  of  local  tenderness  when  the  appendix  is 
in  the  pelvis.  The  tender,  swollen  appendix  can  occasionally  be 
distinctly  felt. 

If  there  is  local  peritonitis,  the  pain  and  tenderness  in  the  right  iliac 
fossa  are  more  severe  and  accompanied  by  greater  rigidity  and  a  more  diffuse 
swelling,  due  to  inflammatory  matting  of  the  parts.  If  it  remains  plastic, 
the  temperature  ranges  between  100°  and  103°  F.  for  about  a  week,  and 
then  gradually  falls  after  a  somewhat  irregular  course.  The  swelling 
becomes  more  and  more  defined,  forms  a  definite  localised  tumour,  and 
disappears  slowly.  The  other  symptoms  are  general  malaise,  anorexia, 
diarrhoea  or  constipation,  and  perhaps  vomiting. 

Unfortunately  mild  cases  of  this  type  are  uncommon,  and  the  more 
serious  ones  end  in  suppuration  and  abscess.  Pus  is  usually  found  at  the 
end  of  4  days  of  acute  symptoms,  or  if  the  temperature  still  remains  up. 
There  may  be  distinct  improvement  after  a  few  days,  localisation  of 
suppuration  and  slow  development  of  the  abscess.  The  temperature  may 
fall,  and  then  rise  and  become  irregular.  In  many  cases  the  temperature 
falls,  pain  lessens,  the  abdominal  swelling  becomes  more  defined  because 
the  abscess  has  burst  into  the  bowel,  and  usually  a  loose  offensive  stool  is 
passed.  The  local  signs  of  abscess  are  more  diffused  pain,  tenderness, 
rigidity  and  swelling  ;  redness  and  oedema  of  the  skin  and  fluctuation,  if 
the  abscess  bulges  anteriorly.  Occasionally  it  develops  slowly  with  few 
symptoms.    The  thigh  is  often  flexed  to  relieve  tension. 

Many  cases  end  in  septic  peritonitis.  In  most  of  these,  previous  mild 
attacks  of  catarrh  have  occurred  and  one  or  more  concretions  formed. 
Gradually  the  concretion  ulcerates  through  and  a  small  pocket  of  pus  is 
shut  off  at  the  tip  of  the  appendix,  or  it  may  rupture  into  the  general 
peritoneal  cavity.  Frequently  from  some  slight  cause,  such  as  strain  or 
injury,  the  ulcerated  patch  already  verging  on  perforation  has  given  way 
and  set  up  acute  perforative  peritonitis.  Unless  this  is  quickly  limited  by 
adhesions,  or  if  the  escaping  matter  is  virulent,  infective  peritonitis  rapidly 
ensues.  Thus,  a  boy,  aged  7,  played  football  in  the  afternoon,  went  home 
on  the  top  of  a  tramcar,  and  eat  a  large  tea  of  buns  and  bloater  paste. 
No  less  than  three  exciting  causes,  strain,  cold  and  unsuitable  food,  were* 
present.  In  the  evening  he  was  seized  with  abdominal  pain  and  vomiting. 
He  was  treated  for  digestive  disturbance,  but  remained  unwell,  con- 
stipated and  feverish.  On  the  fourth  day  a  lump  in  the  right  iliac  fossa  was 
ascribed  to  fsecal  accumulation.  The  bowels  acted  well  after  an  enema  ; 
a  dose  of  castor  oil  produced  three  good  actions  next  day,  and  the  lump 
disappeared.      On  the  evening  of  the  seventh  day  he  became  collapsed, 


344  Chapter  XXX. 

vomited  and  had  abdominal  pain.  When  seen  next  morning,  he  was 
collapsed  and  moribund,  the  abdomen  was  a  little  tense,  and  there  was 
general  tenderness  ;  death  took  place  an  hour  later.  In  a  similar  case,  on 
account  of  the  absence  of  localising  signs  and  very  slight  indications  of 
peritonitis,  operation  had  been  postponed.  It  was  decided,  however, 
to  explore,  and  a  typical  condition  of  acute  septic  peritonitis,  secondary  to 
perforation  by  concretion,  was  found. 

Perforative  Peritonitis  is  characterised  by  sudden  severe  pain  in 
the  right  iliac  fossa,  acute,  lancinating  and  continuous ;  vomiting  of  the 
contents  of  the  stomach  and  then  bile  ;  sometimes  chilliness  or  rigor  ; 
prostration  and  general  appearance  of  serious  illness.  The  vomiting  may 
be  persistent,  and  become  greenish  and  feeculent.  Occasionally  the  perfora- 
tion comes  on  insidiously.  Local  signs  may  be  absent.  The  signs  of  peri- 
tonitis develop  usually  in  3  or  4  days.  The  acute  symptoms  due  to  perfora- 
tion may  have  subsided  and  apparent  improvement  set  in.  The  abdominal 
signs  may  be  slight  or  absent,  or  those  found  in  acute  peritonitis.  Perfora- 
tion can  take  place  suddenly  and  quite  independently  of  apparent 
illness. 

Fulminating  Peritonitis  is  due  to  acute  gangrene  from  virulent  infec- 
tion and  possibly  thrombosis.  The  symptoms  are  intense — more  severe 
pain,  general  tenderness,  early  tympanites,  sometimes  an  initial  rigor. 
The  pulse  is  small  and  frequent,  temperature  subnormal,  and  the  facies 
of  the  abdominal  type.  Pain  may  cease  early  in  the  worst  cases.  Often 
there  are  no  local  signs,  neither  tenderness  nor  swelling.  I  have  seen  all 
these  symptoms  in  one  case  of  acute  tuberculous  peritonitis. 

Diagnosis. — In  infants  under  2  years  diagnosis  is  very  difficult, 
because  of  the  inability  to  answer  questions  and  locate  pain,  and  resistance 
to  palpation.  If  constipation  is  a  prominent  sign,  it  may  suggest  intestinal 
obstruction  or  simulate  intussusception,  but  the  temperature  is  usually 
high  and  there  is  no  bloody  rectal  discharge.  Mild  attacks  at  all  ages  may 
be  diagnosed  as  appendicular  colic.  Such  cases  are  due  to  slight  catarrh,  or 
irritation  of  the  peritoneum  by  a  fish  bone  or  a  pin  sticking  through  the 
appendix.  Attacks  are  liable  to  be  confounded  with  gastro-enteric  dis- 
turbance and  colic  from  any  cause  ;  all  kinds  of  intestinal  obstruction  ; 
acute  indigestion  with  fever  ;  local  causes  of  suppuration  in  the  right  iliac 
fossa,  e.g.,  psoas  abscess  ;  tuberculous  peritonitis  ;  perforative  peritonitis 
from  other  causes  ;  fsecal  accumulation,  and  typhoid  fever  (no  leucocy- 
tosis).  Stomach-ache  is  common  in  children  who  eat  many  odd  articles  of 
diet.  It  is  usually  acute  and  soon  passes  off,  perhaps  with  vomiting  or 
diarrhoea  and  no  rise  of  temperature.  The  pain  of  rheumatism  in  one  hip, 
or  hip  disease  and  flexion  of  the  thigh  may  suggest  appendicitis  ;  so, 
too,  those  cases  of  pleurisy  and  pneumonia  in  which  the  pain  is  referred  to 
the  iliac  region,  but  in  these  breathing  is  rapid  and  the  face  flushed  or 
livid. 


Appendicitis.  345 

The  main  symptoms  on  which  stress  must  be  laid  are  the  history  of 
previous  attacks  and  the  onset,  with  vomiting,  abdominal  pain,  fitful 
crying,  disturbed  sleep,  local  tenderness  and  rigidity,  anxious  face,  rising 
pulse-rate  and  temperature,  and  discomfort  on  extending  the  lower  limbs. 
Pain  is  more  often  absent  in  children  than  in  adults.  Decrease  of  pain  can 
be  deceptive  ;  it  may  indicate  improvement  or  toxaemia.  Rectal  examina- 
tion can  prove  negative,  and  yet  three  days  later  a  large  abscess  may  be 
found.  It  must  never  be  omitted,  except  at  the  onset  of  a  mild  attack. 
Peritonitis  due  to  perforation  is  distinguished  from  other  varieties  by  the 
history  and  severity.  It  is  most  likely  to  be  mistaken  for  the  pneumococcal 
or  gonococcal  form,  both  more  common  in  girls  than  in  boys. 

Prognosis. — Mild  cases  frequently  terminate  in  resolution  within  a 
few  days.  How  often  this  occurs  it  is  impossible  to  tell,  for  the  bulk  of 
mild  cases  must  be  overlooked,  if  we  believe  that  concretion  is  proof  of 
a  former  attack.  Of  the  cases  that  are  recognised  and  come  under  proper 
treatment,  a  certain  number  end  in  resolution,  but  the  majority  terminate 
in  abscess,  concretion,  and  local  or  general  peritonitis.  The  prognosis  is 
very  bad  in  infancy.  Eecovery  under  18  months  of  age  is  rare.  The 
disease  is  more  dangerous  in  infants  than  children,  because  of  the  greater 
difficulty  in  diagnosis  and  the  greater  liability  to  generalised  infection  in 
early  life.  Attacks  are  often  put  down  to  colic.  Suppuration  readily 
occurs.  In  even  the  mildest  cases  the  prognosis  must  be  guarded,  for  the 
clinical  condition  constantly  does  not  correspond  with  the  severity  of  the 
lesion,  and  acute  peritonitis  may  supervene  at  any  time.  The  possibility 
of  recovery  with  a  residual  concretion  necessitates  a  warning  as  to  subse- 
quent attacks.  Yet  recurrence  is  not  common.  A  mild  attack  lasts  for 
1-3  weeks,  and  a  bad  one  may  be  prolonged  for  as  many  months.  Improve- 
ment is  indicated  by  cessation  of  vomiting  and  diminution  of  constipation 
if  present.  A  rise  in  temperature,  pulse  rate  and  number  of  leucocytes 
is  a  sign  of  a  relapse  or  extension.  Neither  pulse  nor  temperature  can  be 
relied  on.  Even  in  very  severe  cases  there  may  be  little  change  in  either. 
Coffee-ground  vomiting  is  ominous  of  paralytic  ileus.  The  most  acute 
cases  may  die  in  36-48  hours  ;  usually  in  about  a  week.  Those  in  which 
an  abscess  forms  do  very  well  under  operative  treatment  and  badly  without. 
A  favourable  result  may  follow  rupture  through  the  abdominal  wall,  rectum, 
or  vagina.  More  often,  if  left  alone,  death  results  from  some  complication. 
Quite  80  per  cent,  die  from  peritonitis,  and  the  remainder  from  asthenia, 
pyaemia,  or  lardaceous  disease  secondary  to  a  permanent  fistula.  In  the 
fulminating  cases  death  is  due  to  toxaemia.  It  has  also  followed  operation, 
from  acute  acidosis.  Temporary  improvement  may  result  from  perforation 
and  relief  of  tension,  or  the  cessation  of  toxic  absorption,  due  to  thrombosis 
■or  gangrene. 

Treatment. — The  child  must  be  kept  in  bed,  in  a  recumbent  position 
with  the  knees  over  a  pillow,  given  a  liquid  diet,  and  carefully  watched. 


346  Chapter   XXX. 

In  very  acute  cases  starvation  and  saline  enemata,  to  relieve  thirst,  are 
useful.  An  ice-bag,  hot  fomentation,  or  belladonna  and  glycerine  is 
applied  locally.  Children  usually  prefer  heat  to  cold.  Opiates,  bleeding, 
leeches  and  blisters  must  be  avoided  ;  so,  too,  purgatives,  because  of  the 
consequent  peristalsis ;  an  enema  of  ordinary  soap  and  water  must  be 
given.  In  the  earliest  stage  of  a  catarrhal  attack  a  dose  of  calomel, 
followed  by  a  saline  aperient  and  an  enema,  is  very  beneficial.  Unfor- 
tunately it  is  often  impossible  to  distinguish  a  mild  attack  from  the 
beginning  of  perforation,  in  which  treatment  by  purgatives  is  dangerous. 
It  is  much  safer  to  avoid  purgatives  and  to  rely  on  enemata.  Expectant 
treatment  is  only  safe  in  mild,  acute  cases  kept  under  skilled  observation. 
As  soon  as  the  diagnosis  and  the  type  of  the  disease  are  established,  small 
doses  of  opium  may  be  given  to  relieve  pain  and  to  keep  the  intestines  at 
rest.  It  is  liable  to  paralyse  the  intestines  and  cause  tympanites,  and 
is  better  avoided.  If  used  early  it  is  apt  to  obscure  symptoms  and  lead 
to  apparent  improvement,  although  the  patient  is  getting  worse.  Hence, 
operation  may  be  fatally  postponed  and  an  unduly  favourable  prognosis- 
given. 

The  question  of  operation  depends  upon  the  circumstances  of  each 
case.  If  all  patients  are  operated  on,  many  cases  which  would  recover 
by  resolution  are  submitted  to  an  unnecessary  and  expensive  ordeal. 
Operation  is  quite  as  dangerous  in  a  mild  attack  as  in  a  severe  one,  and 
many  recover  in  a  few  days  without.  On  the  other  hand,  delay  leaves  the 
patient  to  chance ;  and  there  is  little  prospect  of  localisation  in  childhood. 

In  addition  there  is  a  liability  to  erroneous  diagnosis  in  the  first 
48  hours.  Some  lives  are  sacrificed  to  too  early  and  others  to  too  late 
interference.  If  signs  of  peritoneal  irritation  are  present,  operation  is 
advisable.  In  fulminating  cases  there  is  a  fair  hope  of  recovery  if  operation 
is  done  within  12  hours,  in  a  period  of  quiet  sometimes  present  after  the 
shock  has  passed  off.  In  all  but  the  mildest  cases  it  is  advisable  to  operate 
within  48  hours.  After  that  time  be  guided  by  circumstances.  In  a  case 
of  moderate  severity,  if  the  pulse  rate  is  increasing,  the  temperature  rising, 
and  the  local  and  general  symptoms  getting  worse,  operate  ;  for  there  is 
almost  certainly  suppuration,  and  possibly  perforation.  It  is  still  more 
imperative  if  the  temperature  is  falling  and  the  pulse-rate  rising.  The 
facial  expression  often  indicates  continued  mischief,  and  actual  gangrene 
may  have  begun.  If  on  the  other  hand  the  temperature  is  falling,  the 
pulse-rate  less  frequent,  and  the  local  and  constitutional  symptoms  less 
severe,  operation  may  be  postponed,  provided  a  careful  watch  is  kept  on 
the  case.  Immediate  operation  is  necessary  in  cases  of  perforation  and  of 
abscess.  Increasing  leucocytosis  is  of  some  value  as  a  sign.  In  recurrent 
cases  remove  the  appendix  during  a  period  of  quiescence.  Advise  operation 
if  the  symptoms  do  not  entirely  disappear  after  an  acute  attack.  When 
operating,  seek  for  faacal  fistulse,  for  in  many  quiescent  cases  the  abscess  has 


Appendicitis.  347 

discharged  into  the  small  intestine,  and  one  or  more  fistula?  may  be  left. 
If  these  are  not  properly  closed,  fatal  peritonitis  will  follow  operation. 
The  presence  of  a  distinct  lump  after  an  attack,  although  the  child  seems  well, 
necessitates  operation.  In  a  girl,  aged  4  years,  a  lump  of  this  nature  was 
found  to  be  a  concretion  on  the  verge  of  perforation.  At  and  after  opera- 
tion the  patient  should  be  kept  in  the  Fowler  position,  the  head  and 
shoulders  raised  so  that  the  pus  gravitates  downward,  instead  of  upward 
into  the  dangerous  subphrenic  area.  In  opening  an  abscess,  it  is  advisable 
merely  to  incise  and  drain,  leaving  the  appendix,  for  it  is  shut  off  by 
adhesions.  Flushing  the  abdomen  is  apt  to  be  injurious  in  septic  peritonitis  ; 
it  takes  time  and  spreads  infection.  Give  saline  injections  freely  in  all 
trirulent  and  toxsemic  cases,  to  counteract  shock,  raise  blood  pressure, 
and  eliminate  toxins. 


CHAPTER    XXXI. 

THE    PERITONEUM. 

Ascites — Acute  Peritonitis — Chronic  and  Tuberculous  Peritonitis — Mesen- 
teric Cysts — Pancreatic  Cysts — Neiv  Growths. 

Ascites. — The  area  of  peritoneum  is  about  equal  to  that  of  the  skin 
and  affords  a  large  surface  through  which  absorption  and  effusion  are 
constantly  going  on.  An  excess  of  fluid  in  the  peritoneal  cavity  is  due 
to  inflammation  or  transudation.  Ascites  is  caused  by  transudation  by 
virtue  of  increased  pressure,  altered  conditions  of  the  blood  and  lymph, 
and  nutritional  changes  in  the  epithelium.  The  last  factor  is  most  impor- 
tant, for  probably  no  excessive  effusion  can  take  place  without  impaired 
nutrition.  The  amount  of  osmosis  varies  with  the  specific  gravity  of  the 
fluids.  Absorption  takes  place  through  the  lymphatics  and  blood  vessels  ; 
probably  to  a  great  extent  by  means  of  those  lymphatics  of  the  diaphragm 
which  run  to  the  anterior  mediastinal  glands.  Simple  ascites  is  due  to 
backward  pressure  from  obstructive  heart  or  pulmonary  disease,  pressure 
on  the  vena  cava  inferior,  mediastino-pericarditis,  hepatic  cirrhosis,  throm- 
bosis of  the  portal  vein,  or  occlusion  of  the  vein  by  pressure  of  glands  or 
adhesions  ;  blood  states  leading  to  malnutrition,  such  as  leukemic  affec- 
tions and  renal  disease  ;   and  tumours. 

Hemorrhagic  ascites  is  rare  and  usually  due  to  malignant  tumours, 
tuberculous  disease  or  septic  thrombosis.  In  chylous  ascites  the  fluid 
contains  fat.  It  may  be  due  to  injury  of  the  thoracic  duct,  occasionally 
to  tuberculous  peritonitis.    It  is  very  rare  and  of  bad  prognosis. 

Acute  Peritonitis  is  quite  an  uncommon  affection  after  the  first  few 
weeks  of  life.  In  the  foetus  it  is  due  to  syphilis  or  is  of  unknown  causation, 
rarely  appendicitis  or  placental  infection,  and  leads  to  death  in  utero  or 
intestinal  malformation.  In  the  newborn  it  is  septic  and  results  from 
pyogenic  infection,  usually  through  the  navel.  In  infants  it  is  often  part 
of  a  polyserositis  of  streptococcal  or  pneumococcal  origin,  or  secondary 
to  ileo-colitis,  vulvo-vaginitis,  etc.  At  any  time  after  birth  the  main 
causes  are  microbial  infection,  and  perforation  of  some  viscus  or  direct 
extension.  Exposure  to  cold  and  wet  predispose.  Rheumatic  peritonitis 
is  of  doubtful  existence  ;  such  cases  are  probably  pneumococcal.  Trau- 
matism, accidental  or  surgical,  accounts  for  a  few  cases.  The  chief  secondary 
causes  are  appendicitis  and  typhoid  ulceration,  with  or  without  perforation  ; 


The  Peritoneum.  349 

perforation  of  gastric,  duodenal  or  intestinal  ulcers  ;  various  forms  of 
intestinal  obstruction  ;  abscess  in  a  lymph  gland,  the  liver,  kidney,  pleural 
cavity  or  in  Pott's  disease.  The  gonorrhceal  form  is  secondary,  and  the 
pneumococcal  form  generally  so.  Common  organisms  are  streptococci, 
pneumococci  and  the  bacillus  coli ;  less  often,  staphylococcus  aureus  and 
albus,  gonococcus,  micrococcus  lanceolatus,  B.  proteus,  B.  pyocyaneus, 
B.  typhosus  and  others.    Many  cases  are  mixed  infections. 

Morbid  Anatomy. — At  first  there  is  loss  of  lustre,  and  then  the 
peritoneum  becomes  red  and  injected,  serum  and  lymph  are  effused,  and 
adhesions  form.  Sometimes  the  great  omentum  is  the  part  first  or  mainly 
affected.  In  the  plastic  or  fibrinous  form  there  is  little  effusion  of  fluid. 
In  the  serous  type  there  is  little  lymph  and  much  fluid,  which  may  be  clear, 
turbid  or  blood-stained.  To  a  certain  extent  the  exudation  of  lymph  is 
protective,  for  it  limits  the  absorption  of  toxic  products  by  the  peritoneum. 
In  the  sero-purulent  or  purulent  variety  there  are  much  pus  and  lymph, 
especially  if  it  is  due  to  perforation.  The  pus  may  become  localised  in  the 
iliac  fossa,  pelvis,  centre  of  the  abdomen  or  under  the  diaphragm.  Such 
an  abscess  may  burst  externally,  frequently  at  the  umbilicus  ;  may  burrow 
its  way  into  a  viscus,  such  as  the  liver  ;  or  may  open  into  the  bladder, 
rectum,  vagina,  or  even  the  pelvis  of  the  kidney.  In  streptococcal  peritonitis 
the  fluid  is  thin  and  yellowish,  and  does  not  tend  to  localisation.  The  local 
affection  is  a  part  of  a  general  streptococcal  pygemia. 

Symptoms. — In  infants  the  cause  of  illness  may  be  overlooked,  for 
the  symptoms  are  often  obscure.  In  the  newborn  there  may  be  no  vomiting 
and  little  or  no  fever,  merely  some  refusal  of  food  for  fear  of  sickness. 
Usually  an  attack  commences  suddenly  with  vomiting  and  high  fever, 
round  about  104°  F.  The  abdominal  pain  is  indicated  by  fretfulness, 
restlessness,  sudden  waking,  drawing  the  hand  across  the  abdomen, 
screaming,  and  perhaps  flexion  of  the  knees.  The  pain  is  paroxysmal 
or  continuous,  with  exacerbations.  Older  children  complain  of  pain  when 
it  is  present.  It  is  by  no  means  uncommon  for  most  virulent  attacks  to 
be  quite  unassociated  with  pain  or  with  only  a  little  abdominal  discomfort. 
The  amount  of  tenderness  is  very  variable  and  that  of  muscular  rigidity, 
whether  local  or  widespread,  difficult  to  estimate.  At  first  the  abdomen 
is  retracted,  empty,  and  more  or  less  rigid  and  immobile.  Later  it  becomes 
distended,  uniformly  so  as  a  rule,  and  very  tympanitic.  There  is  not  often 
much  fluid,  merely  sufficient  to  cause  dulness  in  the  flanks.  Occasionally  a 
friction  rub  can  be  heard.  Rigidity  and  tenderness  vary  much,  and  may 
be  absent  in  late  stages.  The  child  assumes  the  dorsal  decubitus  with  the 
knees  drawn  up.  Diarrhoea  is  generally  present  in  streptococcal  and  pneu- 
mococcal infections,  and  is  always  more  common  than  in  adults.  Reten- 
tion or  incontinence  of  urine  and  dysuria  are  frequent. 

Vomiting  usually  stops,  but  may  continue  throughout  and  become 
fseculent  towards  the  end.    The  features  are  pinched,  haggard  and  anxious. 


350  Chapter   XXXI. 

The  characteristic  Abdominal  Fades  is  sometimes  absent  even  a  few  hours 
before  death.  Kespiration  is  thoracic,  shallow,  and  increases  in  frequency 
with  the  distension.  The  pulse  rate  is  more  important  than  the  tem- 
perature ;  the  pulse  is  frequent,  small,  soft  and  running.  Leucocytosis 
rapidly  develops  in  perforation  cases.  In  these  the  temperature  is  low  at 
first,  and  rises  after  the  period  of  reaction.  Prostration  becomes  more  and 
more  profound,  the  extremities  cold,  and  hiccough,  collapse  and  exhaustion 
end  the  scene. 

Pneumococcal  Peritonitis  is  more  frequent  in  children  than  in  adults, 
and  in  girls  than  in  boys,  in  the  proportion  of  3-1.  Annand  and  Bowen 
(1906)  collected  91  cases,  including  16  of  their  own,  in  children  under 
15  years  of  age.  They  regarded  47  as  primary  and  44  secondary.  Several 
cases  have  been  recorded  since.  In  the  primary  cases  infection  is  pro- 
bably carried  by  the  blood  stream.  Of  the  secondary  cases  three-fourths 
are  due  to  lung  mischief,  and  the  remainder  to  otitis  media,  sore  throat, 
umbilical  infection,  and  possibly  a  pneumococcal  appendicitis  or  enteritis, 
or  infection  via  the  genitals. 

The  peritoneal  symptoms  may  be  relatively  slight  or  severe.  The 
exudation  is  profuse,  rich  in  fibrin,  very  coagulable,  greenish  yellow,  and 
not  offensive.  Fibrinous  layers  of  lymph  and  jelly-like  masses  of  pus  are 
often  present.  Adhesions  and  early  localisation,  generally  in  the  lower  part 
of  the  abdomen,  are  common,  but  the  inflammation  may  be  diffuse.  Rarely 
the  exudation  is  haemorrhagic.  It  may  be  offensive  from  post  mortem 
decomposition.  The  lung  affection,  if  present,  may  occur  before  or  after, 
or  be  coincident  with  the  peritonitis. 

The  symptoms  are  those  of  an  acute  peritonitis,  usually  less  severe 
and  more  often  associated  with  diarrhoea.  Its  onset  is  generally  sudden, 
with  vomiting  and  diarrhoea,  colicky  pains,  especially  in  the  lower  part  of 
the  abdomen,  and  high  fever.  In  a  few  days  the  symptoms  become  less 
severe,  but  diarrhoea  persists,  meteorism  develops,  and  pus  collects. 
Pain  may  be  great  and  generalised,  and  the  temperature  hectic.  The 
abdominal  distension  is  sometimes  a  prominent  feature.  Two  varieties 
can  be  distinguished.  There  is  a  diffuse,  violent,  persistent  type  with 
prostration,  cyanosis,  rapid  pulse,  abdominal  facies,  and  rapidly  fatal 
end.  The  other  is  acute  in  onset,  but  becomes  chronic  or  circumscribed,  and 
the  pus  is  encapsuled,  forming  an  Abdominal  Empyema.  The  abscess  is 
usually  sub-umbilical,  median  or  lateral,  and  perforates  the  umbilicus  in 
about  4-6  weeks,  if  untreated.  It  may  discharge  through  the  vagina 
or  bladder.  It  may  fill  the  whole  abdomen.  These  cases  in  their  general 
appearance  simulate  chronic  tuberculous  peritonitis,  and  the  local  abscess 
had  generally  been  regarded  in  the  past  as  a  tuberculous  abscess. 

Gonococcal  Peritonitis  has  been  recorded  as  early  as  5  months  of  age. 
It  is  due  to  infection  spreading  along  the  vagina,  uterus  and  tubes.  It  is 
often  localised,  causing  salpingitis,  which  may  be  felt  per  rectum.     The 


The  Peritoneum.  351 

gonorrhoea  may  be  acute  or  chronic,  and  is  seldom  of  a  severe  type.  The 
onset  is  usually  acute  with  frequent  vomiting,  frequent  micturition,  alter- 
nate diarrhoea  and  constipation,  and  a  temperature  up  to  104°  F.  The  pulse 
is  frequent,  small  and  weak  ;  the  extremities  cold  and  cyanosed  ;  and 
the  abdomen  tender  and  tympanitic.  The  child  lies  with  the  legs  crossed  or 
drawn  up,  screams  with  pain,  is  somewhat  delirious,  and  is  soon  very 
gravely  ill.  An  attack  lasts  from  1-8  days,  and  the  acute  symptoms  may 
subside  rapidly  for  the  vitality  of  the  gonococcus  is  small  in  cellular  tissues. 
A  gonococcal  peritonitis  is  usually  localised,  and  a  rapidly  fatal  generalised 
variety  is  due  to  a  mixed  infection.  The  diagnosis  is  difficult  because  it  is 
unsuspected.  A  simultaneous  occurrence  of  peritonitis  in  sisters  is  very 
suggestive.  It  is  liable  to  be  mistaken  for  appendicitis.  The  prognosis 
is  good  and  relapse  is  exceptional.  Laparotomy  is  said  to  seriously 
aggravate  the  condition. 

Diagnosis. — Peritonitis  at  the  onset  must  be  distinguished  from 
colic.  Later  on  it  may  simulate  cholera,  dysentery,  and  acute  colitis  or 
entero-colitis.  Pneumonia  and  pleurisy  have  been  erroneously  diagnosed 
as  peritonitis  or  appendicitis,  and  the  abdomen  opened.  Such  a  mistake 
ought  not  to  arise,  for  the  breathing  is  rapid  and  out  of  proportion  to  the 
pulse-rate  and  temperature,  the  temperature  is  generally  higher,  cough 
sometimes  present,  and  the  rigidity  of  the  abdominal  muscles  usually 
relaxes  during  inspiration  and  on  steady  pressure.  Henoch's  purpura, 
acute  intestinal  obstruction,  appendicitis,  and  perforation  of  an  abdominal 
viscus  may  be  mistaken  for  peritonitis,  of  which  they  are  often  the  cause. 
Differential  diagnosis  of  the  different  types  is  fairly  easy.  In  the  newborn 
the  disease  is  almost  always  streptococcal.  The  gonococcal  variety  occurs  in 
girls,  usually  over  4  years  of  age,  vulvo-vaginitis  is  almost  invariably  present, 
and  the  pain  at  first  is  often  localised  in  the  lower  part  of  the  abdomen. 
The  presence  of  pulmonary  disease,  herpes  labialis,  and  green  loose 
inoffensive  stools  indicate  the  pneumococcal  type.  A  primary  pneumococcal 
affection  is  not  improbable  in  all  those  cases  of  acute  onset,  without  a  his- 
tory indicative  of  appendicitis  or  a  perforative  lesion.  I  have  known 
tuberculous  peritonitis  so  acute  in  its  onset  as  to  suggest  perforation  and 
secondary  peritonitis.  A  boy,  12  years  old,  was  seized  with  vomiting 
and  abdominal  pain,  and  on  the  third  day  was  almost  moribund  from 
collapse  and  toxsemia.  On  laparotomy  the  intestines  were  found  covered 
with  tubercles  and  much  fluid  was  let  out,  and  the  patient  recovered. 
Some  of  the  acute  cases  of  the  pneumococcal  type  may  be  mistaken  for 
typhoid  fever,  if  a  leucocyte  count  is  not  made.  Eectal  examination  is 
often  of  assistance. 

The  Prognosis  is  very  bad  because  of  the  large  area  for  the  absorption 
•of  toxins.  In  localised  cases  the  inflammation  is  protective.  The  pyogenic 
form  in  infants  ends  fatally  in  2  or  3  days,  but  older  children  live  for  about 
a  week.     After  that  the  outlook  is  more  hopeful,  for  the  mischief  may 


352  Chapter  XXXI. 

become  localised.  The  diffuse  pneumococcal  type  is  generally  fatal,  and 
the  circumscribed  ends  in  recovery.  Sero-fibrinous  effusions  are  the  least 
dangerous,  and  purulent  ones  the  most  fatal,  for  they  are  often  due  to 
perforation,  especially  of  an  appendix,  and  terminate  in  6  or  7  days.  The 
temporary  improvement  after  perforation  must  not  be  regarded  favourably, 
as  it  is  only  the  result  of  reaction,  and  the  onset  of  peritonitis  is  indicated 
by  increased  frequency  of  the  pulse  and  abdominal  distension,  and 
progressive  illness. 

The  Treatment  varies  with  the  nature  of  the  case.  In  acute  general 
peritonitis,  not  due  to  perforation,  cold  or  heat  may  be  applied  locally,  e.g., 
spongiopiline  wrung  out  in  hot  or  cold  water,  an  ice-bag,  bran  poultice, 
or  turpentine  stupes.  Give  a  saline  purge,  if  there  is  constipation  and  no 
appendicitis.  Use  the  common  remedies  for  vomiting  (p.  252).  Give 
opium  gr.  -^  -  T^,  every  2  or  3  hours,  to  control  the  pain  and  peristalsis. 
It  may  keep  up  the  vomiting  and  its  effects  in  minimising  symptoms  must 
be  remembered.  Feed  the  child  carefully  with  peptonised  milk,  whey, 
white  of  egg,  and  other  easily  digestible  foods.  In  severe  vomiting  it  may 
be  necessary  to  omit  food  for  a  time.  Give  a  liberal  supply  of  fluid  by  various 
channels,  and  brandy  and  champagne  as  stimulants.  Laparotomy  is 
necessary  in  pneumococcal  cases  when  pus  has  formed,  in  those  due  to 
perforation,  and  in  most  septic  ones.  The  removal  of  fluid  leads  to  the 
effusion  of  fresh  serum  with  greater  germicidal  power  than  in  that  removed . 
If  on  laparotomy  there  is  a  general  diffused  peritonitis  and  much  purulent 
fluid,  seek  and  remove  the  cause  if  possible  and  drain.  Do  not  mop, 
wash  or  irrigate.  Keep  the  patient  in  a  sitting  posture  and  give  saline 
injections.  On  the  whole  laparotomy  must  be  recommended  with  caution, 
except  in  the  pneumococcal  cases  and  those  due  to  perforation.  An 
abscess  must  be  treated  as  a  chronic  abscess,  opened  and  drained. 

Chronic  Peritonitis  is  generally  tuberculous.  A  few  cases  are  secondary 
to  acute  attacks,  visceral  disease,  vaginal  infection,  cold  or  injury.  Possibly 
some  are  syphilitic.  In  one  case,  prolonged  and  fatal,  it  was  a  sequel  of 
acute  ptomaine  poisoning,  but  no  organisms  were  found  in  the  peritoneal 
exudation. 

Sub-diaphragmatic  or  Sub-phrenic  Abscess  is  an  accumulation  of  pus. 
under  the  diaphragm  and  above  the  liver,  or,  rarely,  the  spleen.  It  is 
due  to  pneumonia,  disease  of  the  liver,  extension  from  tuberculous  cavities, 
and  occasionally  appendix  abscess.  It  is  usually  mistaken  for  empyema, 
or  pneumothorax  if  it  contains  air.  The  physical  signs  are  those  of 
empyema,  and  it  is  treated  by  incision  and  drainage. 

Tuberculous  Peritonitis. — In  acute  miliary  tuberculosis  the  peritoneum 
may  be  studded  with  grey  tubercles,  without  the  spread  of  inflammatory 
changes  to  the  peritoneum,  and  death  occurs  before  the  onset  of  any 
definite  abdominal  symptoms.     If  the  illness  is  more  prolonged  the  tubercles 


The  Peritoneum.  353 

undergo  caseous  degeneration  and  set  up  peritonitis  and  exudation. 
In  rare  instances  acute  peritonitis  is  due  to  this  cause,  and  the  tuberculous 
affection  limited  to  the  abdominal  cavity.  More  commonly  we  have  to  deal 
with  a  chronic  form  divisible  into  the  following  groups,  viz.  : — 

(1)  Adhesive,  fibrous  or  plastic  peritonitis. 

(2)  Peritonitis  with  effusion,  of  serum  or  pus. 

(3)  Caseous  or  ulcerative  peritonitis. 

The  source  of  infection  is  doubtful.  It  may  be  conveyed  by  lymphatics 
or  blood  vessels  from  distant  parts  ;  it  may  spread  from  a  broken  down 
gland  or  from  the  Fallopian  tubes  ;  or  be  due  to  the  breaking  down  of  a 
tubercle  in  the  wall  of  a  small  artery,  and  dissemination  to  the  parts  supplied 
by  that  artery ;  or  secondary  to  tuberculous  ulceration  of  the  intestines. 
The  etiology  is  that  of  tuberculous  disease  generally.  Malnutrition, 
unsuitable  food,  and  insufficient  clothing  of  the  abdomen  render  the 
peritoneum  susceptible  to  infection. 

It  occurs  at  all  ages,  but  is  most  common  at  2-4  years.  Almost  half 
of  306  cases  under  15  years  of  age  were  between  3  and  7,  and  the  sexes 
were  about  equal  (Faludi,  1905).  In  later  life  it  is  very  much  more  frequent 
in  females  or,  perhaps,  is  more  readily  recognised  in  them  because  they 
are  more  liable  to  be  operated  on  for  abdominal  conditions. 

The  symptoms  vary  somewhat  with  the  type  of  disease,  and  include 
anorexia,  wasting,  variable  degree  of  fever,  abdominal  distension  and  ascites. 
The  superficial  veins  are  dilated.  The  distension  depends  upon  tympanites 
and  fluid,  so  the  degree  of  dulness  varies.  Fever  runs  no  definite  course  ; 
it  may  be  hectic  in  the  caseous  type.  Anemia,  sweating  and  prostration 
are  often  present.  In  the  ascitic  type  tubercles  are  present  in  all  stages, 
and  there  are  few  adhesions.  A  localised  serous  effusion  may  be  mistaken 
for  a  cyst.  Any  variety  may  be  associated  with  scattered  lumps,  due  to 
tuberculous  mesenteric  glands.  In  the  caseous  form  caseous  masses  are 
felt.  Sometimes  the  omentum  stretches  across  the  abdomen  as  a  rolled 
up,  hard,  irregular,  nodular,  caseous  band.  In  the  adhesive  variety  there 
is  little  or  no  fluid,  and  a  more  or  less  general  matting  together  of  the 
intestines.  It  is  the  commonest  type  in  children,  and  may  be  secondary  to 
the  more  acute  form  with  effusion  of  serum.  The  fluid  is  usually  clear, 
occasionally  sero-purulent  or  bloody,  less  commonly  purulent.  Effu- 
sions of  pus  are  generally  due  to  rupture  of  a  caseous  gland  or  caseous 
mass  in  the  mesentery,  or  due  to  secondary  infection.  It  may  be  localised 
as  a  chronic  abscess. 

In  the  caseous  variety  the  intestines  are  matted  together  by  ad- 
hesions, with  masses  of  caseous  material  covering  and  separating  the  coils. 
In  the  milder  degrees  there  may  be  only  one  or  more  semi-solid,  in- 
definite lumps  or  a  general  doughy  feeling  of  the  abdomen,  with  patches 
of  irregular   dulness   and   resonance.      This   form   is   differentiated   with 

2a 


354  Chapter  XXXI. 

difficulty  from  the  adhesive  type  with  local  accumulation  of  fasces  and 
localised  flatulent  distension. 

The  course  of  the  disease  is  slow  and  irregular.  The  adhesive  type  is 
tedious  and  may  last  for  12  months,  and  there  may  be  some  effusion  of 
fluid.  In  peritonitis  with  effusion  of  serum  the  acute  stage  lasts  from 
4-8  weeks,  and  sometimes  longer,  the  fluid  then  being  re-absorbed,  and  the 
case  assuming  the  characters  of  the  adhesive  variety.  In  the  caseous  type 
the  course  is  somewhat  similar,  if  there  are  only  1  or  2  localised  masses, 
but  in  the  diffused  caseous  form  the  patient  steadily  gets  worse  and  dies. 
Consequently,  the  prognosis  depends  on  many  different  factors,  such  as  the 
age  of  the  patient,  the  hygienic  and  social  surroundings,  the  pathological 
state,  the  physical  condition,  and  the  presence  of  the  various  complications 
and  sequelae  that  may  arise.  The  adhesive  type  is  rarely  fatal,  unless  it 
produces  intestinal  obstructions  by  adhesions.  Constipation  is  often 
troublesome.  Some  cases  die  from  meningitis,  tuberculosis  of  the  lung, 
or  miliary  tuberculosis.  The  prognosis  is  worst  in  the  caseous  variety. 
The  most  fatal  complications  are  intestinal  ulceration  and  general  dis- 
semination. As  long  as  the  disease  is  confined  to  the  peritoneum,  the  prog- 
nosis is  good,  except  in  the  caseous  variety.  The  gloomy  views  of  past 
physicians  and  surgeons  are  not  supported  by  recent  experience.  Probably 
quite  50  per  cent,  of  hospital  cases  recover,  and,  I  believe,  in  private 
practice  the  percentage  of  recovery  is  considerable  higher,  if  they  are 
properly  treated.     The  prognosis  is  worst  in  the  youngest  cases. 

The  signs  of  the  patient  getting  worse  are  continuous  fever,  rapid 
wasting,  diarrhoea  and  vomiting.  The  prognosis  is  unfavourable  in  the 
presence  of  lung  infection,  recurrent  exacerbations,  pleurisy,  albuminuria, 
dropsy,  localised  suppurations,  caseous  mesenteric  glands,  or  intestinal 
obstruction.  A  rare  complication  is  pigmentation  due  to  pressure  of 
glands  on  the  adrenals. 

Diagnosis. — Undoubtedly  many  mild  cases  are  undiagnosed.  It  is 
impossible  to  be  certain  that  some  of  these  are  not  due  to  simple  flatulent 
distension  from  other  causes.  Such  distension  in  apparently  healthy 
children,  especially  when  accompanied  by  vague  abdominal  pains  or  other 
symptoms  referable  to  the  intestinal  tract,  must  be  regarded  as  possibly 
tuberculous.  Cases  are  sometimes  diagnosed  as  ovarian  cvsts  or  tumours, 
hydatids,  colloid  cancer,  sarcoma  of  the  kidney,  horse-shoe  kidney,  and 
ascites  from  other  causes.  It  may  be  put  down  to  appendicitis  because 
of  a  lump  in  the  iliac  region,  or  the  lump  may  be  regarded  as  faecal.  It 
may  be  ascribed  to  typhoid  fever  because  of  fever  and  diarrhoea.  Early 
cases  are  often  mistaken  for  digestive  disturbance  because  of  the  wasting 
and  large  abdomen,  but  in  these  there  is  neither  fever  nor  ascites.  The  large 
belly  of  rickets  ought  to  give  rise  to  no  difficulty.  Abscess  and  fistula  of  the 
umbilicus  are  almost  always  tuberculous,  but  may  be  pneumococcal. 
Examine  for  tuberculosis  elsewhere,  especially  in  the  lungs  and  mediastinal 


The  Peritoneum.  355 

glands.     In  doubtful  cases  some  of  the  recent  tests  for  tuberculosis  must 
be  tried. 

The  treatment  is  general  and  local,  symptomatic  and  objective.  The 
child  must  be  kept  in  bed  until  all  definite  signs  of  acute  inflammation  have 
subsided.  At  this  stage  the  treatment  is  that  of  acute  peritonitis.  In  very- 
prolonged  cases  going  on  well,  except  for  slight  fever,  the  child  may  be 
moved  out,  while  in  bed  or  on  a  couch,  into  the  open  air.  Open  air  treatment 
is  of  the  greatest  value,  but  in  the  acute  stages  better  results  are  obtained 
from  careful  supervision  and  nursing,  even  in  large  towns,  than  from  sea 
air  or  other  surroundings  which  are  sometimes  supposed  to  render  skilled 
medical  attention  and  nursing  superfluous.  Local  rest  is  obtained  by 
bandaging  the  abdomen  and  careful  diet.  The  more  acute  the  case  the 
more  liquid  must  be  the  diet.  It  may  have  to  be  limited  to  peptonised 
milk  and  meat  juice.  As  improvement  takes  place  the  diet  is  increased  by 
the  addition  of  soups  and  broth,  milk-tea,  Benger's  food,  cocoa  and  gruels 
made  with  milk  and  water,  eggs  beaten  up  with  milk  and  water,  pounded 
up  fish,  meat,  mashed  potatoes  and  cream,  lightly  boiled  eggs  and  bread 
and  butter.  Brandy  is  given  in  acute  stages,  and  port  wine,  Burgundy,  ale 
or  stout  during  convalescence.  Careful  dieting  generally  stops  the  vomiting, 
but,  if  not,  give  bismuth,  small  doses  of  cocaine  or  laudanum.  Constipation 
is  best  treated  by  diet,  cod-liver  oil  and  malt,  and  castor  oil,  small  doses  of 
calomel  or  glycerine  enemata.  Diarrhoea  is  generally  stopped  by  careful 
■diet,  unless  there  is  intestinal  ulceration.  If  troublesome,  it  must  be 
treated  with  large  doses  of  bismuth  and  small  doses  of  opium.  Ulceration 
may  be  present  without  diarrhoea.  Creosote,  guiacol  and  styracol  are 
useful  for  tympanites  and  diarrhoea.  I  generally  prefer  to  give  internally  a 
mixture  of  cod-liver  oil,  maltine,  and  phosphates  of  iron  or  hypophosphites  ; 
together  with  iodoform  gr.  i-2,  or  creosote  m.  ^-2,  in  pill  form  3  times  a  day. 
Locally,  the  abdomen  is  painted  with  a  mixture  of  belladonna  ointment, 
blue  ointment  and  olive  oil  (p. a.),  night  and  morning,  and  a  broad  flannel 
binder  put  on.  Hot  fomentations  and  opium  are  useful  for  the  relief  of 
pain.  Under  treatment  by  careful  diet,  iodoform  internally,  and  local 
applications,  many  cases  have  done  extremely  well.  Most  importance 
must  be  attached  to  diet. 

Operative  Treatment  is  probably  of  little  value  unless  there  is  purulent 
•exudation  or  a  possibility  of  clearing  away  caseous  masses.  In  the  adhesive 
type  it  is  unnecessary.  If  there  is  much  effusion  of  serum,  it  may  do  a 
little  good  by  removing  exudates  containing  toxins  and  relieving  distension. 
Paracentesis  may  injure  the  gut.  Local  caseous  masses  often  dry  up, 
calcify,  and  become  encapsuled.  Even  if  removed  there  is  almost  just  as 
great  a  probability  of  a  fresh  outbreak  from  disease  elsewhere.  Operative 
treatment  has  shown  that  the  disease  is  by  no  means  always  fatal,  while 
medical  treatment  proves  that  operation  is  usually  unnecessary.  Purulent 
effusions  are  generally  localised  and  treated  as  chronic  abscess.    Operation 


356  Chapter   XXXI. 

is  also  needed  for  the  cure  of  intestinal  obstruction,  and  may  be  valuable 
for  small  fistula?. 

Abdominal  Cysts  and  Tumours. — Mesenteric  Cysts  are  of  embryonic 
origin  or  due  to  parasites,  e.g.,  hydatid  cysts.  They  do  not  originate  in 
lymphatic  structures.  Cysts  are  spoken  of  as  serous,  chylous  or  sanguineous, 
according  to  the  nature  of  their  contents.  Embryonic  cysts  are  derived 
from  the  remains  of  foetal  organs,  remnants  of  the  Miillerian  and  Wolffian 
ducts  and  bodies,  commonly  situated  between  the  layers  of  the  mesentery. 
Occasionally  a  cyst  is  due  to  dilatation  of  Meckel's  diverticulum,  which 
becomes  constricted  and  attached  to  the  gut  by  an  impervious  cord,  or  to 
constriction  of  the  ends  of  an  unobliterated  urachus.  A  urachal  cyst  is  not 
a  mesenteric  one.  In  other  instances  it  is  derived  from  a  sequestrated 
portion  of  some  retro-peritoneal  organ,  such  as  the  pancreas  ;  or  it  may 
be  a  dermoid,  derived  from  a  sequestrated  part  of  the  ovary  or  parovarian 
body,  and  containing  an  imperfect  foetus,  which  may  even  be  alive. 
Possibly  the  cyst  may  arise  from  a  snared-ofi  portion  of  the  gut,  or  an 
atypical  intestinal  diverticulum.  Thus,  in  a  girl,  aged  5  weeks,  a  saccular 
dilatation  of  the  small  intestine  communicated  with  the  jejunum  by  a 
small  orifice,  15  ins.  from  the  pylorus.  Its  walls  were  composed  of  normal 
gut.  Had  it  been  entirely  cut  off  it  would  have  developed  into  a  cyst. 
Multiple  diverticula  of  the  large  and  small  intestines  have  often  been 
reported,  and  many  of  them  are  in  the  mesentery.  Pancreatic  diverticula, 
of  the  small  intestine  are  usually  connected  with  the  third  part  of  the 
duodenum,  occasionally  the  upper  part  of  the  jejunum.  At  the  csecal  end 
is  a  glandular  mass  of  pancreatic  tissue.  The  pancreas  is  developed  from 
twin  buds  or  diverticula  of  the  duodenum. 

Mesenteric  cysts  are  more  common  in  females  than  in  males,  and 
may  occur  at  any  age,  e.g.,  a  male,  aged  II  weeks  (Eve).  They  are  situated 
between  two  layers  of  the  mesentery,  and  occasionally  the  mesocolon. 
A  prominent  fluctuating  tumour  is  found  near  the  umbilicus,  and  rarely 
in  other  situations.  It  is  very  mobile,  sometimes  can  be  rotated,  and 
easily  moved  from  side  to  side.  A  zone  of  resonance  round  the  tumour 
and  a  belt  of  resonance  in  front  are  due  to  intestine.  By  pressure  on  the 
gut  it  may  give  rise  to  more  or  less  intestinal  obstruction  and  gastro- 
enteric disturbance.  If  left  alone  it  may  end  in  death  from  emaciation, 
obstruction,  rupture  or  perforation  of  the  gut.     The  treatment  is  surgical- 

Pancreatic  Cysts  are  traumatic  or  non-traumatic.  Coombs  and 
Nash  collected  25  traumatic  cases  of  which  3  were  under  10  years  of  age,, 
and  29  non-traumatic  of  which  only  their  own  patient,  a  girl,  4  years 
old,  was  under  15  years.  It  was  probably  due  to  rupture  of  a  small  pan- 
creatic cyst  into  the  lesser  peritoneal  cavity.  There  are  no  serious  symp- 
toms apart  from  pressure.  Telling  and  Dobson  (1909)  reported  a  case  at 
11  months  of  age.  There  were  no  symptoms  of  ill-health,  except  gradual 
loss  of  weight  and  enlargement  of  the  abdomen.    The  cyst  contained  1  \  pints. 


.     The  Peritoneum.  357 

Pain  is  not  constant.  It  is  sometimes  severe  (Coeliac  neuralgia).  The 
tumour  gives  rise  to  dulness,  tenderness,  and  resistance  in  the  epigastrium 
and  left  hypochondrium,  just  below  the  edge  of  the  ribs.  Its  contents  are 
alkaline,  albuminous,  and  contain  ferments,  if  connected  with  the  pancreas. 
Traumatic  ones  may  be  merely  localised  serous  effusions.  These  cysts  are 
treated  by  incision  and  drainage. 

Tumours  of  the  pancreas  are  very  rare,  and  usually  mistaken  for  renal 
tumour.    Malcolm  (1902)  reported  a  case  of  fibro-sarcoma  in  a  girl  of  4  years. 

Omental  Cysts  and  Tumours. — Cysts  of  the  great  omentum  are  rare. 
In  a  case  of  Mathews  (1905)  the  contents  were  sanguineous.  The  cyst  was 
in  the  middle  line  and  connected  by  a  pedicle  with  the  transverse  colon. 
Sarcoma  may  occur  and  give  rise  to  no  definite  symptoms.  It  usually  begins 
on  the  left  side  and  grows  very  rapidly.  Tuberculous  masses  are  by  no 
means  infrequent.  Eetro-peritoneal  Sarcomata  are  soft  and  fluctuating 
and  may  feel  cystic.     The  gut  is  situated  in  front. 

Tumours  of  the  Alimentary  Canal. — Corner  and  Fairbank  (1901) 
reported  a  case  of  sarcoma  of  the  colon  in  a  boy,  aged  9  years,  causing 
intussusception.  They  state  that  it  is  the  fifth  recorded  instance  of  such 
a  result,  and  the  eleventh  recorded  instance  of  sarcoma  of  the  colon.  In  a 
■resume  of  174  cases  sarcoma  was  twice  as  frequent  in  males,  and  the  round 
cell  variety  was  the  most  common.  Sarcomata  of  the  ileo-caecal  region 
and  colon  are  most  frequent  during  the  first  decade.  The  distribution  of 
155  cases  was: — oesophagus,  14;  stomach,  58;  ileo-csecal,  65;  colon,  11  ; 
rectum,  7.  The  symptoms  vary  with  the  site  ;  and  the  course  of  the 
disease  may  resemble  tuberculous  peritonitis  or  intestinal  obstruction. 
The  prognosis  of  early  operation  for  sarcoma  of  the  colon  is  good  ;  6  were 
free  from  recurrence  1-9  years  later.  Glandular  infection  is  rare,  and  the 
secondary  growths  are  usually  in  the  liver  or  kidneys.  Colloid  carcinoma 
has  also  been  reported  in  the  rectum,  and  generally  distributed  throughout 
the  peritoneum. 

Multiple  Cysts  have  been  found  in  the  wall  of  the  colon  and  even  more 
rarely  in  the  ileum.  They  contain  mucin,  and  are  probably  due  to  occlusion 
of  Lieberkuhn's  ducts.  They  are  situated  between  the  epithelium  and 
serous  coat,  and  may  attain  the  size  of  cherries. 


CHAPTER    XXXII. 

DISEASES  OF   THE  LIVEE. 

Jaundice — Acute  Yellow  Atrophy — Biliary  Cirrhosis — Atrophic  Cirrhosis 
— Syphilis — Tuberculosis — Active  and  Passive  Congestion — Abscess — 
Fatty  Liver — Amyloid  Liver — Hydatids — Tumours. 

The  liver  is  a  most  important  organ  in  foetal  life.  It  is  formed  very 
early  and  grows  rapidly.  By  the  end  of  the  third  or  fourth  month  it 
nearly  fills  the  abdomen  and  almost  equals  half  the  entire  weight  of  the 
foetus.  At  birth  its  weight  is  from  4-5  per  cent,  of  the  body  weight,  or 
4-5  oz.  It  is  equivalent  to  the  weight  of  10  spleens,  9  kidneys,  or  7  hearts 
(Boivard  and  Nicoll,  1906).  In  bulk  it  is  greater  than  that  of  the  2  lungs 
combined,  and  it  contains  about  one-fourth  of  the  total  blood  in  the  body. 
It  doubles  its  weight  in  1  year,  trebles  it  in  2  years,  and  quadruples  it  in 
4  years.  It  is  very  susceptible  to  disease  or  gives  rise  to  disease,  on  account 
of  its  great  size  and  the  relationship  which  it  bears  to  the  foetal  circulation. 
During  intra-uterine  life  the  umbilical  vein  carries  arterial  blood  to  the 
foetus.  Entering  at  the  umbilicus  it  passes  along  the  edge  of  the  sus- 
pensory ligament.  It  gives  off  branches  to  the  left  lobe,  the  quadrate  lobe, 
and  the  lobe  of  Spigelius.  At  the  transverse  fissure  it  divides  into  two 
branches  ;  the  larger  unites  with  the  portal  vein  and  enters  the  right  lobe, 
while  the  smaller  forms  the  ductus  venosus  and  joins  the  left  hepatic  vein 
as  it  enters  the  inferior  vena  cava.  Hence  the  maternal  blood  reaches  the 
vena  cava  by  three  different  channels.  The  main  bulk  passes  through  the 
right  lobe  of  the  liver  and  the  right  hepatic  vein  ;  some  passes  through  the 
left  lobe  and  the  left  hepatic  vein  ;  and  the  rest  joins  that  of  the  left  hepatic 
vein,  and  does  not  pass  through  the  liver  at  all.  On  ligature  of  the  cord  the 
main  blood  supply  of  the  liver  is  at  once  cut  off.  The  umbilical  vein  is 
obliterated  in  2-5  days,  and  forms  the  round  ligament,  and  the  ductus 
venosus  is  closed  in  about  the  same  time.  The  lungs  are  inflated  and 
exercise  their  functions.  The  importance  of  the  liver  is  diminished,  but  it 
still  remains  relatively  larger  and  heavier  than  in  adult  life. 

In  infants  the  ribs  are  more  horizontal  than  in  adults,  and  the  liver 
more  exposed.  At  birth  the  edge  reaches  2-3  ins.  below  the  costal  margin, 
and  during  the  first  3  years  of  life  it  can  usually  be  felt  an  inch  below  the 
edge  of  the  ribs.  The  upper  border  of  dulness  is  higher  than  in  the  adult, 
and  reaches  to  the  lower  edge  of  the  fifth  rib  in  the  nipple  line,  the  seventh 


Diseases  of  the  Liver.  359 

rib  in  the  mid-axillary  line,  and  the  ninth  rib  behind.  The  organ  may  be 
displaced  downward  by  deformity  of  the  chest,  as  in  rickets  ;  by  fluid  or 
new  growths  in  the  thorax  ;  or  from  weakness  of  its  ligamentous  supports 
and  relaxation  of  the  abdominal  muscles  in  great  debility.  The  right  lobe 
may  be  so  much  displaced  as  to  reach  the  crest  of  the  ilium,  leaving  the  left 
lobe  only  in  contact  with  the  diaphragm.  Hepatoptosis  is  sometimes  marked 
in  acute  febrile  diseases.  Displacement  upward  is  due  to  fluid  or  new 
growth  in  the  abdomen,  or  excessive  tympanites.  Transposition  is  rare. 
Bile  is  secreted  in  the  third  month  of  foetal  life  (Zweifel).  Glycogen  for- 
mation begins  in  the  fifth  month.    Fat  is  distributed  throughout  the  lobules. 

Jaundice. — Although  jaundice  is  not  a  disease,  it  is  a  common  and  very 
obvious  symptom,  indicative  of  a  slight  and  transient  disorder  or  severe 
and  rapidly  fatal  disease.  Its  occurrence  in  the  newborn  has  already  been 
considered  (p.  133).  In  the  present  section  the  simple  obstructive  or 
catarrhal  jaundice  will  be  considered.  Its  most  usual  cause  is  catarrhal 
inflammation  of  the  duodenum,  with  or  without  catarrh  of  the  stomach, 
and  hence  it  is  often  called  Duodenitis  or  Gastro-duodenitis.  The  swelling 
of  the  mucous  membrane  blocks  the  opening  of  the  common  duct  into 
the  duodenum,  or  the  inflammation  extends  by  continuity  up  the  common 
duct  and  into  the  hepatic  and  cystic  ducts.  This  is  the  true  catarrhal 
jaundice  of  the  obstructive  variety,  the  bile  passing  into  the  blood  because 
of  its  inability  to  escape  into  the  alimentary  canal.  Obstructive  jaundice 
is  occasionally  due  to  blockage  of  the  duct  by  a  plug  of  mucus  or  inspissated 
bile,  gallstone  or  roundworm,  and,  very  rarely,  to  stricture  of  the  duct  or 
pressure  from  without.  Catarrhal  jaundice  is  common  from  the  date  of 
the  eruption  of  the  first  teeth  up  to  6  years  of  age,  and  after  that  is  some- 
what less  frequent.  The  attack  can  often  be  traced  to  exposure  to  cold 
or  to  food,  unsuitable  in  quality  or  quantity  or  undergoing  decomposition. 
It  is  most  common  in  the  spring  and  autumn,  and  sometimes  occurs  in 
epidemics  ;  possibly  contagious  and  associated  with  septic  symptoms. 
Thus,  there  are  probably  two  classes  of  cases  :  (1)  Simple  catarrhal,  and 
(2)  Infectious. 

In  the  simple  catarrhal  variety  the  attack  is  often  ushered  in  by 
vomiting  or  diarrhoea.  The  child  loses  its  appetite,  is  fretful,  languid  and 
drowsy,  and  in  a  few  days  exhibits  yellow  discolouration  of  the  skin,  con- 
junctivae and  matrix  of  the  nails.  Anorexia,  nausea,  vomiting,  epigastric 
tenderness  and  pain  may  persist  for  some  days,  if  there  is  catarrh  of  the 
stomach.  If  the  catarrh  is  limited  to  the  duodenum,  pain  comes  on  2  or  3 
hours  after  the  ingestion  of  food,  on  its  passage  from  the  stomach  onwards, 
and  there  is  tenderness  in  that  region.  The  urine  shows  the  usual  changes 
in  colour  ;  the  stools  are  offensive,  constipated  or  loose,  and  vary  in  colour 
according  to  the  degree  of  obstruction.  If  no  bile  reaches  the  intestines 
they  are  clay-coloured,  but  if  the  obstruction  is  not  complete  they  are  more 
or  less  yellowish  brown.    The  deficiency  in  bile  prevents  the  proper  digestion 


3G0  Chapter   XXXII. 

and  assimilation  of  fats.  Marked  slowing  of  the  pulse  is  uncommon  in 
children,  and  itching  of  the  skin  is  also  rare,  but  it  does  occasionally  occur, 
and  with  it  a  tendency  to  troublesome  urticarial  rashes.  The  liver  is  almost 
always  enlarged,  and  may  reach  as  low  as  the  level  of  the  umbilicus.  It  is 
sometimes  painful  and  tender.  The  staining  persists  for  2  or  3  weeks,  and 
even  for  as  many  months  without  producing  any  very  great  effect  on 
nutrition.  In  prolonged  attacks  the  mental  condition  is  dull,  and  the  child 
stupid  or  sleepy.    Slight  fever  is  often  present  in  the  early  stages. 

In  the  infectious  or  epidemic  type  the  fever  lasts  for  8-10  days  or  less- 
Occasionally  there  is  prodromal  malaise.  Usually  the  onset  is  sudden,  with 
fever,  chilliness,  vague  pains,  vomiting,  thirst,  offensive  breath  and 
perhaps  delirium.  There  are  pain  and  tenderness  in  the  epigastrium  and 
over  the  liver  ;  the  liver  and  spleen  are  enlarged  ;  the  stools  are  loose  or 
costive,  and  there  is  often  a  trace  of  albuminuria.  Enlarged  congested 
tonsils  are  not  infrequent  and  may  be  the  source  of  infection.  Jaundice 
does  not  necessarily  occur.  This  infectious  type  is  also  seen  in  pneumonia, 
scarlet  fever  and  septic  infections.  Weil's  disease,  or  Icterus  Gravis,  is  a 
severe  type  of  infectious  jaundice,  with  swelling  of  the  spleen  and  liver,  and 
nephritis.  It  is  either  a  toxic  or  severe  jaundice,  or  due  to  infection  by 
micro-organisms,  frequently  the  bacillus  coli.  In  a  4  months  old  infant 
(Briining,  1904),  who  died  in  23  days  from  the  onset,  the  bacillus  proteus 
fluorescens  was  found  in  the  urine,  and  the  serum  agglutinated  the  typhoid 
bacillus.  This  is  a  common  feature  of  the  serum  in  jaundice.  The  bacillus 
was  cultivated  from  various  organs,  blood  and  bile.  Post  mortem  examina- 
tion showed  fatty  infiltration  and  degeneration  of  the  liver  and,  to  a  less 
extent,  of  the  heart ;  purulent  inflammation  of  the  kidneys,  and  swollen 
lymphoid  follicles  in  the  intestines.  Fortunately  the  disease  is  almost 
unknown  in  children.  At  the  onset  it  simulates  simple  jaundice  and  later 
on  may  be  mistaken  for  meningitis  or  typhoid  fever. 

The  diagnosis  of  simple  catarrhal  jaundice  depends  upon  the  history 
of  gastro-intestinal  disturbance  and  some  exciting  cause.  Distension  of  the 
gall  bladder  is  evidence  of  obstruction  of  the  common  duct.  Other  causes 
of  jaundice  must  be  remembered,  and  excluded  as  far  as  possible.  It  is  a 
complication  of  many  infective  diseases. 

The  'prognosis  is  good,  if  due  to  simple  duodenal  catarrh.  As  soon  as 
the  cause  ceases  to  be  operative,  the  blood  and  urine  lose  the  yellow  tint. 
The  re-appearance  of  normal  coloured  stools  indicates  that  the  obstruction 
has  gone.  A  sudden  return  of  colour  implies  sudden  detachment  of  a  plug 
of  mucus,  inspissated  bile  or  other  obstruction  in  the  common  duct.  Gradual 
return  of  colour  occurs  when  the  obstruction  disappears  slowly.  The  skin 
resumes  its  normal  colour  as  soon  as  the  stained  epidermis  is  desquamated. 
In  the  rare  persistent  cases  the  system  appears  to  accommodate  itself  to  the 
presence  of  bile  in  the  tissues  for  many  months.  Eventually  the  obstruction 
leads  to  the  dilatation  of  the  ducts  in  the  liver,  infiltration  of  the  liver  cells, 


Diseases  of  the  Liver.  361 

and  finally  interference  with  their  functions.  Changes  occur  characteristic 
of  a  secondary  biliary  cirrhosis,  and  the  patient  dies  in  a  year  or  two  from 
a  kind  of  toxsemia  or  blood  poisoning.  Such  a  result  is  not  unknown  in 
mild  cases,  but  I  have  never  seen  a  simple  catarrhal  jaundice  in  a  child 
end  fatally.  Complications  are  rare.  Some  children  are  liable  to  frequent 
attacks. 

Drug  treatment  is  rarely  necessary.  In  catarrhal  conditions  diet  the 
child  carefully,  giving  bland  and  easily  digested  food  with  a  minimum 
quantity  of  fat.  Fruit  is  permissible.  Constipation  is  treated  by  drugs 
acting  on  the  lower  intestinal  tract,  e.g.,  saline  laxatives,  mineral  waters, 
and  aloes.  It  is  a  moot  point  whether  cholagogues  should  be  given.  By 
increasing  the  secretion  of  bile  it  may  be  possible  to  raise  the  pressure 
in  the  ducts  and  overcome  the  obstruction.  If  this  fails,  the  treatment  may 
make  the  patient  worse.  Small  frequent  doses  of  calomel  in  my  experience 
are  harmless  and  beneficial,  possibly  by  reducing  inflammation,  preventing 
intestinal  decomposition,  and  keeping  the  bowels  gently  open.  Salol  is 
good  for  offensive  stools.  Mild  diuretics  and  diaphoretics  aid  the  elimination 
of  the  retained  bile.  Effervescing  mixtures  are  pleasant.  Alkalies  are 
useful  by  dissolving  and  liquefying  the  mucus,  and  enabling  the  mucous 
membranes  to  digest  food  more  easily.  Small  doses  of  mix  vomica  and 
dilute  hydrochloric  acid  assist  digestion.  Emetics  are  sometimes  given  in 
the  hope  that  the  act  of  vomiting  may  compress  the  liver  and  bile  ducts 
sufficiently  powerfully  to  drive  out  the  obstruction.  It  is  experimental 
treatment,  and  might  cause  rupture  of  the  duct,  if  the  obstruction  is  due 
to  gallstone. 

Acute  Yellow  Atrophy. — Syn.  :  Malignant  Jaundice — Hemorrhagic 
Jaundice —  Typhoid  Icterus —  Hepatite  Maligne —  Atrophic  Aigue  du  foie — 
Parenchymatous  Hepatitis. — This  disease  is  very  rare  in  children,  and 
closely  resembles  phosphorus  poisoning.  It  has  been  asserted  that  all 
cases  are  due  to  this  cause.  Arsenic  and  antimony  produce  similar  effects 
upon  the  liver.  Possibly  it  is  due  to  microbial  infection,  or  to  ptomaines 
or  leucomaines  acting  as  poison  to  the  liver.  Undoubtedly  it  is  due  to  a 
protoplasmic  poison  which  affects  the  liver  chiefly.  Leucin  and  tyrosin 
are  found  in  the  urine,  on  evaporation  to  a  small  bulk  and  allowing  them  to 
crystallize  out.  It  has  been  recorded  as  early  as  the  tenth  month  of  life, 
and  about  25  cases  under  12  years  have  been  reported.  The  disease  is 
characterised  by  acute  degeneration  of  the  liver,  with  the  abolition  of  its 
functions  and  death  from  toxaemia.  The  symptoms  are  the  same  as  in 
adults.  It  often  begins  insidiously,  like  mild  catarrhal  jaundice,  and  the 
temperature  remains  normal  or  subnormal,  but  may  rise  towards  the  end. 
Sometimes  the  onset  is  acute  with  high  fever  and  hepatic  pain.  The  usual 
symptoms  are  fever,  furred  tongue  which  becomes  dry  and  brown,  foetid 
breath,  sordes  on  the  lips  and  teeth,  nausea  and  vomiting  coffee-ground 
vomit,  tarry  stools,  jaundice,  pain  on  pressure  over  the  liver,  prostration 


362  Chapter   XXXII. 

frequent  variable  pulse  ;  marked  tendency  to  haemorrhages  such  as  epistaxis, 
purpura,  hsemateinesis  and  melama  ;  bile,  leucin  and  tyrosin  in  the  urine  ; 
headache,  nervous  irritability,  somnolence  alternating  with  restlessness, 
insomnia,  delirium,  clonic  and  tonic  spasms,  convulsions,  maniacal  symp- 
toms, and  coma.  The  liver  may  diminish  rapidly  in  size  in  the  second  stage, 
and  is  often  tender.  The  spleen  is  enlarged.  The  pupils  often  become 
dilated  arid  react  badly. 

The  diagnosis  is  impossible  in  the  first  stage.  Later  on  it  simulates 
meningitis  or  typhoid  fever.  In  extreme  fatty  degeneration  the  spleen  is 
not  enlarged,  and  leucin  and  tyrosin  are  absent.  These  substances  may  be 
absent  in  mild  cases  of  acute  yellow  atrophy,  and  possibly  in  the  most 
severe  ones. 

Death  commonly  ensues  within  a  week.  The  early  stages  are  of  variable 
duration,  but  the  closing  toxsemic  stage  usually  ends  fatally  in  1-3  days. 
Bauer  (1893)  reported  a  case  of  recovery,  followed  by  death  3  months 
later  from  acute  miliary  tuberculosis,  with  marked  evidence  of  regeneration 
of  liver  tissue  post  mortem.    No  treatment  is  of  any  value. 

Biliary  Cirrhosis. — Syn.  :  Hanoi's  Cirrhosis — Hypertrophic  Cirrhosis 
wilh  Jaundice. — Cirrhotic  changes  can  be  produced  in  the  liver  by  irritants 
reaching  the  bile  ducts,  and  setting  up  cholangitis  and  pericholangitis,  or 
from  chronic  obstruction  of  the  hepatic  duct  or  common  bile  duct,  or  absence 
of  the  ducts.  Possibly  the  irritant  is  excreted  into  the  smaller  bile  ducts 
and  sets  up  chloangitis  and  proliferation  of  the  surrounding  connective 
tissue  cells.  Such  a  result  was  produced  by  Hunter  as  the  effect  of  experi- 
mental poisoning  by  toluylendiamine.  Hence  the  disease  may  be  a  primary 
infection  of  the  minute  bile  ducts,  or  an  ascending  infection  from  the  larger 
ducts,  or  due  to  obstruction. 

Hanot's  cirrhosis  is  rare  in  children.  It  gives  rise  to  dull  pain  in  the 
region  of  the  liver,  acute  attacks  of  abdominal  colic,  and  slight  jaundice 
which  increases  with  each  attack.  For  some  time  the  health  and  appetite 
are  unaffected.  Gradually  the  liver  and  abdomen  increase  in  size,  the 
spleen  is  enlarged,  the  urine  contains  much  bile  pigment,  and  the  stools 
are  not  clay  coloured.  Fever  is  slight  and  may  become  intermittent.  The 
child  wastes  and  dies  with  symptoms  of  cholaemia.  Subcutaneous  petechial 
spots,  bleeding  from  the  gums  and  nose,  and  intestinal  hsemorrhage  may 
occur.  The  fingers  and  toes  may  be  enlarged,  and  ascites  supervene  towards 
the  end.  The  liver  is  symmetrically  enlarged  and  smooth  ;  cuts  with 
difficulty,  and  has  a  yellow  or  dark  green  hue  on  section  ;  and  the  ducts  are 
pervious.  Microscopically  there  is  found  a  monolobular  cirrhosis  starting 
round  the  bile  ducts  ;  new  fibrous  tissue  in  concentric  layers  round  the 
larger  ducts  ;  and  multiplication  of  bile  ducts  containing  inspissated  bile  and 
minute  calculi.  The  disease  apparently  begins  in  or  around  the  small 
bile  ducts. 


Diseases  of  the  Liver.  363 

Acute  cases  may  end  in  a  few  months  ;  more  usually  the  jaundice  is 
chronic  and  lasts  for  years,  perhaps  with  occasional  intermissions.  Death 
results  from  choleemia,  profuse  haemorrhage,  or  intercurrent  disease. 

Infantile  Biliary  Cirrhosis  is  a  disease  prevalent  in  East  India,  in 
Calcutta  and  other  large  Indian  towns,  and  in  Bengal.  It  is  most  frequent 
in  Hindoos  ;  more  common  among  the  well-to-do  ;  and  generally  begins 
in  the  seventh  or  eighth  month  of  life,  sometimes  within  a  few  days  of 
birth,  and  rarely  after  3  years.  It  runs  in  families,  child  after  child  dying 
from  it  under  the  age  of  2  years.  The  onset  is  insidious,  and  the  liver  may 
be  much  enlarged  before  the  disease  is  suspected.  It  ends  fatally  in  3-12 
months,  and  occasionally  in  2  or  3  weeks.  Its  causation  is  uncertain,  but 
it  is  probably  the  result  of  some  irritant  of  gastric  origin,  e.g.,  condiments, 
acting  directly  on  the  liver  cells  or  on  the  lining  of  the  ducts.  Syphilis, 
malaria  and  alcohol  can  be  excluded.  The  liver  is  enlarged,  deeply  bile 
stained,  and  shows  marked  cirrhosis  of  the  intra-  and  inter-lobular  type, 
and  proliferation  of  bile  ducts.  In  some  parts  the  cirrhosis  is  even  pericellu- 
lar. The  liver  cells  undergo  degeneration.  Similar  changes  have  been 
produced  experimentally  by  ligature  of  the  common  bile  duct  (Wickham 
Legg,  1873),  or  branches  of  the  main  duct  (Vaughan  Harley).  Probably, 
therefore,  it  is  due  to  obstruction. 

The  symptoms  are  languor,  fretfulness,  sallow  skin,  a  voracious 
appetite  alternating  with  anorexia,  nausea,  occasional  vomiting,  great 
thirst,  constipation  and  clay  coloured  stools,  and  some  fever.  The  liver 
may  extend  to  the  level  of  the  umbilicus  or  lower,  with  smooth  surface, 
rounded  or  prominent  edge,  and  no  pain  or  tenderness.  The  spleen  is 
enlarged.  The  sallowness  deepens  into  profound  jaundice  ;  the  urine  is 
bile  stained  ;  ascites  and  pufhness  of  the  hands  and  feet  ensue,  and  death 
results  from  cholaemia,  haematemesis,  melsena  or  coma.  The  liver  contracts 
during  the  progress  of  the  disease.     Treatment  is  entirely  symptomatic. 

Congenital  Cystic  Disease. — Congenital  cystic  disease  of  the  liver  is 
usually  associated  with  cystic  degeneration  of  the  kidneys,  nearly  always 
in  a  more  advanced  form,  and  rarely  with  cystic  degeneration  of  the 
lungs  and  pancreas.  It  has  been  found  with  other  congenital  anomalies, 
e.g.,  hemicephalus  and  transposition  of  the  viscera  (Witzel)  ;  Polydactyly 
and  meningocele  (Rolleston)  ;  Polydactyly,  encephalocele,  hare-lip  and 
malformed  external  genitals  (Couvelaire  and  Porak).  Its  pathology  is 
uncertain,  but  it  is  probably  due  to  maldevelopment  in  most  cases.  It 
gives  rise  to  no  jaundice  or  other  symptoms  indicating  disease  of  the  liver, 
although  the  liver  may  be  so  large  in  the  foetus  as  to  interfere  with  labour, 
and  sometimes  reaches  to  Poupart's  ligament.  It  is  compatible  with  con- 
siderable length  of  life,  and  may  terminate  in  ascites,  cedema  and  pro- 
gressive asthenia.  Rapid  growth  is  indicated  by  pain.  The  liver  is  enlarged, 
yellow,  firm,  and  shows  white  patches.  There  may  be  no  naked-eye  changes. 
The  cysts  are  scattered  throughout  as  minute  white  specks  in  the  early 


364  Chapter   XXXII. 

stages,  and  later  on,  vary  in  size  from  a  pea  to  a  cherry,  or  even  larger,  and 
contain  no  bile.  MacMunn  (1906)  reported  a  case  in  a  man  of  46  whose  liver 
weighed  over  12  lbs.,  and  was  covered  with  large  transparent  cysts,  the  size 
of  a  pea  to  a  Tangerine  orange  and  multilocular.  The  left  lobe  was  con- 
verted entirely  into  cysts,  and  the  right  one  almost  so.  The  kidneys  and 
the  adrenals  were  similarly  affected.  It  is  said  that  the  coloured  fluids 
injected  into  the  bile  duct  do  not  pass  into  the  cystic  spaces,  yet  they  are 
found  in  the  early  stages  lined  by  columnar  epithelium.  A  variable  amount 
of  uni-  and  multi-lobular  cirrhosis  is  present.  In  another  type  of  case  in 
which  numerous  cystic  spaces  are  found  filled  with  bile-stained  debris,  there 
is  evidence  of  prolonged  pericholangitis  and  fibrosis  round  the  bile  ducts. 

Atrophic  Cirrhosis. — The  typical  "  hob-nailed  "  liver  may  occur  in 
children  who  have  never  tasted  alcohol.  It  is  probably  induced  by  toxic 
bodies  absorbed  from  the  intestine  as  a  result  of  gastro-intestinal  catarrh, 
set  up  by  highly  stimulating  food,  alcohol,  and  even  vinegar  ;  or  alcohol 
may  act  as  a  direct  hepatic  irritant.  Some  cases  follow  specific  fevers.  The 
cirrhosis  is  of  the  ordinary  multilobular  type,  an  interstitial  hepatitis  or 
portal  cirrhosis,  with  secondary  fatty  degeneration  of  the  liver  cells.  Palmer 
Howard  (1887)  reported  2  cases  in  one  family  and  collected  61  others  ; 
the  common  age  was  9-12  years.  It  was  twice  as  frequent  in  boys  as  in  girls. 
In  half  the  cases  no  cause  could  be  found  except  defective  diet,  only  10 
could  be  ascribed  to  alcohol  and  7  to  syphilis. " 

The  early  symptoms  are  those  of  hepatic  incompetence  or  lithaernia  ; 
flatulent  dyspepsia,  abnormal  appetite,  headache,  debility,  languor  and 
lithuria.  Morning  sickness  and  attacks  of  biliousness  or  diarrhoea  may 
occur.  Its  course  is  characterised  by  digestive  disorders,  wasting,  dryness 
of  the  skin,  ascites  and  haemorrhages.  Epistaxis  and  cutaneous  haemor- 
rhages are  common,  but  haemateniesis  and  melaena  are  less  frequent  than 
in  adults.  Headache  and  vomiting  are  common  ;  and  jaundice,  fever 
and  diarrhoea  more  frequent  than  in  adults.  In  a  few  cases  the  ordinary 
signs  have  been  absent,  and  there  has  been  a  marked  nervous  disturbance 
with  screaming,  convulsions  and  coma ;  progressive  idiocy,  paralysis, 
emaciation  and  fever  ;  spastic  rigidity  of  the  limbs,  normal  reflexes  and  loss 
of  speech ;  high  fever  and  most  of  the  signs  of  typhoid,  or  of  acute  peritonitis, 
due  to  perforation.  If  there  is  ascites,  it  is  liable  to  be  mistaken  for  tuber- 
culous or  other  forms  of  chronic  peritonitis. 

A  boy,  aged  9.  under  my  care  died  from  severe  haemateniesis.  At 
age  3  or  4  he  had  jaundice  for  8  weeks  ;  at  7  years  he  was  in  hospital 
for  jaundice  and  large  liver.  The  terminal  illness  lasted  4-5  weeks  before 
and  7  weeks  after  admission  to  hospital,  and  was  characterised  by  anaemia, 
wasting,  haematemesis,  melaena,  ascites,  irregular  fever,  and  purpura  2  days 
before  death.    The  liver  weighed  32|  oz.  ;   spleen  11 J  oz. 

The  prognosis  is  extremely  bad,  especially  if  there  are  haemorrhages  or 
nervous  symptoms.    Targett  has  reported  a  case  of  a  boy,  aged  8,  who  was 


Diseases  of  the  Liver.  365 

apparently  in  perfect  health  when  killed  by  accident,  and  yet  had  a  typical 
hob-nailed  liver.    The  treatment  is  essentially  the  same  as  in  adults. 

Syphilitic  Cirrhosis. — Congenital  syphilis  produces  a  patchy  or  diffuse 
generalised  interstitial  hepatitis.  It  takes  the  form  of  an  intercellular  or 
unicellular  cirrhosis  ;  the  individual  cells  being  separated  by  leucocytes  and 
newly-formed  connective  tissues.  The  typical  variety  in  infancy  is  a  diffuse 
acute  infiltration  with  young  cellular  connective  tissue.  Small  yellowish 
points  of  necrotic  liver  tissue,  areas  of  anaemic  necrosis,  are  often  present. 
The  cells  atrophy,  and  both  bile  ducts  and  portal  vessels  may  be  obstructed. 

The  liver  is  enlarged,  usually  yellow  but  varies  much  in  colour,  with 
irregular  outline,  thickened  capsule,  and  dense  consistency.  On  section 
it  may  exhibit  isolated,  small,  greyish  white  or  white  spots,  which  look  like 
miliary  tubercles.  They  are  called  miliary  syphilomata  ;  are  composed  of 
small  round  cells,  differing  only  from  tubercles  in  the  absence  of  the  tubercle 
bacillus ;  and  they  undergo  necrosis.  In  the  patchy  variety  the  yellowish 
grey  areas  are  distinguishable  by  their  colour  from  normal  liver. 

The  diagnosis  is  based  on  the  hepatic  enlargement,  in  conjunction 
with  other  signs  of  congenital  syphilis  and  enlargement  of  the  spleen.  There 
are  no  special  symptoms  and  jaundice  is  rarely  marked.  Nutrition  is 
generally  greatly  impaired.  Gummata,  associated  with  the  cirrhosis,  are  rare 
in  infancy  and  uncommon  in  later  childhood.  They  vary  in  size,  are  single 
or  multiple,  surrounded  by  new  connective  tissue  cells,  and  may  break 
down  in  the  centre.  The  liver  cells  are  active,  and  sometimes  there  are 
amyloid  changes.  A  polylobular  cirrhosis  may  occur  from  other  causes  in 
syphilitic  children. 

The  prognosis  is  not  very  bad,  provided  that  the  primary  disease  is 
energetically  treated.  Fatal  cases  die  early.  Wollstein  (1902)  states  that 
11  out  of  14  died  under  4  months  of  age,  and  the  others  at  7,  13,  and  19 
months.  Broncho-pneumonia  is  a  common  cause  of  death.  Many  terminate 
in  complete  recovery. 

The  Liver  in  Tuberculosis. — Miliary  tubercles  are  frequently  seen  on  the 
surface  in  miliary  tuberculosis.  Occasionally  a  capsular  hepatitis,  spreading 
into  the  lobules,  is  tuberculous  in  origin.  Earely  tuberculous  masses  are 
found.  Cirrhotic  changes  may  be  secondary  to  cardiac  failure  and  venous 
stasis,  or  due  to  the  tuberculous  toxin.  Alcohol,  syphilis,  and  malaria  must 
be  excluded  in  these  cases,  for  they  are  probably  due  to  mixed  infections. 

Active  Congestion  of  the  Liver. — Active  congestion  occurs  in  malaria, 
phosphorus  poisoning,  infectious  fevers,  in  the  first  stages  of  suppuration, 
and  from  high  external  temperatures  or  the  habitual  ingestion  of  rich  and 
stimulating  foods.  It  gives  rise  to  chilliness,  fever,  headache,  anorexia, 
vomiting,  constipation,  and  perhaps  mild  delirium.  The  child  lies  on  the 
right  side  with  the  knees  drawn  up.  The  liver  is  enlarged,  tender  and 
painful.  It  must  be  diagnosed  from  gastritis  and  perihepatitis.  The  pain 
and  tenderness  can  be  relieved  by  hot  fomentations,  mustard  leaf,  leeches, 


366  Chapter  XXXII. 

or  cupping.  Calomel  or  grey  powder,  followed  by  salines,  should  be  given 
freely.  Free  sweating  and  diuresis  must  be  encouraged,  and  light  diet 
given.  Ammonium  chloride  is  said  to  be  beneficial.  The  attack  is  soon  over, 
unless  it  ends  in  suppuration. 

Abscess  of  the  Liver  has  been  recorded  in  112  collected  cases  in  young 
children  (Legrand,  1906),  and  as  early  as  the  second  year  of  life.  It  is  due 
to  dysentery,  traumatism,  appendicitis,  migration  of  roundworms  into 
bile  ducts,  tubercle,  pyaemia,  pylephlebitis  and  umbilical  phlebitis, 
typhoid  fever  and  influenza.  Traumatism  is  relatively  a  more  common 
cause  than  in  adults,  the  abscess  developing  immediately  or  not  for  some 
weeks.  In  pyaemia  the  abscesses  are  small  and  multiple,  and  the  symptoms 
those  of  the  primary  disease. 

Liver  abscess  gives  rise  to  hectic  fever,  rigors,  prostration,  sweating, 
vomiting,  diarrhoea  and  wasting ;  jaundice,  if  there  is  any  pressure  on  or 
secondary  catarrh  of  the  bile  ducts  ;  more  or  less  constant  pain,  often 
intense,  not  necessarily  localised  over  the  liver  ;  downward  enlargement 
of  the  liver,  bulging  of  the  ribs,  and  a  tumour  if  it  is  situated  on  the  anterior 
surface  and  not  between  the  liver  and  diaphragm.  Hiccough  may  result 
from  irritation  of  the  diaphragm.  The  inflammation  may  extend  to  the 
thorax,  or  the  abscess  may  rupture,  giving  rise  to  pleurisy,  empyema, 
pneumo-thorax  and  pneumonia.  Or  it  may  rupture  through  the  skin, 
into  the  alimentary  tract  or  peritoneal  cavity.  Metastatic  abscesses  and 
endocarditis  complicate  pyseniic  cases.  Spontaneous  cure  has  followed 
rupture  through  the  skin  or  into  the  respiratory  passages.  The  abscess  may 
remain  quiescent  for  a  time  and  then  grow  rapidly. 

It  must  be  diagnosed  from  abscess  of  the  abdominal  wall.  It  cannot  be 
differentiated  from  subphrenic  abscess,  which  for  all  practical  purposes 
may  be  included  in  this  description.  Marked  local  signs  are  in  favour 
of  the  abscess  being  single.  An  exploratory  puncture  is  necessary,  for  a 
quiescent  abscess  simulates  hydatid  or  new  growth.  Grumous  liver  pus  is 
obtained.  The  prognosis  is  good,  if  it  is  single  and  treated  by  incision  and 
drainage.  Pyosmic  cases  are  almost  invariably  fatal,  and  the  multiple 
abscesses  only  diagnosed  post  mortem. 

Passive  Congestion  is  due  to  the  same  causes  as  in  the  adult,  and 
produces  cardiac  cirrhosis  or  the  "Nutmeg  Liver."  It  may  also  follow  on 
asphyxia  neonatorum  and  chronic  mediastinitis.  The  early  engorgement 
is  followed  by  more  or  less  fibrosis  and  enlargement.  Over-distension  of  the 
liver,  due  to  backward  pressure  from  rapid  heart  failure,  is  indicated  by 
pain  and  tenderness  in  the  hepatic  region,  sometimes  generalised  deep 
abdominal  tenderness,  or  tenderness  over  the  seventh  to  the  tenth  dorsal 
vertebra?.  The  enlargement  may  subside  if  cardiac  compensation  is 
established.  If  not,  it  becomes  chronic  ;  pain  and  tenderness  increase,  and 
ascites  and  oedema  develop.  The  superficial  abdominal  veins  over  the  liver 
are  dilated ;   jaundice  is  slight  and  the  skin  has  a  dirty  greenish  hue,  and 


Diseases  of  the  Liver.  367 

gastro-intestinal  symptoms  ensue.     The  spleen  is  large,  but  contracts  a 
good  deal  in  late  stages.    Mitral  disease  is  the  most  common  cause. 

Fatty  Liver. — Fat  globules  are  normally  present  in  the  liver  cells,  and 
in  great  excess  from  overfeeding,  alcohol,  deficient  exercise  and  imperfect 
aeration  of  the  blood.  Extreme  fatty  infiltration  is  most  common  in  obese 
children,  who  take  little  exercise.  It  is  apt  to  be  produced  in  tuberculosis, 
pneumonia,  acute  infectious  disease  and  intestinal  disorders.  It  is  incon- 
stant in  marasmus,  rickets  and  congenital  syphilis.  Fever  leads  to  fatty 
changes  of  the  nature  of  infiltration,  or  a  finely  granular  degeneration 
preceded  by  cloudy  swelling.  A  fatty  liver  may  be  present  at  any  period 
of  life,  even  in  utero,  and  is  extremely  common  under  6  months  of  age. 
It  gives  rise  to  uniform  and  painless  hepatic  enlargement  with  no  jaundice, 
ascites,  or  splenic  hyperplasia.  Its  colour  varies  with  the  amount  of  blood 
it  contains,  and  may  resemble  that  of  simple  anaemia.  Its  surface  is  smooth 
and  shiny,  pits  on  pressure,  and  has  a  doughy  and  greasy  feeling.  On 
section  it  is  soft,  friable  and  yellow,  and  oil  globules  can  be  scraped  off  it 
with  a  warm  knife.  Diet  and  exercise  are  the  most  important  factors  in 
its  treatment. 

Amyloid  Liver. — Amyloid  disease  affects  the  liver,  spleen,  kidneys, 
intestines  and  pancreas.  It  is  due  to  prolonged  suppuration,  tuberculosis, 
and  congenital  syphilis.  It  is  rare  under  10  years  of  age,  and  runs  the  same 
course  as  that  of  adults.  The  child  presents  a  waxy  pallor,  suffers  from 
vomiting  and  diarrhoea,  with  very  offensive  stools,  and  develops  oedema  and 
ascites.  There  is  no  jaundice ;  sometimes  slight  irregular  fever ;  much  urine, 
containing  much  albumin  and  hyaline  casts.  Death  results  from  exhaustion, 
pleurisy,  pneumonia  or  peritonitis.  The  ascites  is  due  to  the  kidney  affec- 
tion, and  failure  of  nutrition  and  circulation.  The  abdomen,  liver  and 
spleen  are  much  enlarged. 

Hydatid  Disease. — Although  the  taenia  echinococcus  is  common  in 
dogs,  hydatid  disease  is  rare  in  this  country.  Infection  is  acquired  by 
swallowing  water,  lettuce,  watercress,  etc.,  contaminated  with  the  faecal 
discharges  of  dogs  affected  with  worm.  Many  cases  in  adult  life  have 
probably  been  acquired  in  childhood.  The  symptoms  are  mechanical  in 
origin,  and  vary  with  the  situation.  A  case  was  reported  in  a  child  of 
5  months  by  Malcolm  (1895)  ;  another  by  Stiles  (1904),  in  a  girl,  aged  9  years, 
containing  about  a  gallon  of  fluid.  A  thrill  and  hydatid  fremitus  were 
present. 

Tumours. — Non-parasitic  cysts  are  rare,  but  have  been  reported  in  the 
foetus  and  the  newborn,  possibly  a  variety  of  cystic  disease.  Various  cases 
of  congenital  tumour  of  the  liver  and  one  or  both  adrenals  are  on  record. 
They  are  generally  round-celled  sarcomata,  sometimes  spindle-celled,  or 
described  as  lympho-sarcomata  or  lymph-adenomata.  Primary  carcinoma 
has  also  been  reported  in  a  few  cases,  with  secondary  deposits  in  various 
organs,  and  perhaps  of  the  nature  of  the  multiple  adenomata.     The  true 


368  Chapter   XXXII. 

character  of  many  of  these  tumours  is  doubtful    because  of  imperfect 
examination  and  report. 

Some  cases  have  occurred  in  utero  ;  a  few  have  followed  injury ;  no 
inherited  tendency  has  been  proved.  The  symptoms  include  rapid  develop- 
ment of  the  tumour,  sometimes  the  only  sign,  hepatic  pain,  enlargement 
of  the  abdomen  and  dilated  superficial  veins,  gastro-intestinal  symptoms, 
tumour,  rarely  jaundice,  no  splenic  enlargement  cr  ascites,  occasionally 
fever,  and  oedema.    They  are  fatal  in  a  few  days  to  several  months. 


CHAPTER    XXXIII. 

THE    NOSE   AND   ACCESSOKY   SINUSES. 

Congenital    Anomalies — Nasal    Obstruction — Nasal    Discharges — Rhinitis, 
acute  and  chronic — Epistaxis — Sinusitis — Osteomyelitis  of  the  upper  jaw. 

The  nose  is  an  organ  of  smell  and  the  main  channel  for  respiration. 
Obstruction  exerts  a  serious  influence  on  development  and  on  the  general 
health.     In  infancy  it  interferes  with  suckling. 

Congenital  Anomalies. — In  rare  instances  the  nose  is  entirely  absent, 
rudimentary,  cleft,  or  extraordinarily  flattened.  Any  part  of  the  nasal 
passages,  especially  the  choanse  or  posterior  nares,  on  one  or  both  sides, 
may  be  narrowed  or  occluded.  The  occlusion  may  be  membranous  or 
bony.  Sometimes  it  is  due  to  adhesion  of  the  soft  palate  to  the  naso- 
pharynx. More  anteriorly,  obstruction  is  commonly  due  to  a  deflected 
septum,  deformity  of  the  inferior  turbinal  bones,  or  a  hypertrophic  state 
of  the  mucous  membrane  covering  these  bones,  especially  at  the  posterior 
ends.  Rarely  there  is  adhesion  of  the  walls  of  the  nasal  fossa? ;  and  mem- 
branous occlusion  of  the  exterior  nares  is  a  pathological  curiosity. 

In  the  newborn  the  nasal  passages  and  naso-pharynx  are  very  narrow. 
The  adjacent  sinuses  are  small  or  undeveloped.  Congenital  maldevelop- 
ment  of  the  base  of  the  skull,  with  a  low  naso-pharyngeal  vault  and  a 
high  palate,  exaggerates  the  condition.  Congenital  nasal  stenosis  is 
usually  associated  with  narrow  nostrils,  a  high  V-shaped  palate,  a  Y-shaped 
dental  arch,  crowded  teeth  and  mouth-breathing.  Schroder  (1902)  devised 
a  mechanical  apparatus  for  stretching  the  alveolar  arch.  It  consists  of  a 
gold  plate  and  a  transverse  rod  of  two  parts  united  by  a  screw  which  is 
slowly  tightened.     Extreme  caution  is  needed  in  its  application. 

Nasal  Obstruction  depends  on  congenital  abnormalities  or  post-nasal 
causes,  such  as  various  forms  of  rhinitis,  new  growths  and  foreign  bodies, 
enlarged  tonsils  and  adenoid  hypertrophy,  and  occasionally  cicatricial 
obliteration  of  the  nares,  usually  syphilitic,  but  known  also  to  have 
followed  diphtheria  and  noma. 

Mouth-breathing  causes  dryness  of  the  mouth  and  throat  on  waking, 
and  a  constant  undue  dryness  of  the  mouth,  pharynx  and  larynx.  It 
predisposes  to  pharyngitis,  laryngitis,  bronchitis  and  tuberculosis.  Nasal 
obstruction  is  more  common  among  the  phthisical.  The  obstruction  also 
leads  to  the  development  of  pigeon-breast,  indrawn  ribs,  and  retraction  of 

2  B 


370  Chapter   XXXIII. 

the  membrana  tympani,  due  to  catarrh  of  the  Eustachian  tube  and  the 
middle  ear.  In  cases  of  deflected  septum  the  retraction  is  worst  on  the 
narrowed  side.  During  sleep  the  tongue  drops  back  on  to  the  pharynx 
and  induces  partial  asphyxia.  Hence  arise  morning  lassitude,  headache, 
deficient  growth,  ill  health,  and  possibly  enuresis  nocturna. 

There  is  great  difference  of  opinion  as  to  the  effects  on  the  shape  of  the 
jaw.    Four  types  of  deformity  can  be  recognised  : — 

(1)  The  arch  of  the  lower  jaw  is  larger  than  and  surrounds  that  of 

the  upper  jaw.  The  lower  jaw  is  prognathous,  and  the  molar 
teeth  overlap  those  of  the  upper  jaw.     The  palate  is  high. 

(2)  The  upper  jaw  is  badly  developed  and  atrophic.    The  curve  of  the 

alveolar  arch  is  small,  and  the  upper  teeth  are  consequently  on  the 
inner  side  of  the  lower  ones.  The  palate  is  very  high,  and  the 
turbinal  bones  are  approximated  to  the  septum. 

(3)  The  sides  of  the  upper  jaw  are  approximated  and  push  forward 

the  incisor  teeth,  which  project  and  overlap  the  lower  ones. 

(4)  The  lower  jaw  is  normal,  but  the  mouth  cannot  be  closed  (open- 

bite)  because  the  upper  alveolar  process,  anterior  to  the  molars, 
deviates  upward  at  a  considerable  angle.    The  palate  is  V-shaped. 

Either  the  malformations  are  due  to  adenoids,  nasal  stenosis  or  other 
■cause  of  nasal  obstruction,  or  these  conditions  are  secondary  to  the 
-deformity,  from  developmental  defects  dependent  on  our  advancing 
■civilisation,  and  comparable  with  the  early  decay  of  the  teeth  and  loss  of 
hair.  Undoubtedly  adenoid  hypertrophy  causes  a  well  recognised  type  of 
facial  contour  and  expression,  but  this  facies  can  exist  without  the  presence 
of  adenoids,  and  adenoids  do  not  invariably  produce  it.  These  peculiarities 
are  neither  hereditary  nor  racial  in  origin.  They  are  the  result  of  impeded 
nasal  respiration  and  excessive  external  atmospheric  pressure.  In 
mouth-breathing  the  current  of  air,  passing  through  the  mouth  to  the 
lungs,  abstracts  some  from  the  nasal  chambers,  rarefies  the  remainder,  and 
reduces  the  pressure  within  them  and  on  their  walls.  Thus,  there  is  negative 
pressure  within  the  nasal  cavities  and  positive  pressure  from  outside.  In 
addition,  the  nasal  chambers  are  imperfectly  developed  from  disuse. 
According  to  this  explanation  deflection  of  the  septum  nasi  can  be  pro- 
duced by  unilateral  nasal  obstruction.  Another  factor,  which  aids  develop- 
ment, is  in  abeyance  during  mouth-breathing.  This  is  the  action  of  the 
tongue.  If  the  mouth  is  shut,  the  tongue  exerts  lateral  pressure  on  the  molar 
teeth  and  forces  them  outwards,  widening  the  palatal  arch  and  preventing 
overcrowding  of  the  teeth. 

Against  these  views  it  must  be  pointed  out  that  palatal  deformities 
are  often  present  without  mouth-breathing  or  nasal  obstruction,  and 
may  be  absent  in  well  marked  cases  of  the  latter  condition.  It  might, 
therefore,  be  assumed  that  they  are  due  to  a  common  cause,  and  that  there 
is  no  causal  relationship. 


The   Nose    and   Accessory    Stiluses.  371 

The  association  of  dolichocephaly  and  a  highly  arched  palate  is  quite 
■common,  and  it  is  likely  that  they  are  both  the  result  of  impeded  anterior 
nasal  breathing,  for  this  affects  all  the  sinuses  connected  with  the  nose. 
Long  continued  excess  of  external  atmospheric  pressure  on  young  and  soft 
bones  will  induce  narrowing  of  the  face  and  upper  jaw.  It  is  not  due  to 
adenoids,  and  there  is  no  association  with  them  greater  than  normal. 

According  to  W.  B.  Parsons  (1905)  anterior  nasal  obstruction  causes 
deformity  of  the  maxillae  and  posterior  obstruction  affects  the  bridge  of  the 
nose.  The  lower  jaw  is  apparently  but  not  really  affected.  In  posterior 
•or  naso-pharyngeal  obstruction  the  air  pressure  in  the  sinuses  is  increased, 
and  causes  the  depression  and  widening  of  the  bridge  of  the  nose.  It  is 
important  to  recognise  that  both  anterior  and  posterior  nasal  obstruction 
can  exist  in  the  same  patient,  and  that  the  removal  of  adenoids  will  not 
<mre  the  results  of  anterior  obstruction.  In  post-nasal  catarrh  the  congestion 
and  blockage  give  rise  to  symptoms  like  those  of  adenoids.  It  is  often 
.associated  with  crowded  teeth,  receding  chin  and  a  small,  narrow  naso- 
pharynx. These  are  the  kind  of  cases  in  which  there  is  so-called  recurrence 
•of  adenoids,  i.e.,  adenoids  are  present  and  are  removed  with  a  certain 
.amount  of  temporary  benefit,  but  the  signs  of  nasal  obstruction  soon  recur. 

Nasal  Discharge  is  the  chief  indication  of  nasal  mischief.  It  may  be 
unilateral  or  bilateral,  acute  or  chronic,  serous,  sero-purulent  or  muco- 
purulent, purulent,  blood-stained  or  offensive.  A  unilateral  discharge 
is  generally  due  to  a  foreign  body,  sometimes  to  myiasis  or  new  groAvth, 
•occasionally  to  affections  which  produce  bilateral  mischief,  and  rarely  to 
disease  of  the  antrum,  frontal  or  ethmoidal  sinuses.  Bilateral  discharges 
.are  set  up  by  the  various  forms  of  inflammation  of  the  nasal  mucosa. 

Acute  Coryza,  acute  catarrhal  rhinitis  or  simple  nasal  catarrh,  is  common 
in  newborn  infants  and  during  the  first  three  years  of  life.  Blockage  of  the 
nose  by  the  swollen  mucosa  leads  to  inability  to  suck,  mouth-breathing, 
refusal  of  food,  wasting,  fatigue,  dyspnoea  and  sleeplessness.  It  is  commonly 
■due  to  microbial  infection  by  the  influenza  bacillus  of  Pfeiffer,  the  bacillus 
•coryzae  segmentosus  (Cautley)  or  b.  septus,  the  micrococcus  catarrhalis 
>(Kirchner),  micrococcus  paratetragenus,  Hoffmann's  bacillus,  etc.  Prob- 
ably numerous  organisms  of  the  influenza  group  give  rise  to  it.  Some- 
times it  indicates  the  onset  of  measles  or  influenza.  The  predisposing 
•causes  are  indoor  life,  heated  rooms,  closed  windows,  excess  of  clothing,  lack 
•of  exercise,  malnutrition,  adenoids  and  rickets.  A  deficiency  of  protein 
and  fat,  with  excess  of  carbohydrate  food  in  the  diet,  is  a  concomitant 
cause  by  lowering  vitality  and  impairing  nutrition. 

The  exciting  cause  is  some  organism,  perhaps  normally  an  inhabitant 
•of  the  nose  or  naso-pharynx,  but  its  virulence  is  actually  or  relatively  exag- 
gerated by  lowered  local  or  general  resistance  from  chill,  cold  winds,  wet, 
sweating,  etc.  Even  a  strong  and  healthy  child,  without  a  trace  of  adenoids 
<and  brought  up  on  the  most  hygienic  principles,  may  develop  an  attack 


372  Chapter   XXXIII. 

from  being  out  on  a  cold  and  windy  day  and  inhaling  germ-laden  dust, 
that  of  wood  pavement  being  particularly  irritant  to  mucous  membranes. 
At  all  ages  the  bulk  of  the  cases  are  due  to  direct  infection  from  some  one 
already  suffering  with  a  "  cold  in  the  head."  The  symptoms  and  signs 
are  too  well  known  to  need  description.  It  frequently  starts  in  the  throat, 
and  extends  upwards.  Fever  is  often  marked  in  babies  at  the  onset. 
Extension  may  take  place  to  the  eyes,  lachrymal  ducts  and  the  various 
nasal  sinuses.  Earache  and  deafness  are  common.  Alimentary  disturbance 
and  pulmonary  affections  arise  from  the  fever,  or  by  direct  extension. 

Usually  the  disease  runs  its  course  in  about  a  week  and  clears  up 
completely.  Often  it  leaves  behind  a  certain  amount  of  congestion  of  the 
mucosa,  a  tendency  to  recurrence,  and  the  development  of  lymphoid 
hypertrophy  as  the  result  of  repeated  attacks.  Occasionally  a  vasomotor 
type  is  seen,  in  which  profuse  watery  discharge  and  frequent  sneezing  per- 
sist for  a  few  hours  up  to  a  day  or  so.  Nasal  catarrh  must  be  regarded 
seriously  in  the  newborn  and  in  delicate  infants,  for  it  is  apt  to  end  in 
fatal  bronchitis,  atelectasis,  or  even  sudden  death. 

Treatment  is  more  essential  in  infancy  than  in  later  life.  Keep  the- 
child  in  bed  in  a  warm  room,  at  60-70°  F.,  and  have  the  air  moistened 
in  dry  weather  by  a  bronchitis  kettle.  Place  a  pledget  of  absorbent  wool, 
soaked  in  0-001  per  cent,  adrenalin  solution,  in  each  nostril  alternately  for 
2  or  3  minutes.  It  may  be  repeated  every  3  or  4  hours  in  bad  cases,  before 
feeding.  The  introduction  of  a  little  borated  vaseline  into  the  nares 
induces  sneezing  and  clears  away  mucus.  Apply  to  the  edges  of  the  nose 
and  to  the  upper  lip,  to  prevent  excoriation,  cold  cream  or  an  ointment  of 
boric  acid  gr.  20,  salicylic  acid  gr.  3,  vaseline  oz.  \ .  For  crusts  use  weak 
white  precipitate  ointment.  Other  topical  applications,  instead  of  adrenalin,, 
are  chloral  hydrate  gr.  5-10,  or  menthol  gr.  2-5,  in  olive  oil  oz.  J  ;  menthol 
gr.  1,  camphor  gr.  1,  liquid  albolene  oz.  1.  It  may  be  necessary  to  insert 
a  soft  rubber  catheter  in  each  nostril  to  keep  the  passage  open.  In  the 
later  stages,  when  the  discharge  is  chronic  and  purulent,  the  adrenalin 
application  is  followed  by  a  drop  of  0-5-1-0  per  cent,  solution  of  silver- 
nitrate  into  each  nostril ;  or  by  painting  the  mucosa  with  a  1-2  per  cent, 
solution,  after  washing  away  mucus  with  an  alkaline  lotion. 

Small  doses  of  aspirin  or  salicin,  mild  diaphoretics,  and  a  dose  of 
grey  powder  or  calomel  are  also  needed.  The  diet  must  be  light  and 
digestible.  Strong  infants  can  be  starved  temporarily,  say  for  24  hours^ 
and  at  any  rate  they  need  not  be  pressed  to  take  food.  Feeble  infants, 
must  be  fed,  by  gavage  if  necessary,  and  often  require  alcohol  and  strych- 
nia. Older  children  are  treated  on  the  same  lines.  A  hot  mustard  foot-bath,, 
hot  diaphoretic  drink  and  Dover's  powder  may  cut  short  an  attack. 
Inhalations  of  turpentine,  ol.  pini  sylvestris,  ol.  eucalypti,  formaldehyde 
and  menthol,  or  menthol  and  camphor  with  eucalyptus  oil  can  be  used. 
Protargol,  10  per  cent.,  may  be  sprayed  or  painted  on  the  nasal  mucosa 


The   Nose    and   Accessory    Sinuses.  373 

once  or  twice  in  the  early  stages.  Borated  vaseline,  10-20  per  cent., 
snuffed  up  into  the  nose,  which  is  then  blown  at  the  end  of  10  minutes, 
is  also  useful.  In  blowing  the  nose,  only  one  nostril  should  be  closed  at  a 
time.  Snuffs  are  inadvisable  for  children,  and  douching  is  rarely  necessary, 
though  undoubtedly  it  can  be  used  with  great  benefit  if  the  child  will  submit 
to  the  treatment.      Vaccine  treatment  is  only  on  trial. 

Nasal  lotions  or  Collunaria  are  applied  by  spray,  medicine  dropper, 
syringe,  irrigation,  brush,  absorbent  wool,  or  probe  and  cotton.  Plain 
water,  strong  antiseptics  and  astringents  must  not  be  used,  except  silver 
nitrate  as  already  mentioned.  Order  lotions  in  such  strength  as  to  render 
•dilution  with  twice  the  amount  of  hot  water  necessary,  for  they  must  be 
used  warm.  If  ordered  at  the  required  strength,  the  bottle  must  be  stood 
in  warm  water  until  the  temperature  of  the  lotion  reaches  90°  F.  Up 
to  the  third  year  the  lotion  is  dropped  into  the  nostrils  with  the  child 
on  its  back.  Syringing  or  irrigation  may  be  used  for  older  children,  as  long 
as  it  is  not  done  with  sufficient  force  to  drive  infection  up  the  Eustachian 
tubes. 

Syringing. — Use  a  glass  syringe  of  h  oz.  capacity,  and  cover  the  nozzle 
with  a  piece  of  soft  rubber  tubing  for  insertion  into  the  nostril  to  prevent 
injury.  Place  the  child  on  its  back  with  the  head  turned  to  one  side. 
Stand  behind  the  head  and  syringe  through  the  upper  nostril,  allowing  the 
rluid  to  flow  out  through  the  lower  nostril  or  the  open  mouth.  Or  the 
child  may  be  in  the  sitting  posture  with  the  head  well  forward  and  a  basin 
under  the  chin.  For  older  children  a  small  rubber  ball  syringe  can  be 
used.  The  stream  is  directed  along  the  floor  of  each  nostril  alternately, 
while  the  child  breathes  deeply  through  the  mouth.  Irrigation  is  inadvis- 
able for  children  under  4  years  of  age,  and  very  little  force  must  be  exerted. 

The  chief  nasal  lotions  are  :  (1)  Normal  saline  ;  (2)  Dobell's  solution  : 
sod.  bicarb,  dr.  1,  sod.  biborat.  dr.  1,  glyc.  ac.  carbol.  dr.  2  (or  Listerine 
•dr.  4),  aqua  ad  oz.  10  ;  (3)  Equal  parts  of  common  salt,  bicarbonate  and 
biborate  of  soda,  dr.  1  to  the  half  pint  of  water  ;  (1)  One  part  each  of  sod. 
bicarb.,  sod.  biborat.,  pot.  chlorat.  and  2  parts  of  white  sugar,  dr.  1-2  to  the 
half  pint  of  water.  As  an  astringent  lotion  use  sulphocarbolate  of  zinc, 
grs.  5  to  the  ounce,  by  spray  or  dropper  ;  or  hazeline  20  drops  to  the  ounce. 

Rhinitis  due  to  Adenoids  causes  a  chronic,  irritating,  mucoid  discharge, 
sometimes  muco-purulent  and  sanious,  occasionally  unilateral.  It  may  be 
continuous,  but  more  often  varies  from  time  to  time.  Discharge  and 
excoriation  of  the  external  nares  may  be  the  only  signs  of  adenoids.  It  is 
really  a  simple  chronic  rhinitis  or  post-nasal  catarrh,  a  variety  of  snuffies, 
often  occurring  in  acute  and  recurrent  attacks.  Epistaxis,  eczema,  impetigo 
and  swelling  of  the  upper  lip  are  not  infrequent  complications.  In  its  more 
advanced  form  the  affection  involves  all  the  nasal  mucosa,  especially  that 
of  the  inferior  turbinals,  and  is  known  as  Hypertrophic  Rhinitis.  This 
induces   chronic   catarrh   and   bilateral   nasal   stenosis.      Salt   and   water 


371  Chapter  XXXIII. 

is  used  to  keep  the  nose  clean.  The  galvano-cautery  is  useful,  and  pendulous 
masses  can  be  removed  by  snares.  Sometimes  it  is  necessary  to  excise 
the  inferior  turbinals. - 

Acute  purulent  rhinitis  of  infancy  is  set  up  by  infection  at  birth  by 
gonorrhoeal  or  leucorrhoeal  discharge.  It  comes  on  a  day  or  two  after 
birth  with  redness,  swelling  and  purulent  discharge,  and  prevents  sucking. 
In  later  childhood  it  may  be  also  due  to  pneumococcal  infection  or  measles. 
It  is  treated  by  alkaline  lotions  and  painting  with  silver  nitrate  solution, 
1  per  cent.,  or  other  silver  compound. 

Snuffles  is  a  symptom,  but  the  name  is  generally  used  for  the  rhinitis 
which  occurs  in  congenital  syphilis.  It  must  not  be  assumed  that  every 
baby  with  snuffles  has  got  syphilis,  for  it  may  be  due  to  any  of  the  numerous 
causes  of  nasal  catarrh.  The  syphilitic  type  comes  on  later  in  babyhood 
than  the  acute  purulent  rhinitis  of  infancy,  or  the  acute  coryza  apt  to  occur 
in  the  newborn.  It  generally  begins  in  2  or  3  weeks,  and  there  is  a  family 
history  or  other  evidence  of  syphilis  obtainable.  The  inflammation  is  sub- 
acute, chronic  and  persistent,  with  muco-purulent  discharge,  nasal  obstruc- 
tion, thickening  of  the  mucosa  and  the  formation  of  crusts  on  the  top  of 
raw  mucous  membrane.  It  may  be  acute,  and  followed  by  sloughing  of  the 
mucosa  and  necrosis  of  bone.  In  later  childhood  the  disease  takes  the 
form  of  a  gummatous  periostitis  and  necrosis  of  cartilage  and  bone, 
ulceration  and  ozsena.    Use  yellow  oxide  of  mercury  ointment,  1  in  8. 

Foreign  bodies  are  the  chief  cause  of  a  unilateral  discharge,  which 
varies  in  character  more  with  the  nature  of  the  object  than  the  duration 
of  its  presence  in  the  nose.  At  first  it  merely  causes  a  little  mechanical 
irritation,  perhaps  none  at  all  if  it  is  a  smooth  bead  or  button.  Frequently 
the  discharge  is  chronic,  profuse,  muco-purulent  or  purulent,  often  blood- 
stained, and  excoriates  the  nares.  The  foreign  body  is  nearly  always  in  the 
inferior  meatus.  A  recently  inserted  smooth  one  can  often  be  evacuated 
by  exciting  sneezing,  or  getting  the  child  to  blow  strongly  through  the 
nose,  with  the  unblocked  nostril  compressed.  If  this  fails,  apply  cocaine 
as  an  astringent  and  anaesthetic,  stand  behind  the  child,  and  push  a  probe 
or  director  gently  along  the  floor  of  the  nose,  displacing  the  foreign  body 
upward.  Then,  using  the  margin  of  the  floor  as  a  fulcrum  for  the  instru- 
ment, push  the  object  upward  and  forward,  and  it  will  frequently  glide 
forward  and  out.  A  general  anaesthetic  may  be  needed.  Subsequently 
apply  an  alkaline  mildly  disinfectant  lotion. 

Myiasis  (maggots)  is  due  to  the  meat  fly,  musca  vomitaria,  laying  its 
eggs  in  a  fold  of  mucous  membrane.  It  sets  up  acute  rhinitis,  which  may 
end  in  ulceration,  perforation  of  the  septum  and  even  foetid  atrophic  rhinitis. 
The  maggots  can  be  killed  by  chloroform  vapour,  or  the  insertion  of  a 
warm  oily  fluid,  which  suffocates  them  by  blocking  up  the  pores  or  stigmata 
of  the  respiratory  system.  They  are  then  syringed  out.  Nasal  polypus, 
mucous  or  fibrous,  is  rare.     It  causes  unilateral  obstruction  and  serous 


The   Nose  and    Accessory  Sinuses.  375 

discharge  ;  sometimes  bilateral  symptoms  and  headache,  sneezing,  reflex 
cough  and  asthma.  It  is  removed  by  snare  or  forceps.  Only  about  8  cases 
of  tuberculous  disease  are  on  record.  It  may  produce  a  large  tumour  of 
granulation  tissue,  simulating  sarcoma,  and  ulceration  and  destruction  of 
the  cartilaginous  septum.  It  is  diagnosed  by  microscopical  examination, 
and  treated  by  curettage.  Fibrinous  or  membranous  rhinitis  is  almost 
always  due  to  diphtheria  (q.v.).  Rhinitis  caseosa  is  rare  and  generally 
unilateral.  It  is  probably  a  sequel  of  chronic  suppuration  and  retention  of 
pus,  with  subsequent  changes  in  the  pus  rendering  it  caseous,  putty-like 
and  foetid.  It  differs  from  tuberculous  disease  in  the  absence  of  tubercle 
bacilli,  and  from  choleastoma  in  its  freedom  from  cholesterin.  Atrophic 
rhinitis  is  almost  unknown  under  12  years  of  age.  It  has  ensued  on  myiasis 
and  congenital  syphilis.  Cartilaginous,  sarcomatous  and  other  tumours 
are  very  uncommon. 

General  Diagnosis. — Examination  is  difficult  in  the  young,  because  of 
the  small  size  of  the  nose  and  the  nervousness  of  the  child.  Elevation  of 
the  tip  of  the  nose,  and  lifting  the  ala  upward  and  outward  with  a  probe 
often  give  a  good  view  of  the  inferior  meatus,  and  enable  a  diagnosis  to  be 
made  of  foreign  body,  sinus  disease,  diphtheria,  etc.  A  mirror  and 
speculum  are  frequently  needed.  A  history  of  the  insertion  of  a  foreign 
body,  exposure  to  the  infection  of  acute  coryza,  influenza,  measles  or 
diphtheria,  or  evidence  of  congenital  syphilis  is  of  much  assistance. 
Chronicity  of  discharge  favours  adenoids  or  syphilis,  and  a  prolonged 
duration  suggests  the  presence  of  a  foreign  body.  Thick  muco-pus  generally 
means  adenoids  or  syphilis.  A  blood-stained  discharge  is  most  commonly 
due  to  syphilis,  diphtheria,  or  foreign  body.  Pus  and  blood  may  be 
present  in  tuberculous  disease.  Pure  liquid  pus  is  sometimes  due  to 
foreign  body,  more  often  to  sinusitis.  In  atrophic  rhinitis  the  nasal  cavity 
is  large,  the  mucosa  atrophied,  the  discharge  mucoid  and  watery,  large 
brownish  or  greenish-grey  crusts  are  formed,  and  there  is  distinct  ozsena. 
In  rare  instances  a  profuse  watery  discharge  is  due  to  the  escape  of 
cerebrospinal  fluid. 

General  treatment. — The  prevention  of  rhinitis  depends  on  general 
hygiene,  judicious  hardening,  proper  diet  and  clothing,  and  the  avoidance 
of  exposure  to  infection.  The  last  precaution  is  of  the  utmost  importance 
in  the  newborn,  during  the  first  year  of  life,  and  for  the  weak  and  delicate. 
Cleanliness  is  the  chief  feature  in  the  treatment  of  all  nasal  affections. 
Alkaline  lotions  are  used  to  dissolve  mucus  ;  mild  antiseptics  are  added 
if  the  discharge  is  offensive  ;  and  any  local  cause,  such  as  adenoids  or  a 
foreign  body,  must  be  removed.  For  suggestions  refer  to  the  treatment 
of  acute  coryza. 

Epistaxis  is  uncommon  in  infancy.  It  may  occur  in  the  hemorrhagic 
disease  of  the  newborn,  sepsis  or  congenital  syphilis.  The  ordinary 
type  of  epistaxis  takes  place  from  a  vein,  generally  in  the  mucosa  over  the 


376  Chapter   XX XI II. 

cartilaginous  septum  or  any  part  of  the  anterior  nares.  It  is  more  common 
in  boys  than  girls.  The  latter  are  most  subject  to  it  at  puberty.  The 
predisposing  factors  are  those  which  lead  to  deficient  vascular  tone  and 
alterations  in  the  coagulability  of  the  blood.  A  few  cases  are  due  to 
general  plethora.  Others  result  from  local  injury  or  nasal  affections. 
It  may  occur  at  the  onset  or  in  the  course  of  fevers,  such  as  typhoid, 
measles,  scarlatina,  pneumonia,  and  the  malignant  types  of  all  specific 
fevers  ;  during  diphtheria  ;  in  blood  diseases,  e.g.,  anaemia,  leukaemia, 
purpura,  scurvy  and  haemophilia  ;  and  in  the  paroxysms  of  pertussis. 
The  rheumatic  diathesis  is  a  predisposing  cause.  Obstructive  and  con- 
genital morbus  cordis  may  induce  it,  through  causing  passive  venous 
congestion.  Stooping  and  tight  collar  bands  may  accentuate  or  start  an 
attack.  Often  it  follows  mental  or  physical  excitement  or  sudden  change 
in  temperature  from  heat  to  cold.  It  is  most  common  in  hot  muggy 
weather.  A  family  type,  associated  with  multiple  telangiectases  of  the 
skin  and  mucous  membranes,  not  connected  with  haemophilia,  is  also 
recognised  in  later  life. 

Bleeding  is  the  first  sign,  but  it  may  be  preceded  by  a  feeling  of  fulness 
in  the  head.  It  is  unilateral,  drop  by  drop,  variable  in  amount,  and  rarely 
enough  to  cause  grave  anaemia  or  death.  It  may  be  overlooked  through 
the  blood  being  swallowed. 

In  simple  cases  the  bleeding  is  a  trivial  matter.  If  recurrent,  usually 
about  puberty,  it  produces  the  usual  signs  and  effects  of  loss  of  blood. 
At  the  onset  of  typhoid  fever  it  is  unimportant,  but  it  is  a  bad  sign  in  late 
stages  of  diphtheria,  and  generally  an  indication  of  severity  in  the  course 
of  specific  fevers  and  in  blood  diseases. 

Preventive  treatment  consists  in  toning  up  the  system  generally  by 
fresh  air,  cold  baths,  exercise  and  general  hygiene.  Tight  bands  round  the 
neck  must  be  avoided.  The  bowels  of  the  plethoric  must  be  kept  freely 
open  with  salines.  In  these  children  no  other  measures  are  needed.  A 
glass  of  milk  on  waking  in  the  morning  sometimes  prevents  the  recurrent 
attacks  which  occur  in  children  at  puberty. 

Treatment  of  an  attack. — Compress  the  nose  with  the  finger  and  thumb, 
the  patient  being  in  a  sitting  posture  with  the  arms  raised  behind  the 
head.  Discourage  sniffling  and  nose-blowing.  Syringe  clot  away  with 
tepid  water,  and  make  the  child  breathe  deeply  through  the  nose.  Reflex 
constriction  of  the  arteries  supplying  the  mucosa  can  be  induced  by  a 
cold  key,  or  similar  object,  put  down  the  back  of  the  neck,  and  ice  or  some 
cold  substance  in  the  mouth.  Alternate  douching  with  hot  and  cold 
water  may  be  needed.  Loosen  the  clothes  round  the  neck.  Always  look 
for  the  bleeding  spot  and,  if  it  is  seen,  touch  it  with  caustic,  chromic  acid, 
pure  carbolic,  or  the  actual  cautery.  Mild  local  astringents,  such  as 
diluted  lemon  juice  and  tannic  acid,  and  gauze  soaked  in  hydrogen  per- 
oxide, 5  volume  strength,  are  often  useful.     Adrenalin  applications  are 


The   Nose    and   Accessory  Sinuses.  377 

generally  followed  by  vascular  dilatation  and  recurrence.  A  simple 
plug  of  gauze  or  wool  inserted  for  an  inch  within  the  nostril,  and  lateral 
pressure  with  the  finger  on  the  ala,  is  efficacious.  Astringent  powders 
are  unsatisfactory,  for  they  induce  sneezing.  Should  all  other  methods  fail, 
plug  the  anterior  and  posterior  nares  by  the  insertion  of  strips  of  gauze 
along  the  floor  of  the  nasal  cavity  until  the  nose  is  completely  plugged. 
Remove  it  in  24  hours.  Syringe  with  weak  carbolic  lotion  if  there  is  any 
bleeding,  and  insert  another  plug.  Drugs  internally  are  of  little  value. 
Calcium  salts  may  be  tried. 

Acute  Sinusitis  is  often  overlooked  and  regarded  as  part  of  acute 
rhinitis.  Chronic  cases  attract  attention  by  the  discharge  of  pus  from 
the  nose,  usually  from  one  side.  The  pus  may  be  swallowed  and  give 
rise  to  dyspeptic  symptoms  only.  Empyema  of  the  antrum  is  more 
common  than  empyema  of  the  frontal  sinus,  but  both  are  infrequent.  The 
antrum  can  be  distinguished  at  birth.  It  has  dental,  nasal  and  orbital 
walls,  and  is  situated  just  above  the  alveolus  of  the  first  pre-molar  tooth, 
and  a  little  below  the  infra-orbital  groove.  Inflammation  may  spread 
from  it  to  the  nasal  cavity.  Even  at  the  age  of  15  days  it  has  given  rise 
to  marked  proptosis  of  sudden  onset  and  the  subsequent  discharge  of 
thick,  odourless,  pneumococcal  pus  through  the  nose,  the  babe  soon 
recovering  (Beauvois).  In  the  case  of  a  boy,  9  years  of  age,  the  onset  was 
with  vomiting,  fever,  and  symptoms  suggestive  of  gastric  disturbance. 
On  the  third  day  the  temperature  was  104-6°  F.,  tongue  foul,  and  breath 
offensive.  Considerable  discharge  took  place  during  the  night,  with 
profuse  sweating  and  fall  of  temperature,  rising  again  in  the  morning  to 
104°  F.  The  course  of  the  case  suggested  a  general  nasal  infection,  and 
bilateral  otitis  media  ensued,  ending  in  satisfactory  recovery.  The 
diagnosis  of  sinusitis  generally  depends  on  localised  pain  and  a  discharge 
of  pus,  which  can  sometimes  be  actually  seen  exuding  from  the  antrum 
-and  on  transillumination.  An  alkaline  antiseptic  douche  should  be  used 
gently  and   fomentations  applied  externally.    Operation  may  be  needed. 

Osteomyelitis  or  Osteitis  of  the  Upper  Jaw,  sometimes  called  maxillary 
and  orbital  periostitis  or  phlegmon  of  the  orbit,  is  often  erroneously 
described  as  empyema  of  the  antrum.  It  is  said  to  resemble  a  similar 
affection  in  adults,  though  in  them  it  is  by  no  means  certain  that  the 
disease  is  a  primary  antral  affection.  There  is  strong  evidence  that  it  is 
due  to  injury  or  infection,  and  that  it  is  an  osteomyelitis  of  the  superior 
maxilla.  Probably  in  infants  it  is  sometimes  secondary  to  inflammation 
•of  the  dental  sac.  The  superior  maxilla  in  infancy  is  spongy  throughout 
and  contains  many  dental  sacs.  The  antrum  is  very  small,  and  an  empyema 
is  more  likely  to  discharge  through  the  nose  than  to  make  its  way  through 
the  fairly  thick  bone  into  the  soft  tissues  of  the  cheek  and  a  dental  sac. 

In  many  instances  no  cause  can  be  found.  Some  cases  are  due  to 
injury  at  birth  by  pressure  of  forceps  or  on  the  pubic  arch,  and  others  to 


378  Chapter   XXXIII. 

infection.  Probably  the  infection  starts  in  the  alveolus,  extends  to  the- 
dental  sac,  and  then  to  the  bone.  It  may  begin  in  the  nose  or  by  way  of  the- 
lachrymal  duct,  secondary  to  gonorrhceal  conjunctivitis.  The  spongy 
bone  affords  a  ready  means  of  spread.  The  dental  sac  of  the  first  molar- 
is  large  and  prominent,  and  likely  to  be  affected  early.  Eupture  leads  to 
extrusion  of  the  tooth  and  the  formation  of  sinuses. 

Brown  Kelly  (1904)  states  that  out  of  15  collected  cases,  9  started 
at  8-21  days  after  birth,  and  6  at  1-9  months.  The  early  origin  is  strongly 
suggestive  of  injury  during  labour.  At  the  onset  there  may  be  no  special 
symptoms,  or  the  child  is  feverish,  cries  constantly  and  may  have  con- 
vulsions. Almost  always  there  are  swelling  and  redness  of  the  eyelids  on 
the  affected  side,  sometimes  enough  to  cause  closure  of  the  lids  ;  occasion- 
ally conjunctivitis,  chemosis  and  exophthalmos.  The  swelling  may 
extend  to  the  naso-labial  fold.  The  cheek  is  swollen  and  the  hard  palate- 
bulges.  In  2-3  days  an  abscess  forms  below  the  inner  angle  of  the  eye,  and 
eventually  bursts  externally  through  the  alveolus  or  into  the  lachrymal 
sac.  Simultaneously  there  is  a  purulent  discharge  from  the  nose  on  the- 
same  side,  increased  by  pressure  on  the  sub-orbital  swelling.  Examination 
of  the  mouth  shows  bulging  of  the  hard  palate,  swelling  of  the  alveolus,  and 
probably  a  partially  erupted  canine  or  molar  tooth  whose  removal  gives 
free  exit  to  pus.  A  probe  can  then  be  passed  into  a  cavity,  which  is 
generally  mistaken  for  the  antrum  and  is  really  a  dental  sac,  and  it  may 
impinge  on  bare  bone.  Fluid  injected  into  the  cavity  may  escape  through 
the  nose.    Sometimes  the  alveolus  is  primarily  and  severely  affected. 

Gradually  the  dead  bone  separates,  sequestra  are  discharged,  the- 
secretion  dries  up,  and  the  sinuses  close.  The  illness  may  be  much  pro- 
longed because  of  the  slow  separation  of  dead  bone,  and  may  end  fatally 
from  inanition  or  sepsis,  with  multiple  pyaemic  abscesses,  purulent  pleurisy 
and  pericarditis.  Quite  one-fourth  of  the  patients  die.  The  entire  superior 
maxilla  may  be  necrosed. 

It  may  simulate  an  alveolar  abscess.  Usually  it  starts  in  the  anterior 
surface  of  the  maxilla,  and  the  nasal  discharge  appears  later  or  not 
at  all.  All  cases  show  pathological  changes  in  the  mouth,  either  a  sinus  or 
bulging  of  the  hard  palate. 

Treatment  consists  in  free  evacuation.  Make  an  opening  in  the 
alveolus,  canine  fossa,  or  where  the  abscess  points,  and  enlarge  any  sinus 
which  has  formed.  Syringe  regularly.  Guard  against  the  passage  of 
pus  into  the  mouth,  to  lessen  absorption  and  general  infection.  Radical 
operations  are  unnecessary,  usually  unsatisfactory  and  deforming. 


CHAPTER    XXXIV. 

LARYNGEAL  AFFECTIONS. 

The  Larynx  — Examination  —  Croup  —  Laryngitis  Stridulosa  —  Catarrhal, 
Membranous  and  Chronic  Laryngitis — (Edema  Glottidis  —  Congenital 
Laryngeal  Stridor — Neiv  Growths. 

The  infantile  larynx  is  small  and  yielding.  Its  superior  orifice  is 
bounded  by  the  epiglottis,  the  artytenoids,  and  the  ary-epiglottic  folds. 
These  folds  are  readily  sucked  in  on  deep  inspiration,  becoming  approxi- 
mated and  causing  inspiratory  stridor.  The  thyroid  cartilage  is  almost 
semicircular  in  transverse  section.  Up  to  the  fourth  year,  and  notably  in 
the  newborn,  the  cricoid  plate  is  inclined  posteriorly.  Growth  is  rapid  at 
puberty. 

Examination. — For  many  reasons  the  examination  of  the  larynx 
is  difficult.  Certain  anatomical  peculiarities  are  obstructive.  The  frsenum 
linguae  is  short,  and  up  to  the  age  of  three  years  interferes  with  traction  of 
the  tongue.  The  vertical  measurement  of  the  mouth  and  fauces  is 
relatively  very  short,  so  that  the  uvula  disappears  behind  the  base  of  the 
tongue.  The  soft  palate  is  more  horizontal  than  in  the  adult,  and  the 
posterior  wall  of  the  pharynx  slopes  more  backward  ;  the  angle  of  the 
head  and  spine  is  less  acute.  These  peculiarities  are  favourable  to  Kirstein's 
method  of  examination.  The  epiglottis,  instead  of  being  spread  out,  is 
curved  and  folded  on  itself,  so  that  it  forms  a  protective  hood  over  the 
vestibulum  laryngis,  and  almost  conceals  the  short  vocal  cords.  Voluntary 
or  reflex  spasm  of  the  pharynx  or  larynx,  or  the  copious  secretion  of  mucus, 
may  render  the  view  impossible.  An  older  child  may  refuse  to  open  the 
mouth,  resist  traction  on  the  tongue,  does  not  readily  understand  and  carry 
out  directions  as  to  breathing  and  phonation,  holds  its  breath,  retches 
and  secretes  mucus  copiously.  With  patience  and  training  it  is  possible 
to  overcome  these  difficulties. 

Lack's  method  requires  depression  and  traction  of  the  tongue,  thus 
drawing  the  epiglottis  forward.  No  instrument  and  no  force  are  needed. 
The  infant  is  supported  in  the  usual  position.  The  left  index  finger  is 
placed  in  the  mouth  and  hooked  round  the  hyoid  bone,  pulling  it  forward. 
The  finger  acts  as  a  tongue  depressor  and  the  knuckle  as  a  gag,  while  the 
left  thumb  under  the  chin  steadies  the  head.  A  small  mirror  is  used.  The 
younger  the  infant,  the  less  is  the  resistance  and  the  easier  the  examination. 
A  suitably  bent  spatula  must  be  used  for  older  children  with  teeth. 


380  Chapter  XXXIV. 

Escat  recommends  the  use  of  a  light  tongue  depressor,  merrythought 
shaped,  terminating  in  two  blunt  prongs  curved  so  as  to  fit  into  the  base 
of  the  tongue,  one  fork  lodging  in  each  sinus  pyriformis  on  the  side  of  the 
laryngeal  orifice.  It  controls  the  tongue  and  pulls  forward  the  larynx 
from  the  posterior  pharyngeal  wall.  A  small  mirror,  mounted  on  a 
short  stem,  is  used  to  push  back  the  uvula  and  the  posterior  pharyngeal 
wall.  It  is  a  "  forced  "  examination.  The  child  must  be  rolled  up  in  a 
blanket,  and  the  mouth  may  have  to  be  forcibly  opened.  Cocaine  is 
necessary  ;   sometimes  a  general  anaesthetic  and  a  gag. 

In  Kirstein's  method  a  special  autoscope  is  used.  The  child's  head 
is  drawn  over  the  edge  of  the  table  and  held  by  an  assistant.  A  spatula  is 
directed  downward  to  press  the  tongue  forward,  and  the  autoscope  is  held 
in  the  left  hand.  The  head  is  raised  or  lowered  until  the  larynx  comes 
into  view.  Tubular  specula,  mounted  at  a  right  angle  on  strong  handles, 
are  more  useful.  If  the  child  sits  upright  with  the  head  thrown  far  back, 
such  a  speculum  can  be  passed  without  much  difficulty  or  discomfort,  after 
thorough  cocainisation  ;  or  under  anaesthesia  in  the  supine  or  lateral 
position.  Valuable  information  can  be  sometimes  obtained  by  external 
examination,  internal  palpation  and  X-rays. 

Croup  should  never  be  used  as  the  name  for  a  special  disease,  for  it 
merely  indicates  a  group  of  symptoms  due  to  several  causes.  "  True  " 
croup  is  an  acute  laryngitis  of  a  simple  or  membranous  type,  generally 
diphtheria.  "  False  "  or  "  spasmodic  "  croup  is  either  laryngospasm  or 
laryngitis  stridulosa.  The  symptoms  of  croup  are  hoarseness,  inspiratory 
crowing  or  stridor,  cough,  dyspnoea  and  recession  of  the  soft  parts  of  the 
chest.  In  other  words  it  means  laryngeal  obstruction  due  to  catarrh,  with  or 
without  muscular  spasm,  to  membranous  exudation,  or  to  simple  spasm. 
The  cough  is  husky,  dry,  suppressed,  inefficient  and  stridulous. 

Laryngitis  stridulosa,  catarrhal  laryngeal  spasm,  spasmodic  laryngitis, 
spasmodic  or  catarrhal  croup. — There  is  little  doubt  that  this  is  nothing 
more  than  a  very  mild  type  of  catarrh,  with  secondary  adductor  laryngeal 
spasm,  which  is  especially  apt  to  occur  in  rachitic  infants,  and  those  with 
a  long  uvula,  enlarged  tonsils  or  adenoids,  and  a  neurotic  ancestry.  It  is 
infrequent  in  children  unless  it  has  previously  occurred  in  infancy.  The 
common  age  is  1-4  years,  and  boys  are  more  liable  to  it  than  girls.  The 
usual  history  is  that  the  child  has  a  slight  cold,  a  little  hoarseness  or  nasal 
catarrh,  perhaps  a  hollow,  barking  or  slightly  metallic  cough.  It  is  put 
to  bed,  and  wakes  up  in  a  few  hours  with  cough,  dyspnoea,  crowing  in- 
spiration, restlessness  and  alarm.  In  mild  cases  we  find  hoarseness,  croupy 
cough,  general  discomfort,  no  dyspnoea  and  perhaps  slight  fever.  In 
severe  ones  the  child  sits  up  in  bed  in  a  state  of  excitement,  terror  and 
urgent  dyspnoea,  struggling  for  breath.  There  is  loud  inspiratory  stridor, 
great  recession,  hoarseness,  stridulous  hoarse  or  metallic  cough,  laboured 
and  slow  breathing,  rapid  pulse,  and  a  temperature  of  99-101°  F.     Slight 


Laryngeal    Affections.  381 

cyanosis,  progressing  to  asphyxia,  may  be  present,  with  profuse  sweating, 
prostration  and  the  appearance  of  impending  death.  The  attack  lasts 
from  ^-3  hours,  ends  suddenly  or  subsides  slowly,  and  may  recur  on  the  next 
two  or  three  nights,  and  every  few  weeks  or  at  longer  intervals.  During 
the  day  the  child  is  quite  well  or  presents  a  little  hoarseness  and  cough,  and 
perhaps  stridor. 

Occasionally  the  child  goes  to  bed  apparently  quite  well.  Sometimes 
the  voice  is  clear,  although  stridor  is  marked.  Slight  catarrhal  sounds  may 
be  heard  in  the  chest  on  the  following  day.  Some  attacks  last  only  a  few 
minutes.  Although  the  attacks  may  be  very  alarming  they  are  rarely,  if 
ever,  fatal.  The  parents  must  be  warned  that  they  are  liable  to  recur, 
especially  after  indiscretions  in  diet  and  exposure  to  cold.  A  cold  bed- 
room, full  of  fog,  is  very  likely  to  induce  an  attack.  Few  cases  occur  after 
the  seventh  year. 

The  treatment  is  essentially  that  appropriate  for  simple  laryngitis, 
combined  with  that  for  laryngospasm.  For  immediate  relief  rely  on  hot 
applications  to  the  larynx,  a  hot  mustard  bath,  an  emetic  of  vin.  ipecac, 
dr.  1  or  pulv.  ipecac,  gr.  5  half  hourly  until  vomiting  is  induced,  and 
inhalations  of  steam.  Inhalations  of  amyl  nitrite  or  a  few  whiffs  of  chloro- 
form are  more  efficacious.  Whitla  recommends  vin.  ipecac,  vin.  antimon., 
syr.  scillae  aa  m.  10,  every  J  hour.  As  attacks  are  variable  in  duration 
and  sometimes  last  only  a  few  minutes  it  is  difficult  to  estimate  the  value 
of  the  medicine.  A  dose  of  bromide,  chloral  or  phenazone  at  bedtime 
acts  as  a  preventive.  Between  the  attacks  attend  to  the  general  health 
and  search  for  the  exciting  cause.  A  warm  dry  climate  is  the  most  suitable. 
Arsenic,  cod-liver  oil  and  belladonna  are  often  useful. 

Catarrhal  Laryngitis  varies  much  in  severity.  It  may  occur  at  any  age 
but  is  quite  infrequent  after  the  fourth  year  of  life,  for  the  child  is  hardier 
and  less  susceptible.  The  common  predisposing  causes  are  rickets,  bad 
hygienic  surroundings  and  confinement  in  hot,  ill-ventilated  rooms.  An 
attack  is  induced  by  the  conditions  liable  to  set  up  catarrh  of  the  respiratory 
mucosa,  e.g.,  damp,  cold  air,  irritant  vapours,  steam,  scalds  of  the  mouth, 
caustics,  dust  and  microbial  infections.  It  is  frequent  in  measles  and  less 
common  in  pertussis,  influenza,  typhoid  fever,  scarlatina  and  other 
infections. 

The  onset  is  more  or  less  acute.  After  a  scald  the  symptoms  come  on 
in  a  few  hours  or  almost  at  once.  In  infancy  the  symptoms  are  severe 
because  of  the  small  and  yielding  larynx.  The  oedema  of  the  mucous 
membrane  of  the  arytenoids,  upper  orifice  of  the  larynx  or  in  the  sub- 
glottic region,  produces  serious  obstruction  in  a  few  hours.  A  mild 
attack  may  pass  into  a  severe  one.  The  main  sign  is  the  inspiratory  diffi- 
culty in  breathing,  with  no  intermission  and  often  considerable  fever. 
The  temperature  ranges  from  101-105°  F.  Sometimes  the  symptoms 
are  limited  to  hoarseness,  partial  or  complete  loss  of  voice,  a  hard  cough 


382  Chapter   XXXIV. 

which,  is  worst  at  night,  pain  and  soreness  over  the  larynx  and  very  slight 
malaise.  Such  attacks  are  seen  in  older  children.  In  the  more  serious 
and  the  infantile  type  all  the  signs  of  laryngeal  obstruction  are  present.  The 
cough  is  constant,  harsh,  barking  or  stridulous.  Dyspnoea  is  inspiratory, 
mainly  paroxysmal,  and  exaggerated  at  night.  As  the  case  increases 
in  severity,  the  pulse  and  breathing  become  more  frequent  and  the  tem- 
perature higher.  Restlessness  is  excessive  and  the  child  throws  itself  all 
over  the  bed,  the  colour  turns  more  and  more  livid,  sweat  stands  out  on 
the  forehead,  recession  of  the  chest  becomes  extreme,  all  the  accessory 
respiratory  muscles  are  brought  into  play,  stridor  is  loud,  and  on  listening 
to  the  chest  little  or  no  vesicular  breathing  is  heard.  Dyspnoea,  cyanosis, 
pallor  and  prostration  may  be  as  severe  as  in  diphtheria.  Unless  relief 
is  obtained,  death  ensues  from  collapse,  cardiac  failure,  an  attack  of 
suffocation  and  cyanosis,  or  asphyxial  convulsions. 

The  duration  varies  from  1-6  weeks.  Severe  symptoms  subside  in  2-3 
days  ;  the  child  becomes  more  comfortable  and  falls  asleep  as  the  respira- 
tory obstruction  abates.  In  rare  instances  the  inspiratory  dyspnoea 
persists  for  weeks  without  any  paroxysmal  attacks.  The  chief  compli- 
cations are  spasm  of  the  glottis,  oedema  of  the  glottis,  collapse  of  the 
lungs  and  convulsions.  Catarrh  of  the  trachea  and  bronchi  is  common 
and  liable  to  end  in  broncho-pneumonia.     Recurrence  is  not  infrequent. 

It  is  often  impossible  to  be  certain  that  the  case  is  not  diphtheria. 
Chief  stress  must  be  placed  on  the  absence  of  signs  of  this  disease  in  the 
nose  or  fauces.  Laryngitis  is  generally  rapid  in  onset  and  not  accom- 
panied by  constitutional  disturbance,  beyond  that  due  to  the  dyspnoea. 
In  older  children  a  laryngoscopic  examination  may  settle  the  diagnosis. 
The  laryngitis  at  the  onset  of  measles  is  often  extremely  acute  in  onset 
and  development,  subsiding  with  the  appearance  of  the  rash.  The  presence 
of  buccal  spots  must  be  sought  for.  Laryngospasm  and  congenital  laryn- 
geal stridor  are  unlikely  to  be  mistaken  for  this  affection. 

The  prognosis  depends  on  the  age  and  strength  of  the  child,  the  degree 
of  rickets,  the  cause  and  severity  of  the  attack,  and  the  treatment.  The 
younger  the  child,  the  worse  is  the  outlook.  The  glottic  oedema,  so  often 
present,  is  almost  invariably  fatal  in  the  newborn.  Even  in  the  mildest 
cases  there  is  always  a  liability  to  fatal  spasm.  In  measles  the  child  is 
generally  out  of  danger  from  the  laryngitis  as  soon  as  the  rash  appears. 
Tracheotomy  affords  immediate  relief,  but  increases  the  gravity  of  the 
prognosis,  for  death  may  result  from  profuse  bronchial  secretion  and 
cyanosis,  pulmonary  collapse  and  broncho-pneumonia,  or  infection  of  the 
wound.  The  only  sequel  of  an  ordinary  attack,  untreated  by  operation, 
is  a  certain  degree  of  hoarseness  or  huskiness  and  stridor  for  about  2-3  weeks, 
and  in  rare  cases  persistent  throughout  life. 

Treatment. — The  mildest  cases  must  be  treated  with  care  and  watched, 
because  of  the  risk  of  spasm  and  oedema,  and  the  sudden  development  of  a 


Laryngeal    Affections.  383 

more  severe  type.  The  child  must  be  kept  in  bed,  in  a  warm,  well- 
ventilated  room,  fed  on  light  diet,  and  given  a  calomel  or  saline  purge. 
Apply  to  the  throat  frequent  hot  light  compresses  or  a  mustard  leaf.  An 
ice  bag  is  sometimes  more  efficacious  in  severe  cases  and  in  acute  oedema 
■due  to  scalds.  A  tent  or  a  half-tent  should  be  rigged  up  and  a  bronchitis 
kettle  used,  with  eucalyptus,  tr.  benzoin  co.,  creosote  or  turpentine  added 
to  the  water.  These  drugs  may  be  given  by  inhalation  at  100-120°  F., 
using  an  inhaler  with  a  large  face  piece.  An  emetic  may  be  given  to  a 
strong  lusty  child  and  chloroform  used  for  the  relief  of  spasm,  as  in  the 
treatment  of  laryngitis  stridulosa.  Preparations  of  antimony  and  ipecac- 
uanha are  often  given  in  frequent  small  doses,  but  on  the  whole,  I  prefer  a 
diaphoretic  and  diuretic  mixture.  If  the  skin  and  kidneys  act  freely  the 
symptoms  are  usually  relieved.  Bleeding  is  rarely  advisable.  For  high 
fever,  great  respiratory  distress  and  objections  to  operation,  a  couple  of 
leeches  can  be  applied  above  the  sternum.  Should  the  above  treatment 
fail,  recourse  must  be  had  to  intubation  or  tracheotomy.  In  all  doubtful 
severe  cases  it  is  advisable  to  give  a  dose  of  antitoxin.  If  the  child  has 
been  in  bed  for  at  least  an  hour  and  grave  obstruction  shows  no  sign  of 
yielding  to  treatment,  but  is  rather  getting  worse,  operate.  The  main 
indications  are  increase  in  the  fever,  frequency  of  the  pulse  and  breathing, 
restlessness,  stridor,  recession,  lividity,  pallor  and  prostration.  Should 
there  be  strong  evidence  in  favour  of  a  non-diphtheritic  type,  tracheotomy 
may  be  postponed  as  long  as  possible,  provided  the  doctor  is  on  the  spot 
and  able  to  open  the  trachea  at  a  moment's  notice  in  case  of  sudden  spasm. 
Intubation  is  satisfactory,  if  it  can  be  carried  out,  and  leaves  no  scar. 
The  method  is  described  in  the  chapter  on  diphtheria.  Failing  expertness 
in  intubating,  it  is  better  to  rely  on  tracheotomy,  although  the  subsequent 
risks  are  greater.  Tracheotomy  must  be  avoided,  if  possible,  in  girls 
who  may  have  to  wear  low-necked  dresses. 

In  cases  treated  without  operation  the  treatment  by  bed,  fomentations 
and  inhalations  must  be  continued,  until  practically  convalescent.  Subse- 
quently attend  to  preventive  measures.  Guard  against  chill,  damp  beds 
and  unwarmed  rooms.  Sponge  the  neck  daily  with  cold  water.  Remove 
adenoids  and  large  tonsils,  if  present.  Attend  to  the  general  health. 
Fresh  air  and  cold  bathing  are  most  beneficial. 

Membranous  Laryngitis  is  commonly  diphtheria  and  is  described  under 
that  head.  Occasionally  it  is  due  to  the  pneumococcus  or  streptococcus, 
or  to  scalds  and  caustics.  In  primary  laryngeal  diphtheria  the  diagnosis 
is  difficult,  because  of  the  slow  absorption  of  toxins  from  the  mucous 
membrane  of  the  larynx  and  the  preponderance  of  the  obstructive  laryn- 
geal symptoms  over  the  constitutional  ones.  The  signs  of  a  membranous 
laryngitis  are  like  those  of  the  catarrhal  type,  but  the  onset  is  more  gradual, 
the  course  more  steadily  progressive  and  the  fever  less  marked.  Hoarseness 
is  succeeded  by  loss  of  voice.     Dyspnoea  steadily  increases,  and  becomes 


384  Chapter  XXXIV. 

inspiratory  and  expiratory  in  character  ;  and  all  the  features  of  obstruc- 
tion are  added  to  an  increasing  pallor,  lividity  and  prostration.  Unless  the 
obstruction  is  relieved,  the  restlessness  passes  into  a  state  of  semi-stupor, 
coma,  and  death  from  exhaustion,  sometimes  preceded  by  fits.  Towards 
the  end  the  temperature  may  rise  rapidly  or  fall  below  normal. 

Some  cases  run  a  milder  and  more  chronic  course,  the  symptoms  being 
merely  indicative  of  laryngeal  catarrh,  with  little  fever  or  dyspnoea.  Even 
in  infants  I  have  known  such  attacks  to  last  for  weeks,  the  child  recovering 
after  coughing  up  membrane  or  after  tracheotomy.  Generally  in  infants 
death  results  in  a  day  or  two.  More  prolonged  cases  are  complicated  by 
extension  downwards  of  the  membrane,  and  tree-like  casts  of  the  whole 
bronchial  system  may  be  coughed  up,  as  in  fibrinous  bronchitis.  Broncho- 
pneumonia is  a  common  fatal  termination. 

The  membranous  type  has  to  be  diagnosed  from  other  forms  of  laryn- 
gitis, foreign  bodies  in  the  larynx,  capillary  bronchitis  and  broncho- 
pneumonia, and  from  retro-pharyngeal  abscess.  The  treatment  is  that  of 
diphtheria.  Calomel  fumigations  have  been  used,  when  antitoxin  is  not 
available  and  for  cases  due  to  other  organisms.  The  child  lies  down  in  a 
closed  tent  and  from  10-15  grs.  are  vapourised  every  1-3  hours.  The  danger 
of  fire  must  be  guarded  against. 

Chronic  Laryngitis  sometimes  follows  the  acute  form,  especially  when 
due  to  measles  or  diphtheria  ;  may  be  due  to  a  papilloma  or  foreign  body  ; 
sometimes  depends  on  bad  hygiene  ;  and  in  a  mild  form  is  the  result  of 
general  congestion  of  the  fauces,  secondary  to  adenoids  or  mouth-breathing. 
It  is  treated  on  general  principles,  and,  in  older  children,  by  astringent 
sprays,  inhalations  or  insufflations,  e.g.,  ac.  tannici  gr.  20,  glycerini  m.  90, 
aquae  ad.  oz.  1.  The  syphilitic  formis  described  in  the  chapter  on  congenital 
syphilis.  Tuberculous  laryngitis  is  practically  unknown  before  the  fourth 
year  and  rare  at  a  later  age.  It  has  occurred  although  the  lungs  were 
healthy,  but  is  generally  secondary  to  pulmonary  tuberculosis.  The  signs 
are  hoarseness,  cough,  and  muco-purulent  sputa  in  which  tubercle  bacilli 
may  be  found.  It  differs  from  the  syphilitic  type  in  the  greater  local 
sensitiveness,  more  discomfort  or  pain  on  cough  and  swallowing,  greater 
swelling  of  the  arytenoids  and  less  destruction  of  the  epiglottis.  Unless 
there  are  definite  lung  signs  it  is  usually  mistaken  for  syphilitic  ulceration. 
Laryngoscopic  examination  in  the  early  stages  shows  little  difference,  but 
local  tubercles  may  be  seen  and  the  process  is  more  superficial.  The  prog- 
nosis is  almost  hopeless,  and  the  treatment  the  same  as  in  adults. 

CEdema  Glottidis  is  either  serous  or  inflammatory.  It  is  induced  by  the 
stings  of  insects,  inhalations  of  steam  or  irritants,  foreign  bodies,  injury  to 
the  larynx,  laryngitis,  perichondritis,  faucial  affections  and  post-pharyngeal 
abscess.  Or  it  depends  on  nephritis,  morbus  cordis,  venous  congestion, 
the  effects  of  potassium  iodide,  and,  in  rare  instances,  angioneurotic 
cedema.     In  all  cases  the  ary-epiglottic  folds  are  infiltrated  with  effusion 


Laryngeal   Affections.  385 

and  form  diffuse  swellings,  which  block  the  upper  orifice  of  the  larynx. 
The  arytenoids  and  epiglottis  may  be  similarly  swollen.  In  serous  oedema 
the  swelling  is  pale  red  in  colour  ;  in  the  inflammatory  type  it  is  brighter 
red,  more  diffuse  and  involves  the  adjacent  structures. 

Symptoms  develop  with  great  rapidity  and  may  prove  fatal  in  a  few 
hours.  Sometimes  the  onset  is  preceded  by  tickling  in  the  throat,  pain  on 
swallowing,  alteration  in  the  voice  and  fever.  The  swelling  gives  rise  to 
great  inspiratory  dyspnoea,  stridor  and  attacks  of  suffocation.  Expiration 
is  stridulous  or  unaffected.  Pallor,  cyanosis,  restlessness,  rise  of  tempera- 
ture, and  increased  frequency  of  pulse  and  respiration  are  present.  Simple 
oedema  rarely  causes  the  pain,  dysphagia,  hoarseness  and  cough  of  the 
inflammatory  affection.  On  digital  and  laryngoscopic  examination  the 
swellings  are  found  in  approximation  near  the  base  of  the  tongue.  They  can 
be  seen  on  pulling  the  tongue  forward.  The  affection  may  be  mistaken  for 
diphtheria,  erysipelas  of  the  throat  or  asthma. 

For  true  oedema  apply  ice  externally,  give  ice  to  suck,  and  scarify  or 
make  multiple  local  punctures.  Inject  pilocarpin,  if  it  is  of  renal  origin. 
For  inflammatory  cases  adopt  like  measures,  and  leeches  or  tracheotomy 
if  necessary.     Attend  to  the  cause. 

Congenital  Laryngeal  Stridor  is  an  abnormality  of  respiration  which 
may  be  present  at  birth  but  is  more  usually  noticed,  or  comes  on  suddenly, 
during  the  first  few  days  of  life.  In  all  other  respects  the  child  seems 
healthy  and  the  naso-pharynx  is  normal.  It  varies  in  intensity  from  a 
purring,  crowing,  cackling,  grunting  or  harsh  croaking  inspiratory  sound 
up  to  distinct  stridor.  In  severe  cases  a  slight  noise  is  heard  on  expiration. 
The  maximum  intensity  is  at  the  end  of  inspiration  and  during  excitement 
it  may  terminate  in  a  "  crow  "  like  that  of  laryngospasm.  It  is  almost  alway 
absent  during  sleep.  In  one  case  under  my  care  it  persisted  to  a  slight 
extent.  It  is  worst  in  the  dorsal  position  ;  increased  by  catarrh  and  any 
cause  of  deeper  breathing  ;  and  there  is  often  a  certain  amount  of  recession 
of  the  soft  parts  at  the  root  of  the  neck,  the  epigastrium  and  even  the  lower 
ribs.  As  a  rule  there  is  neither  dyspnoea  nor  cyanosis  ;  possibly  dyspnoea 
indicates  a  complication.  In  one  instance  I  noted  frequent  attacks  of 
urgent  dyspnoea  and  inspiratory  stridor  for  which  no  cause  could  be  found. 
Vocal  utterance  is  clear,  crying  and  cough  are  unaffected,  and  the  vocal 
cords  are  normal. 

Pathology. — In  a  fatal  case  of  my  own,  and  in  5  out  of  8  collected  cases 
the  anatomical  state  was  practically  identical ;  so  too  in  cases  examined 
during  life.  The  epiglottis  is  abnormally  long  and  folded  longitudinally 
on  itself,  so  that  its  edges  are  approximated,  leaving  a  narrow,  median 
chink-like  slit.  It  curves  backwards  over  the  larynx  and  the  ary- 
epiglottic  folds  are  closely  approximated,  converting  the  upper  orifice  into 
a  mere  chink.  The  cartilages  of  Santorini  may  touch  each  other  and  the 
opening  of  the  larynx  may  be  smaller  than  normal. 

2c 


336  Chapter   XXXIV. 

The  infant's  larynx  is  normally  soft  and  collapsible,  the  epiglottis 
gutter-shaped,  and  the  ary-epiglottic  folds  are  drawn  together  during 
inspiration  and  narrow  the  orifice.  The  sucking  in  of-  these  folds  during 
inspiration  has  been  observed  by  Dundas  Grant  in  a  3-year  old  boy  with 
inspiratory  stridor  since  birth.  For  these  reasons  J.  Thomson  and  Logan 
Turner  have  argued  that  the  stridor  is  not  due  to  the  anatomical  defect 
and  that  it  is  simply  an  exaggeration  of  the  normal  state,  dependent  on 
defective  coordination  of  the  respiratory  movements,  a  stammering  of  the 
respiratory  muscles,  the  sound  being  due  to  imperfect  action  of  the 
abductors  and  aided  by  the  soft  yielding  character  of  the  structures  forming 
the  superior  orifice  of  the  larynx.  Similar  stridor  may  occur  during  recovery 
from  chloroform  narcosis,  during  excitement  and  on  sudden  deep  inspira- 
tion. Hence,  the  presence  of  a  congenital  deformity  is  not  essential  to  its 
production.  On  the  other  hand  there  is  no  evidence  of  abnormal  breathing 
from  this  supposed  incoordination  ;  and  during  anaesthesia  of  these  patients, 
breathing  is  regular  and  stridor  very  marked.  Furthermore,  it  is  a  con- 
tinuous stridor,  sometimes  persists  during  sleep,  has  been  noted  immediately 
after  birth  (Variot),  and  is  unassociated  with  other  evidence  of  incoordina- 
tion ;  and  definite  anatomical  peculiarities  have  been  found  in  the  third 
month  of  life  (Refslund). 

By  reason  of  the  anatomical  findings  it  has  been  ascribed  to  congenital 
deformity  of  the  superior  laryngeal  aperture  plus  flaccidity  (Sutherland  and 
Lack)  ;  malformation  of  the  larynx  ;  malformation  of  the  epiglottis  and 
superior  opening  of  the  larynx  ;  valvular  action  of  the  superior  laryngeal 
orifice  on  inspiration  ;  or  flabbiness  of  the  vocal  cords.  Possibly  more  than 
one  factor  is  concerned  in  its  production.  Post-mortem  evidence  strongly 
supports  the  anatomical  theory  and  until  typical  cases  are  found,  which 
present  no  such  changes  after  death,  we  must  regard  the  incoordination 
theory  with  suspicion. 

Thomson  and  Turner,  in  5  children  from  7-9  years  of  age,  found  the 
anatomical  condition  persistent  long  after  the  stridor  had  ceased.  The 
subsidence  of  the  stridor  is  probably  the  result  of  increase  in  size  of  the 
larynx.  Cases  in  which  the  stridor  begins  and  ceases  suddenly  may  be  due 
to  incoordination,  perhaps  affecting  the  vocal  cords  and  not  the  upper 
laryngeal  orifice,  the  rima  glottidis  remaining  closed  when  it  should  open 
for  inpiration  :  cf.  "  blue  fits  "  and  "  crowing  "  due  to  temper  in  neurotic 
children.  Stridor  has  been  ascribed  also  to  a  lax  epiglottis  (Dundas  Grant), 
vibration  of  a  flap  of  loose  mucous  membrane  on  the  summit  of  the  ary- 
tenoids (Brown  Kelly),  and  vibration  of  soft  structures  on  the  posterior  wall 
of  the  larynx,  the  arytenoids  and  folds  being  drawn  downward  (Paterson). 

Prognosis.— About  ten  fatal  cases  are  on  record  but  death  is  due  to 
intercurrent  disease,  possibly  caused  by  spasm  in  one.  The  stridor  may  last 
for  several  years.  As  a  rule  it  increases  in  loudness  for  a  few  months  and 
terminates  before  the' end  of  the  first  or  second  year  of  life,  perhaps  quite 


Laryngeal   Affections.  387 

suddenly.     The  malformation  persists  for  years,  though  the  stridor  ceases, 
but  may  recur  under  sudden  emotion. 

The  diagnosis  is  comparatively  easy.  It  must  not  be  confused 
with  the  noisy  breathing  of  laryngitis,  palatal  palsy  or  macroglossia. 
Laryngospasm  does  not  occur  before  the  third  month  of  life.  Adenoids 
and  other  forms  of  nasal  obstruction  are  the  main  cause  of  error.  The 
laryngeal  spasm  set  up  by  adenoids  increases  during  sleep,  during  feeding 
.and  on  closure  of  the  mouth,  ceases  under  chloroform,  and  may  be  associated 
with  severe  suffocative  attacks.  The  stridor  due  to  pressure  on  the  trachea 
is  usually  expiratory  and  associated  with  more  dyspnoea,  and  is  rarely 
•congenital.  Respiratory  or  laryngeal  spasm  sometimes  occurs  in  the 
newborn.  An  attack  of  crying  is  succeeded  by  crowing  inspiration,  apnoea 
.and  lividity.  The  initial  crow  may  be  absent.  These  attacks  may  prove 
fatal,  temporary,  or  persist  in  a  mild  form  for  some  months.  They  are  due 
to  glottic  spasm  or  of  the  nature  of  mild  laryngitis  stridulosa. 

Treatment  is  of  little  value.  The  child  must  be  protected  from  spasm, 
laryngitis  and  bronchitis.  Intubation  is  too  difficult  to  be  of  use.  Possibly 
tracheotomy  may  be  required  if  the  anatomical  state  is  extreme. 

New  Growths. — Sarcoma  is  rare.  Papillomata  are  not  uncommon. 
They  are  more  frequent  in  boys  than  girls.  About  25  per  cent,  are  con- 
genital. They  are  most  common  in  the  third  year  of  life,  and  may  arise  or 
develop  rapidly  after  laryngeal  catarrh.  They  are  single  or  multiple, 
variable  in  size,  pedunculated  or  sessile,  and  usually  on  the  true  vocal 
cords.  Sometimes  they  are  found  in  the  trachea,  immediately  below  the 
larynx,  and  may  set  up  tracheal  stenosis.  They  give  rise  to  the  symptoms 
of  chronic  laryngitis,  viz.,  hoarseness,  spasmodic  cough,  perhaps  loss  of 
voice,  and  sometimes  attacks  of  glottic  spasm.  Hoarseness  and  dyspnoea 
may  date  from  birth.  Later  on,  suffocative  attacks  and  dyspnoea  are  due 
to  obstruction  and  stenosis. 

Papilloma  must  be  suspected  in  all  cases  of  chronic  laryngitis,  and  a 
laryngoscopic  examination  made.  It  may  disappear  spontaneously,  be 
coughed  up  or  cause  sudden  death  from  spasm. 

Symmetrical  nodules  have  been  found  on  the  cords  in  cases  of  hoarse- 
ness, sometimes  congenital.  They  are  possibly  due  to  the  non-absorption 
of  the  embryonic  web  between  the  anterior  thirds  of  the  cords.  Unilateral 
ones  are  more  common  and  cause  huskiness.  They  should  be  left  alone  for 
they  may  disappear  at  puberty  or  cause  no  trouble. 

A  papilloma  can  be  removed  by  the  endo-laryngeal  method,  if  the 
child  is  tractable  and  the  surgeon  prepared  for  tracheotomy  in  case  of 
necessity.  Briining's  speculum  is  the  best  instrument.  Either  forceps 
or  a  wire  snare  is  used.  Tracheotomy  alone  is  sometimes  followed  by  com- 
plete disappearance  of  the  growth  and  recovery  of  the  voice.  If  it  fails, 
the  growth  is  removed  by  the  above  method  or,  as  a  last  resort, by  thyrotomy 


388  Chapter  XXXIV. 

or  laryngo-fissure  and  curettage.  This  greatly  endangers  the  integrity  of 
the  voice.  Operations  may  be  followed  by  bronchitis  and  broncho-pneu- 
monia. Eecurrence  is  common.  Bronner  recommends  the  use  of  1  per 
cent,  formalin  spray  as  a  preventive.  In  view  of  the  fact  that  many  dis- 
appear without  operative  interference,  it  should  not  be  too  lightly  under- 
taken.   Papillomata  often  seems  to  grow  more  rapidly  after  operation. 


CHAPTER    XXXV. 

THE    RESPIRATORY    SYSTEM. 

The  Thorax — The  Lungs  and  Respiration — Respiratory  Symptoms — 
Atelectasis — Hypostatic  congestion — The  Trachea — Foreign  bodies  in 
the  air-passages — Gangrene — Abscess — New  growths — Emphysema. 

At  birth  the  chest  is  almost  circular.  Towards  the  end  of  the  first 
year  the  transverse  diameter  exceeds  the  antero-posterior,  and  by  the 
tenth  year  bears  the  proportion  of  3-2.  The  permanent  shape  is  almost 
attained  by  the  fifth  year.  Measurements  of  the  chest  are  of  little  value  as 
a  standard.  The  circumference  at  the  nipple  level  is  about  13  ins.  at  birth, 
17  at  1  year,  19  at  2  years,  21  at  5  years  and  24  at  10  years  of  age. 
Relatively  to  the  spine  the  sternum  is  a  vetebra  higher  than  in  the  adult. 
The  ribs  are  nearly  horizontal  and  the  epigastric  angle  very  obtuse. 

The  muscles  are  weak,  the  ribs  pliable,  and  the  whole  chest  wall  soft 
and  yielding.  This  flexibility  allows  considerable  alterations  in  shape  from 
respiratory  obstruction  and  atmospheric  pressure.  It  also  affects  the  ex- 
pansion of  the  lungs  in  infants  kept  lying  on  their  backs  and  may  partially 
explain  the  better  results  of  private  practice.  In  hospital  cases  more  or 
less  collapse  of  the  posterior  parts  of  the  lower  lobes  is  often  found  after 
death.  The  weight  of  the  lungs  at  birth  is  about  2  oz.,  4-5  oz.  at  1  year,  and 
10  oz.  at  7  years  of  age. 

Examination  of  the  chest. — The  chest  must  be  carefully  inspected  in  a 
good  light  for  abnormalities,  irregularities  in  shape  and  uneven  expansion. 
Measurements  are  taken  by  a  tape  measure,  callipers  and  a  crytometer 
at  the  level  of  the  junction  of  the  fifth  rib  and  cartilage.  A  small  child  has 
a  small  chest.  An  abnormally  small  chest  is  due  to  naso-pharyngeal  obstruc- 
tion or  insufficient  air  and  exercise.  The  intercostal  spaces  are  small,  the 
ribs  unduly  oblique  and  the  lower  ones  turned  inwards.  The  back  is 
straight,  the  abdomen  retracted,  and  there  is  a  tendency  to  bring  the 
shoulders  forward.  Respiratory  obstruction  must  be  cured  and  deep 
breathing  taught  in  these  cases.  The  outlook  is  good.  Respiratory  obstruc- 
tion has  a  marked  effect  in  rachitic  infants,  producing  the  rachitic  chest 
(pp.  181,  185).  If  the  obstruction  is  marked,  this  form  of  chest  may  be 
present  at  an  early  age,  before  the  development  of  rickets  and  indepen- 
dently of  this  disease.  The  deformity  may  entirely  disappear  in  the 
course  of  growth.  Pigeon-breast  is  apt  to  occur  from  debility  and  un- 
complicated respiratory  obstruction. 


390  Chapter   XXX  V. 

Unilateral  flattening  is  due  to  chronic  tuberculous  lung  disease, 
collapse,  imperfect  expansion  of  the  lung  after  pleural  effusion,  or  fibroid 
contraction  of  the  lung.  In  lateral  curvature  of  the  spine  the  chest  is 
prominent  on  one  side  and  flattened  on  the  other,  and  there  may  be  a 
groove  above  the  level  of  the  liver  or  spleen  equivalent  to  half  a  Harrison's 
sulcus.  Unilateral  bulging  is  seen  in  pleural  effusions,  lateral  curvature 
of  the  spine  and  intra-thoracic  tumours.  In  slight  effusions  the  affected 
side  maybe  relatively  small,  because  of  over-expansion  of  the  opposite  lung. 
Local  bulging  is  caused  by  cardiac  hypertrophy,  pericardial  effusion,  point- 
ing empyema,  congenital  malformation,  greenstick  fracture  of  the  ribs, 
or  local  affections  of  the  chest  wall.  Bilateral  over-expansion  is  seen  in 
emphysema,  chronic  bronchitis  and  asthma. 

Signs  obtained  by  percussion  of  the  back  below  the  middle  third  of  the 
scapula  can  be  disregarded,  for  the  diaphragm  reaches  this  level  in  the  very 
young  and  abnormalities  below  it  require  very  great  experience  for  an 
accurate  estimation  of  their  value.  Note  the  sense  of  resistance  ;  it  is 
much  increased  over  consolidated  lung  and  to  a  greater  degree  over  effusions. 
The  percussion  note  on  the  right  side  above  the  middle  of  the  scapula  is 
tympanitic  in  character  because  of  the  nearness  of  the  bronchus  to  the 
surface.     For  further  details  refer  to  Chapter  I,  pp.  5-6. 

The  Lungs  and  Respiration. — The  foetal  lungs  are  lobulated,  dark 
red,  firm,  solid,  airless  and  sink  in  water.  They  contain  much  connective 
tissue  in  the  form  of  septa.  The  blood  is  carried  to  them  by  the  pulmonary 
and  bronchial  arteries.  The  latter  vessels  supply  the  bronchial  glands,  air 
passages,  large  arteries,  interlobular  tissues  and  pleura.  At  birth  the 
placental  circulation  is  cut  off  and  the  blood  is  deprived  of  its  supply  of 
oxygen.  The  lack  of  oxygen  and  the  cutaneous  stimulation  of  the  peri- 
pheral nerves  excite  the  respiratory  centre,  and  cause  respiratory  move- 
ments and  expansion  of  the  lungs.  At  first  the  breathing  is  chiefly  thoracic 
and  air  does  not  penetrate  all  the  alveoli.  Much  of  the  lung  remains 
unexpanded  for  hours  and  often  expansion  is  only  complete  at  the  end 
of  the  second  day.  Thus  there  may  be  partial  atelectasis,  an  important 
point  forensically.  The  anterior  edges  of  the  upper  lobes  are  first  expanded, 
then  the  upper  lobe  as  a  whole,  and  finally  the  posterior  portions  of  the 
lower  lobes.  The  presence  of  mucus,  etc.,  in  the  tubes  causes  patchy  and 
irregular  expansion.  Atelectasis  has  been  already  described  (p.  117). 
During  the  first  few  days  the  interchange  of  gases  is  feeble  but  it  soon 
becomes  relatively  greater  than  in  adults.  The  average  tidal  air  amounts 
to  35  c.c,  and  may  attain  a  maximum  of  120  c.c.  Lymphatics  are  situated 
in  the  alveolar  walls  between  the  capillaries,  opening  into  perivascular  lymph 
spaces,  and  in  the  walls  of  the  bronchi.     They  enter  the  bronchial  glands. 

The  respiration  rate  is  40-45  per  minute  in  the  newborn,  25-30  at  6 
months,  24  at  2  20  at  3,  and  18  at  7  years  of  age.  A  chart  of  the  rate 
is  of  much  more  value. than  a  single  estimation.    It  increases  to  a  greater 


The  Respiratory  System.  391 

extent  and  is  of  less  serious  significance,  the  younger  the  child.  It  is 
decreased  in  sleep  ;  increased  by  crying,  excitement  and  exertion  ;  often 
irregular  up  to  the  third  year  ;  diaphragmatic  in  nurslings  and  abdominal 
up  to  the  seventh  year.  It  is  normally  high  in  severe  rickets,  because  of 
deficient  lung  expansion,  and  is  modified  in  disease  by  the  presence  of 
rickets.  It  varies  with  the  temperature,  obstruction  to  the  entry  of  air, 
the  amount  of  lung  involved,  and  is  affected  by  rapid  involvement  of  lung, 
pleural  pain,  weak  respiratory  muscles  and  yielding  ribs.  If  the  breath  is 
held  for  long  there  is  no  serious  lung  trouble.  Compared  with  adults  there 
is  more  oxygen  absorbed  and  more  C02  eliminated  in  proportion  to  body 
weight  and  less  in  proportion  to  body  surface. 

General  Symptoms. — Apart  from  changes  in  respiration,  cough, 
expectoration  and  haemoptysis  are  the  chief  symptoms  of  pulmonary 
disease.  Cough  is  useful  or  useless.  Its  object  is  to  get  rid  of  normal 
or  abnormal  secretions  from  the  fauces  and  air  passages,  or  it  may  simply 
result  from  reflex  irritation  of  the  vagus  nerve.  A  normal  reflex  can  produce 
or  maintain  a  cough,  if  there  is  undue  irritability  of  the  nervous  system. 
The  chief  causes  are  pharyngeal  affections,  laryngeal  and  respiratory 
disorders,  and  reflex  irritation. 

The  Physiological  Cough  of  Infancy. — Sometimes  a  baby  begins  to 
cough  a  few  days  after  birth,  usually  on  the  second  or  third  day,  and 
continues  to  do  so  for  even  a  year.  This  cough  is  rare  after  bottle-feeding  ; 
most  common  in  well-nourished,  breast-fed  babies  after  the  first  nursing 
of  the  day.  It  is  often  associated  with  regurgitation,  a  sign  of  over- 
distension of  the  stomach.  It  is  a  reflex  stomach  cough  and  assists  in 
driving  the  food  through  the  pylorus.  Reduce  the  duration  of  each  nursing, 
if  necessary. 

Nocturnal  or  Spasmodic  Night  Cough  comes  on  in  young  children 
about  the  middle  of  the  night  or  shortly  after  being  put  to  bed.  It  is 
spasmodic,  somewhat  like  whooping  cough,  lasts  a  long  time,  and  often 
causes  nausea,  retching  and  vomiting.  It  is  almost  always  due  to  adenoids 
and  post-nasal  catarrh  ;  sometimes  to  large  tonsils  or  elongated  uvula  ; 
occasionally  to  post-pharyngeal  abscess,  and  the  pressure  of  enlarged  glands 
or  the  abscess  of  Pott's  disease  on  the  trachea.  Rarely  it  is  of  purely  nervous 
origin  or  due  to  the  reflex  irritation  of  intestinal  parasites.  Its  spasmodic 
character  is  caused  by  mucus  dropping  into  the  larynx  and  collecting  in  the. 
region  of  the  arytenoids,  setting  up  glottic  spasm  and  attacks  of  suffocation. 
Or  an  elongated  uvula  drops  back  when  the  child  lies  down.  A  cough  from 
this  cause  comes  on  shortly  after  going  to  bed  ;  that  of  post-nasal  catarrh 
comes  on  later  and  occurs  by  day  also. 

Reflex  Cough. — A  knowledge  of  the  branches  and  distribution  of  the 
vagus  enables  us  to  account  for  many  troublesome  coughs.  Wax,  foreign 
bodies  and  catarrh  of  the  external  auditory  meatus  irritate  the  auricular 
branch  (ear  cough).    The  pharyngeal  branches  are  stimulated  by  affections 


392  Chapter  XXXV. 

of  the  throat,  a  long  uvula,  irritant  dusts  and  vapours,  changes  of  tempera- 
ture, hairs,  fluff,  fish  bones,  etc.,  and  possibly  pertussis.  The  superior 
laryngeal  supplies  the  larynx,  epiglottis  and  base  of  the  tongue.  The 
tracheal  branches  are  stimulated  by  pressure  on  the  trachea  and  inflam- 
matory affections,  while  those  to  the  lungs  and  pleura  are  excited  by  various 
affections  of  these  organs  and  passive  cardiac  congestion.  There  is  no 
clear  evidence  of  a  reflex  cardiac  cough,  but  a  hard  and  painful  one  is 
sometimes  noted  in  pericarditis.  "  Stomach  cough  "  is  harsh,  short  and 
dry.  It  arises  from  digestive  troubles  and  disappears  when  the  stomachic 
state  gets  well. 

Hysterical  Cough  is  a  peculiar  barking  cough  at  about  puberty,  more 
common  in  girls.  The  child  is  often  said  to  "  bark  like  a  dog."  Sir 
"William  Jenner  held  that  a  "  loud  barking  cough  in  boys,  unrelieved  by 
treatment,  is  always  connected  with  masturbation."  The  connection  is 
doubtful,  though  the  two  conditions  may  co-exist.  Sometimes  it  is  due  to 
pharyngeal  causes  or  dentition.  The  child  is  usually  neurotic  or  of  neurotic 
ancestry  ;  often  overfed  and  allowed  too  much  alcohol ;  and  shows  other 
signs  of  neurosis.  The  cough  is  rhythmical,  more  or  less  regular  or  paroxys- 
mal, harsh  and  unmelodious.  It  may  simulate  an  ordinary  cough  or  be 
curiously  monotonous.  There  is  no  pain  or  expectoration.  It  ceases  during 
sleep  and  is  increased  by  emotion.  Its  onset  and  termination  are  sudden 
or  gradual,  and  relapse  is  frequent. 

Consideration  of  the  above  varieties  of  cough  shows  that  it  is  by  no 
means  a  constant  proof  of  lung  troubles.  In  quite  half  the  cases  it  depends 
on  throat  affections.  Some  coughs  are  due  to  habit.  The  nervous  and 
reflex  types  do  not  affect  the  health.  Sources  of  reflex  irritation  may  be 
present  and  yet  not  the  actual  basis  of  the  cough.  The  treatment  is 
essentially  that  of  the  cause. 

Hcemoptysis  is  quite  uncommon  under  6  or  7  years  of  age.  Even  if 
there  is  bleeding,  the  young  child  rarely  expectorates.  It  is  secondary  to 
pulmonary  phthisis,  gangrene,  infarction,  or  the  rupture  of  a  caseous  gland 
into  the  trachea  or  bronchus.  In  malignant  forms  of  specific  fevers  and 
blood  states,  such  as  haemophilia,  purpura,  etc.,  it  is  primary.  A  fatal 
case  in  a  boy,  aged  3  years,  was  caused  by  perforation  of  the  right  bronchus 
and  the  branch  of  the  right  pulmonary  artery  to  the  upper  lobe  by  a 
suppurating  caseous  gland.  In  a  boy,  aged  4,  cavitation  of  a  gland  at  the 
root  of  the  right  lung  communicated  with  a  bronchus.  In  the  cavity  were 
three  branches  of  the  pulmonary  artery,  one  of  which  presented  a  fusiform 
aneurysmal  enlargement  and  had  ruptured. 

Post-mortem  examination  generally  shows  tuberculous  arteritis, 
softening  and  perforation,  sometimes  preceded  by  aneurysmal  dilatation  ; 
perforation  of  the  trachea  or  bronchus  ;  or  excavation  of  the  lung,  primary 
or  secondary  to  a  tuberculous  gland.  Expectoration  may  be  tinged  with 
blood  for  a  day  or  two  before  the  fatal  bleeding. 


The  Respiratory  System.  393 

Expectoration  affords  little  information,  for  children  swallow  the 
sputum.  It  can  be  obtained  by  making  the  child  cough  and  collecting  the 
sputum  from  the  fauces  on  a  swab  of  wool,  or  by  lavage  of  the  stomach  in 
the  morning  before  food. 

Collapse  or  acquired  atelectasis  is  an  effect  of  obstruction  of  the  air 
passages  by  secretions  and  foreign  bodies.  Rickets,  marasmus  and 
debility  are  the  main  predisposing  causes.  It  depends  partly  on  feeble 
inspiration,  and  is  frequent  in  all  forms  of  bronchitis  and  broncho-pneu- 
monia. Powerful  respiratory  movements  in  these  diseases  are  more 
likely  to  produce  emphysema.  Compression  collapse  is  seen  in  pleural  and 
pericardial  effusions,  great  cardiac  hypertrophy,  deformity  of  the  chest 
sufficient  to  prevent  complete  lung  expansion,  new  growths  and  dia- 
phragmatic hernia. 

The  collapsed  areas  are  dark  red  to  purple  in  colour,  airless,  solid  and 
sunk  below  the  level  of  the  surrounding  lung,  which  is  emphysematous, 
sometimes  to  a  marked  extent.  They  are  most  common  in  the  lower  lobes 
and  posterior  portions  01  the  upper  ones.  Pleural  conditions  and  fibroid 
or  pneumonic  changes  in  the  collapsed  lung  interfere  with  re-expansion. 

The  symptoms  and  physical  signs  are  much  the  same  as  in  the  con- 
genital type  (p.  117)  and  vary  with  the  degree.  Usually  they  come  on 
gradually.  Dyspnoea,  recession  and  cyanosis  may  be  very  marked.  The 
patches,  if  large  enough,  cause  impairment  of  resonance,  deficient  air 
entry  and  diminished  vocal  resonance.  The  diagnosis  from  pneumonic 
consolidation  is  generally  based  on  the  development  of  dulness  within  24 
hours,  the  air  from  the  obstructed  lung  being  slowly  absorbed  by  the  blood, 
and  without  further  rise  of  temperature.  Crepitations  are  absent.  Small 
patches  give  rise  to  no  physical  signs  for  the  dulness  is  obscured  by  the 
surrounding  emphysema. 

The  prognosis  is  that  of  the  disease.  In  bronchitis  of  the  larger  tubes 
it  generally  is  recovered  from.  Pneumonia  is  a  common  sequel.  Avoid 
prolonged  decubitus  in  the  affections  liable  to  cause  collapse  and  encourage 
deep  breathing. 

Hypostatic  congestion  is  of  the  same  causation  and  produces  the  same 
effects  as  in  adults. 

The  Trachea  is  rarely  malformed,  sometimes  the  oesophagus  opens  into 
it.  Partial  stenosis  has  occurred.  Tracheal  obstruction  is  due  to  foreign 
bodies  ;  inflammation  of  the  mucosa,  or  "  tracheitis,"  commonly  part  of 
laryngitis  or  bronchitis,  set  up  by  similar  causes  and  treated  in  the  same 
manner  ;  or  by  pressure  from  without  by  an  enlarged  thyroid,  a  large 
thymus,  intra-thoracic  glands  which  may  be  caseous,  abscess,  cyst,  dermoid 
•or  new  growth. 

Stenosis  causes  difficulty  in  breathing,  especially  on  inspiration,  epigas- 
tric and  episternal  recession,  a  brassy  or  metallic  cough,  perhaps  inspiratory 
stridor,  feeble  breath  sounds  over  the  lungs,  and  sometimes  severe  cyanosis. 


39-i  Chapter   XXXV. 

Occasionally  the  dyspnoea  is  relieved  by  leaning  forward  in  the  sitting- 
posture.  Attacks  of  paroxysmal  dyspnoea  are  set  up  by  the  difficulty  in 
getting  rid  of  viscid  mucus,  and,  rarely,  by  reflex  irritation  of  the  recurrent 
laryngeal  nerve.  It  may  be  relieved  by  belladonna.  The  voice  is  clear.  If 
the  stenosis  is  caused  by  pressure,  the  usual  signs  of  pressure  on  the  vena 
cava  superior  may  be  also  present,  and  there  may  be  evidence  of  an  intra- 
thoracic tumour  (p.  396).  In  stenosis  of  a  bronchus  the  pulmonary  signs- 
are  unilateral. 

Foreign  Bodies  in  the  Air  Passages. — The  habit  children  have  of 
putting  objects  into  the  mouth  is  a  potent  source  of  their  entrance  into  the 
larynx,  trachea  or  bronchi.  The  actual  cause  is  a  sudden  inspiration,  such 
as  is  produced  in  older  children  by  violent  laughter  or  an  unexpected  slap  on 
the  back.  In  infants  allowed  to  crawl  about  the  floor  the  history  of  the 
accident  is  often  unobtainable  and  the  mother  is  positive  it  cannot  have 
happened.  The  presence  of  a  foreign  body  may  not  be  suspected  until  it  is- 
coughed  up  or  found  after  death.    The  variety  of  objects  is  innumerable. 

The  effects  are  immediate  and  remote.  They  vary  with  the  size  and 
nature  of  the  object  and  its  location.  A  roundworm  has  caused  death- 
Smooth  hard  bodies,  such  as  beads  and  buttons,  produce  the  least  imme- 
diate effect,  but  may  cause  recurrent  attacks  of  glottic  spasm  through  being; 
coughed  up  into  the  larynx.  Soft  bodies,  and  those  which  are  softened  by 
soaking  in  warm  mucus,  are  less  likely  to  be  coughed  up.  On  swelling  they 
become  firmly  impacted  and  cause  complete  obstruction.  Pins  and  other- 
sharp  bodies  are  very  dangerous  and  difficult  to  extract. 

A  foreign  body  entering  the  larynx  causes  symptoms  of  spasm,  often 
alarming.  Dyspnoea  is  great  and  the  child  may  become  black  in  the  face- 
and  die  from  suffocation.  The  initial  choking  fit  may  be  absent  if  the 
body  comes  to  rest  at  once.  Occasionally,  with  a  small  smooth  body,  there- 
is  merely  an  attack  of  spasmodic,  convulsive  or  suffocative  cough,  over  as 
soon  as  the  object  passes  into  the  trachea.  The  symptoms  recur  if  the  body- 
is  again  coughed  up  into  the  larynx.  A  small  hard  body  in  the  larynx 
causes  paroxysmal  cough  and  perhaps  hoarseness,  dyspnoea  and  stridor. 
If  subglottic  or  in  the  vestibidar  region,  the  voice  may  be  unaffected. 
Paralysis  of  the  laryngeal  adductors  has  been  noted  as  an  immediate  effect- 
In  the  trachea  the  body  gives  rise  to  respiratory  obstruction,  recession,, 
stridor  and  occasionally  pain  on  swallowing.  It  remains  at  the  bifurcation 
or  passes  into  a  bronchus,  more  commonly  the  right  as  it  is  larger.  In  the- 
bronchus  it  gives  rise  to  unilateral  physical  signs.  The  movement  of  the 
chest  is  deficient  and  there  is  unilateral  recession,  resonance  is  impaired,, 
the  breath  sounds  are  weak  or  absent  over  the  lower  lobe  or  the  whole  lung, 
and  the  voice  sounds  weak.  Less  often  there  is  stridulous  wheezing 
on  deep  inspiration,  paroxysmal  cough,  and  pain  in  the  side  or  epigastrium. 
Moist  sounds  develop  later.  Cough  varies  and  may  be  absent  until  septic 
pneumonia  results  from  decomposition  of  retained  secretions,  local  ulceration 


The  Respiratory  System.  395 

and  microbial  infection.  The  lung  mischief  terminates  in  multiple 
abscesses,  some  times  subpleural,  a  variable  degree  of  fibrosis,  bronchiec- 
tasis, empyema  and  rarely  gangrene.  Compensatory  emphysema  and 
fatal  haemoptysis  may  occur. 

At  first  the  pulse  is  unduly  frequent,  the  respiration  hurried,  and  the 
temperature  rises  about  two  degrees,  a  rise  which  is  difficult  to  explain. 
Cough  and  expectoration  come  on  within  a  week,  and  a  considerable  amount 
of  pus  may  be  found  in  5-6  days.  The  later  symptoms  are  those  of  sepsis  : — 
hectic  fever,  troublesome  cough,  purulent  and  offensive  sputa,  diarrhoea 
and  malnutrition.  On  account  of  the  absence  of  early  symptoms  the  patient 
may  not  come  under  notice  until  local  ulceration  and  suppuration  have  begun. 

The  diagnosis  is  very  difficult  or  very  easy.  In  every  case  of  unilateral 
lung  disease  with  purulent  expectoration  and  signs  of  a  cavity,  a  foreign 
body  must  be  suspected.  Emphasis  is  lent  to  this  probability  by  a  past 
history  of  a  choking  attack,  even  though  remote  in  time,  and  the  absence 
of  signs  of  empyema  or  tuberculosis.  Recurrent  attacks  of  choking  and 
dyspnoea  afford  strong  confirmation,  if  laryngeal  mischief  can  be  excluded. 
An  X-ray  examination  affords  conclusive  proof  in  many  cases.  The  lung 
signs  suggest  bronchiectasis  or  tuberculosis. 

Prognosis. — Untreated  patients  may  get  well  in  time  by  expulsion  of 
the  object  or  its  encapulation,  but  quite  half  of  them  die  from  secondary 
septic  inflammation,  sudden  cardiac  failure  or  some  complication. 
Bronchiectasis  is  a  common  sequel.  Foreign  bodies  have  been  retained  for 
many  years.  Paroxysmal  dyspnoea  and  fatal  glottic  spasm  may  occur  at 
any  time. 

Treatment. — Emetics,  patting  the  back  and  inversion  of  the  body  are 
dangerous  if  the  body  has  passed  beyond  the  larynx.  They  may  cause  it 
to  pass  back  into  the  larynx  and  bring  on  fatal  spasm.  It  is  a  justifiable 
method  if  everything  is  at  hand  for  an  immediate  tracheotomy  and  if  the 
object  is  small  and  smooth.  The  proper  treatment  is  by  bronchoscopy, 
using  Killian's  method  of  direct  laryngoscopy  and  forceps,  if  the  body  is  in 
the  larynx.  Immediate  tracheotomy  is  safer  for  bodies  lower  down,  for  it 
stops  the  risk  of  glottic  spasm  and  provides  a  better  means  of  escape  for  the 
foreign  body,  which  will  often  be  at  once  coughed  up  through  the  widely 
opened  wound,  if  the  child  is  inverted.  If  this  fails,  an  attempt  must  be 
made  to  locate  it  with  a  probe  and  remove  it  by  crocodile  forceps,  wire  loop 
or  other  suitable  appliance.  The  tube  can  be  taken  out  next  day,  unless 
portions  of  a  soft  and  friable  body  are  left  behind.  It  is  rarely  advisable  to 
attempt  removal  through  the  pleural  cavity  and  posterior  mediastinum, 
or  through  the  anterior  mediastinum  if  the  object  is  in  the  right  bronchus. 
The  bronchoscope  and  the  X-rays  have  added  enormously  to  the  means  of 
successfully  locating  and  removing  foreign  bodies. 

Gangrene  is  rare.  It  is  probably  as  common  in  children  as  in  adults  ; 
especially  in  marasmic  infants  under  3  years  of  age.    It  is  liable  to  follow 


396  Chapter  XXXV. 

measles,  sometimes  in  conjunction  with  cancrum  oris,  and  is  most  frequent 
in  the  broncho-pneumonia  and  pneumonia  of  marasmic  infants.  Occasion- 
ally it  is  secondary  to  septic  infection  of  the  mouth  and  pharynx,  caries  of 
the  petrous  bone  or  middle  ear  disease,  septic  bronchitis  and  pysemic 
conditions  generally,  foreign  bodies  in  the  bronchus,  pulmonary  infarction, 
abscess  of  the  lung,  chronic  pneumonia  and  tuberculous  broncho-pneumonia. 

It  is  the  result  of  thrombosis  and  secondary  infection  with  a  pyogenic 
organism.  The  primary  cause  is  in  the  blood  vessels,  bronchi  or  parenchyma 
of  the  lungs.  In  one  variety  there  is  a  general  moist  gangrene,  diffuse, 
involving  probably  a  whole  lobe,  with  a  dirty  green  or  brownish  colour  and  a 
gangrenous  odour.  The  lung  tissue  may  be  semi-solid  or  completely 
liquefied.  More  often  it  is  of  the  nature  of  a  patchy  necrosis,  the  result 
of  local  thrombosis  or  embolism,  perhaps  septic.  This  affects  several  areas, 
is  circumscribed,  in  wedge-shaped  patches  like  infarcts,  and  free  from 
gangrenous  odour.  These  patches  are  liable  to  break  down  and  form 
abscesses,  filled  with  broken  down  lung  tissue  and  offensive  foetid  pus. 
In  late  stages  the  odour  may  be  gangrenous. 

The  outlook  is  best  in  cases  due  to  a  foreign  body.  An  isolated  patch 
may  be  coughed  up  and  end  in  cicatrisation.  Empyema  and  pneumothorax 
are  occasional  sequels. 

It  is  rarely  diagnosed  during  life  for  it  may  give  rise  to  no  definite 
indications  before  death,  especially  in  pneumonic  cases.  If  mouth  affections 
can  be  excluded,  a  foetid  or  gangrenous  odour  of  the  breath,  prostration 
and  the  typhoid  state  are  the  most  suspicious  signs.  Older  children  may 
expectorate  necrotic  lung  tissue  or  even  have  attacks  of  haemoptysis.  The 
treatment  is  on  general  principles,  with  a  liberal  supply  of  food  and 
stimulants. 

Abscess  of  the  Lung. — Multiple  minute  abscesses  are  found  in  pysemia, 
septic  broncho-pneumonia  and  the  secondary  infection  of  tuberculous 
broncho-pneumonia.  Tuberculous  cavities  are  single  or  multiple  and 
variable  in  size.  A  single  abscess  in  the  lung  is  rare  ;  usually  the  result  of 
necrosis,  as  in  some  cases  of  gangrene,  and  occasionally  due  to  the  breaking 
down  of  a  mediastinal  gland  involving  the  lung.  A  large  single  abscess 
might  give  rise  to  signs  like  those  of  empyema.  The  small  multiple  ones  are 
diagnosed  after  death. 

Intra-thoracic  Tumours  are  mediastinal,  pulmonary  or  pleural  in  origin, 
arising  in  the  glands,  bronchi,  lungs,  etc.  Sarcoma  of  these  structures 
may  be  primary  in  the  glands,  or  secondary  in  the  glands  or  lung.  Lym- 
phadenoma  may  be  primary  in  the  glands  or  secondary  to  Hodgkin's  disease. 
Primary  sarcoma  of  the  lung  is  extremely  rare.  A  boy  in  his  fourth  year 
had  a  round-celled  sarcoma  of  the  glands  on  the  right  side,  softened 
hemorrhagic  areas,  and  no  secondary  growths.  He  died  seven  weeks  after 
the  onset  of  symptoms.  Dermoids,  hydatids,  cysts  and  actinomycosis  are 
great  rarities.    Dermoids  are  often  latent  until  puberty.    They  arise  in  the 


The   Respiratory  System.  397 

anterior  mediastinum  and  give  rise  to  the  signs  of  a  tumour  under  the  upper 
half  of  the  sternum.    Many  are  discharged  through  a  bronchus. 

The  symptoms  are  those  of  pressure  on  adjacent  structures.  In  the 
early  stages  there  may  be  pain  in  the  side  or  abdomen,  cough,  emaciation, 
increasing  dyspnoea  and  unduly  frequent  pulse.  If  the  diaphragm  is  in- 
volved, there  may  be  much  pain  and  dyspnoea  or  pleurisy  at  the  onset.  In 
the  case  mentioned  the  pain  occurred  in  spasmodic  attacks,  and  was  referred 
to  the  navel  and  the  right  side.  The  attacks  were  associated  with  dyspnoea 
and  cyanosis,  and  suggestive  of  diaphragmatic  spasm.  In  later  stages  the 
chest  bulges  and  the  heart  is  displaced.  Pressure  on  the  vena  cava  superior 
causes  puffy  swelling  of  the  head,  neck,  chest  wall  and  arms,  lividity, 
slight  exophthalmos,  swelling  of  the  thyroid,  and  dilatation  of  the  super- 
ficial epigastric  and  mammary  veins.  Pressure  on  the  bronchus  causes 
deficient  air  entry,  impaired  resonance  and  subsequent  dulness  ;  later, 
bronchiectasis  through  infection  of  stagnant  secretions,  and  then  perhaps 
bronchial  breathing. 

Because  of  the  pain  and  physical  signs  a  diagnosis  of  pleurisy  or 
pleural  effusion  is  likely  to  be  made.  Examination  shows  dulness  which 
may  extend  to  or  beyond  the  sternum,  weak  breath  sounds,  diminished 
vocal  vibrations  and  vocal  resonance,  and  perhaps  areas  of  bronchial 
breathing  over  the  bronchus  in  front  and  behind.  In  my  case  the  apex 
of  the  heart  was  an  inch  outside  the  nipple  line,  and  the  liver  so  depressed 
that  its  convex  upper  surface  was  felt  in  the  right  hypochondrium  and 
the  epigastrium  and  its  edge  as  low  as  the  umbilicus.  There  was  no 
bronchial  breathing  and  breath  sounds  were  absent  over  the  lower  two- 
thirds  of  the  right  chest.  A  moderate  degree  of  fever  has  been  found  in 
certain  cases,  and  the  evidence  in  favour  of  empyema  has  been  so  strong 
that  portions  of  rib  have  been  resected.  Exploration  may  reveal  the 
presence  of  fluid,  serous  or  bloody.  In  the  case  referred  to  gentle 
aspiration  withdrew  2*1  oz.  and  12  oz.  of  dark,  fluid,  altered  blood  on 
successive  occasions.  It  flowed  out  quite  easily,  was  a  little  brighter  at 
the  end  than  at  the  beginning  of  the  operation,  and  did  not  cause  faintness. 
It  did  not  clot  and  no  sarcoma  cells  could  be  found  in  it.  Its  removal 
had  no  effect  on  the  physical  signs  over  the  lungs  or  the  position  of  the 
heart,  and  very  little  on  that  of  the  liver.  After  death  it  was  found  to  have 
come  from  a  hsemorrhagic  cavity  in  the  growth  and  not  from  the  pleural 
cavity. 

Diagnosis  is  impossible  in  early  stages.  If  there  is  fluid  complicating 
the  case,  its  removal  will  not  definitely  exclude  the  possibility  of  a  new 
growth  as  the  cause  of  the  effusion.  Much  stress  can  be  laid  on  the  absence 
of  fluid  on  exploration,  and  on  the  absence  of  much  improvement  in  the 
physical  signs  if  fluid  is  present  and  is  removed.  Bloody  effusions  are  often, 
of  tuberculous  origin.     Lymphadenoma  may  be  associated  with  pyrexia.. 


398  Chapter   XXXV. 

■Chronic  pneumonia,  bronchiectasis,  fibroid  phthisis  and  tuberculosis  must 
be  excluded. 

The  progress  is  rapid.  As  the  tumour  grows  it  involves  more  and  more 
lung  tissue  or  compresses  it,  producing  greater  dyspnoea  and  an  increase 
in  the  physical  signs.  Death  results  from  interference  with  the  action  of 
the  heart,  syncope  during  diaphragmatic  spasm,  or  asthenia.  Anorexia, 
weakness  and  emaciation  are  progressive  ;  sometimes  there  are  cough  and 
haemoptysis.  Careful  search  must  be  made  for  a  primary  focus  before 
accepting  a  tumour  of  the  lung  as  primary.  The  glands  may  be  involved 
or  entirely  unaffected,  or  the  tumour  purely  glandular,  displacing  and 
compressing  the  lung  in  the  process  of  growth  and  not  infiltrating  it. 
The  tumour  may  start  in  either  the  root  or  substance  of  the  lung.  The 
growth  may  become  adherent  to  the  chest  wall  and  diaphragm,  and  may 
involve  a  rib  by  direct  extension,  the  heart  and  pericardium,  and  adjacent 
structures. 

Emphysema  is  never  primary.  It  is  found  in  the  lungs  and  sub- 
<;utaneously  as  a  complication  of  other  diseases.  General  emphysema  is 
due  to  interference  with  cough  and  expiration.  It  is  present  in  whooping 
oough,  bronchitis,  broncho-pneumonia,  asthma  and  laryngeal  obstruction. 
Delicate  children  develop  it  by  blowing  trumpets  and  wind  instruments. 
In  the  newborn  it  may  be  due  to  mechanical  inflation  of  the  lungs.  Pertussis 
and  asthma  are  the  most  powerful  causes.  Compensatory  emphysema  is  a 
sequel  of  imperfect  expansion  of  lung  damaged  or  impeded  in  its  action, 
as  by  the  adhesions  of  old  pleurisy,  the  contraction  of  empyema,  rachitic 
and  spinal  deformity,  pneumonia  and  tuberculosis.  Patches  are  often  found 
surrounding  isolated  areas  of  collapse  and  consolidation. 

It  is  most  marked  at  the  anterior  edges  of  the  upper  lobes,  the  bases  of 
the  lower  lobes  and  at  the  root  of  the  lung.  Emphysematous  lung  is  lighter 
and  paler  than  normal.  The  vesicles  are  quite  small,  visible  through  a 
magnifying  glass,  and  universally  distributed  in  the  general  type.  If  the 
septa  give  way,  the  vesicles  vary  in  size  from  a  pin  head  to  a  cherry. 
In  rare  instances  the  affection  is  interstitial  or  interlobular,  and  it  may 
extend  to  the  connective  tissue  of  the  body,  via  the  mediastinum. 

In  a  well-marked  case  of  general  emphysema  the  chest  is  fully  expand- 
ed, barrel-shaped,  with  little  or  no  respiratory  excursion.  The  diaphragm 
moves  freely  and  there  may  be  epigastric  pulsation  from  dilatation  of  the 
right  ventricle.  The  face  and  lips  show  a  bluish  pallor,  breathing  is  rapid 
and  shallow,  the  pulse  frequent,  and  there  are  cough  and  general  distress. 
The  physical  signs  are  high  pitched,  resonance,  obliteration  of  the  cardiac 
dulness,  feeble  respiratory  murmur,  and  weak  or  distant  heart  sounds. 
The  temperature  is  normal  or  subnormal.  When  part  of  a  general  disease, 
acute  emphysema  usually  ends  in  complete  recovery.  The  prognosis  is 
that  of  the  disease.    If  there  is  no  evidence  of  an  exciting  cause,  the  outlook 


The  Respiratory  System.  399 

is  bad  and  the  child  may  die  from  cardiac  failure,  ante-mortem  clotting  in 
the  right  auricle  or  broncho-pneumonia. 

The  treatment  is  that  of  the  primary  disease  and  in  convalescence 
must  be  directed  to  maintaining  nutrition  and  strengthening  the  right 
side  of  the  heart  by  cod-liver  oil,  iron,  dry  and  equable  climate,  clothing,  etc. 
The  ordinary  precautions  against  attacks  of  bronchitis  must  be  rigidly 
enforced. 

Subcutaneous  emphysema  appears  above  the  clavicles  and  spreads 
downward  over  the  chest,  upward  to  the  face,  and  perhaps  over  the  whole 
body.  The  chief  causes  are  obstruction  to  the  bronchial  tubes,  tracheotomy 
and  artificial  respiration,  pertussis,  rupture  of  the  lung,  air  tubes  or 
oesophagus,  tuberculosis,  the  bronchitis  of  measles  and  pneumonia.  It 
originates  in  the  interlobular  and  interstitial  emphysema  of  the  lungs,  a 
condition  which  cannot  be  diagnosed  during  life.  Sometimes  the  medias- 
tinal tissues  are  full  of  air  bubbles.  Kirschgessner  (1904)  has  recorded  a  case 
in  a  newborn.  He  ascribed  it  to  extension,  via  the  mediastinum,  from  an 
interstitial  emphysema  of  the  lungs  produced  by  intra-uterine  expiration 
during  extraction,  there  being  no  injury  to  the  clavicles  or  ribs.  The 
child  got  well  in  10  days.  Localised  emphysema  may  surround  an  opening 
into  the  pleural  cavity,  after  operation  for  empyema.  Subcutaneous 
emphysema  is  generally  fatal  if  associated  with  tuberculosis  or  lobar 
pneumonia. 


CHAPTER    XXXVI. 

ASTHMA. 

Hay  Fever — Catarrhal   Asthma — Spasmodic   Asthma. 

Hay  Fever. — Paroxysmal  sneezing  is  sometimes  called  paroxysmal 
coryza,  vasomotor  coryza,  or  vasomotor  rhinitis.  It  is  essentially  the 
same  as  hay  fever,  and  due  to  irritation  of  the  terminal  filaments  of  the 
nasal  nerves,  occasionally  to  irritation  by  a  spur  on  a  turbinal.  Patches 
of  hypereesthesia  of  the  nasal  mucosa  may  be  found.  Many  attacks  of  hay 
fever  appear  to  be  primarily  conjunctival.  They  begin  with  itching  of  each 
inner  canthus  and  irritation  of  the  nose.  Examination  reveals  slight 
hyperemia  of  the  bulbar  conjunctiva,  a  fan-shaped  arrangement  of  vessels 
analogous  to  pterygium,  with  redness  and  swelling  of  the  eyelids,  lachry- 
mation  and  photophobia.  It  is  quickly  followed  by  sneezing,  nasal 
obstruction  and  profuse  nasal  catarrh.  The  attack  lasts  for  about  3  weeks. 
It  differs  from  paroxysmal  sneezing  in  its  extent,  the  ocular  involvement 
and  duration.  Thus  there  are  grades  of  these  affections.  Possibly  in  one 
instance  the  nasal  mucosa  is  alone  susceptible  to  the  irritant,  and  in  the 
other  the  conjunctival  mucosa  is  equally  or  even  more  susceptible.  The 
youngest  case  under  my  observation,  was  a  girl,  3  years  old,  who  had 
suffered  from  paroxysmal  sneezing  since  the  end  of  the  first  year  of  life. 
The  smell  of  horses  was  a  definitely  exciting  cause.  The  etiology  of  the 
condition  is  the  same  as  that  of  true  asthma. 

A  spray  of  adrenalin  solution,  1  in  1000,  affords  immediate  but 
temporary  relief.  Local  tender  or  hyperaesthetic  spots  on  the  nasal  mucosa 
are  painted  with  silver  nitrate  solution  2  per  cent.,  or  touched  with  a 
galvano-cautery.  Adenoids,  enlarged  tonsils  and  hypertrophied  turbinals 
should  be  removed  and  proper  respiratory  exercises  prescribed.  Dunbar's 
antitoxin  or  serum  (pollantin)  is  instilled  in  fluid  form  into  the  eyes,  or  as  a 
powder  into  the  nose,  for  hay  fever.  A  mixture  of  resorcin  gr.  2-4,  sodium 
chloride  gr.  4  in  water  oz.  1,  with  or  without  acetic  acid  m.  2,  is  a  valuable 
nasal  lotion.  Eesection  of  the  nasal  nerve  has  been  suggested  for  intract- 
able cases.  High  altitudes  and  sea  voyages  are  useful,  if  the  attack  is  due 
to  the  pollen  of  certain  grasses. 

Asthma  is  catarrhal  or  spasmodic  in  type.  It  occurs  in  paroxysms, 
with  or  without  pulmonary  catarrh  and  little  or  no  dyspnoea  between  the 
attacks.     It  is  not  infrequent  in  infants    though    often    overlooked    or 


Asthma.  401 

diagnosed  as  bronchitis.  Out  of  225  cases  collected  by  Salter  no  less  than 
71  began  in  the  first  ten  years  of  life  and  eleven  of  these  began  in  the  first 
year,  one  as  early  as  14  days.  The  catarrhal  type  is  much  more  common 
in  infants  than  the  spasmodic  one.  The  earliest  case  of  typical  spasmodic 
asthma  under  my  own  observation  occurred  at  9  months  of  age,  and  I 
have  records  of  12  others  under  one  year.  Cases,  which  begin  after  the 
age  of  4  years,  are  more  often  of  the  spasmodic  variety.  They  usually  begin 
in  the  seventh  or  eighth  year  after  repeated  attacks  of  bronchitis. 

The  family  history  is  one  of  asthma,  hay  fever,  various  neuroses,  gout 
or  eczema.  It  is  comparatively  infrequent  among  the  poor  and  not 
uncommon  among  the  better  classes,  especially  the  Jews.  It  occurs  in  all 
countries,  but  is  least  common  in  dry  climates.  It  may  coincide  or  alternate 
with  eczema  or  urticaria.  Sometimes  it  is  associated  with  enlarged  tonsils, 
and  cured  by  their  removal,  or  follows  whooping  cough. 

Instability  of  the  respiratory  centre  must  be  regarded  as  the  pre- 
disposing cause.  The  exciting  causes  may  be  central  or  reflex.  The  chief 
one  is  a  catarrhal  condition  of  the  respiratory  system,  or  a  hypersensitive- 
ness.  Once  an  attack  has  occurred,  other  paroxysms  are  induced  by 
reflex  causes,  such  as  reflex  stimulation  of  the  vagus  by  aerial  emanations, 
an  east  wind,  the  pollen  of  plants,  various  dusts  and  smells.  None  of  these 
causes  can  produce  an  attack  unless  the  predisposition  is  present.  Digestive 
disturbance,  dilatation  of  the  stomach  or  colon  and  constipation  are  so 
frequent  that  a  special  gastric  type  has  been  named  by  Henoch  "  asthma 
dyspepticum."  Other  reflex  causes  are  affections  of  the  nose  and  naso- 
pharynx, adenoids,  foreign  bodies  in  various  orifices,  teething,  dilated  heart, 
and  possibly  enlarged  bronchial  glands.  Perhaps  they  are  merely  coincident. 
Sometimes  a  hypera^sthetic  area  or  an  unhealthy  state  of  the  nasal 
mucosa,  especially  oedema  of  a  small  area  of  the  upper  part  of  the  triangular 
■cartilage  opposite  and  immediately  above  the  level  of  the  anterior  third 
of  the  middle  turbinal  bone,  has  been  blamed.  Cauterisation  of  this  area 
has  relieved  or  cured  some  cases,  even  when  it  has  appeared  perfectly 
healthy. 

There  is  very  little  evidence  of  central  stimulation  as  an  exciting  cause. 
Attacks  are  occasionally  produced  by  emotion  and  excitement.  Toxic- 
poisons,  e.g.,  carbonic  acid  and  those  of  uraemia,  are  known  to  induce 
dyspnoea  and  act  directly  on  the  respiratory  centre. 

Pathology. — It  has  been  regarded  as  a  spasmodic  neurosis,  analogous 
to  epilepsy  and  migraine,  or  as  a  lung  disease  with  a  marked  neurotic 
element,  or  due  to  a  specific  irritation  in  the  lung  which  excites  bronchial 
spasm.  The  actual  paroxysm  is  due  to  spasm  of  the  muscle  in  the  small 
bronchioles,  or  the  swelling  of  the  mucosa,  or  a  combination  of  these  two 
factors.  In  favour  of  spasm  is  the  relief  obtained  by  inhalations  of  chloroform 
and  amyl  nitrite,  by  morphia  subcutaneously,  and  by  the  ingestion  of 
.nitrites   which   are   supposed   to    act    by   reducing   the   contractility   of 

2  D 


402  Chapter   XXXVI. 

unstriped  muscle.  There  is  sometimes  evidence  of  swelling  of  the  mucosa  in 
the  associated  swelling  of  the  nasal  and  tracheal  mucosa,  and  the  frequency 
of  bronchitis  as  an  exciting  cause.  This  swelling  of  the  mucosa  is  due  to 
hypersemia,  vaso-dilatation  or  angioneurotic  cedema.  It  has  been  suggested 
that  the  cedema  is  an  urticaria  of  the  vagus  nerve.  According  to  Dixon  and 
Brodie  the  pulmonary  vessels  are  devoid  of  vasomotor  nerves.  On  the 
whole  the  evidence  is  in  favour  of  vaso-dilatation.  An  attack  may  be 
induced  by  exposure  of  the  chest  to  cold,  or  be  exaggerated  by  the  inhala- 
tion of  hot  air.  It  is  associated  with  vaso-constriction  elsewhere  causing 
cold  skin  and  extremities,  pallor  and  a  feeble  small  pulse.  It  is  relieved  by 
remedies  which  induce  general  vaso-dilatation  or  local  vaso-constriction, 
by  cardiac  depressants,  and  by  local  or  general  bleeding.  Probably  some 
attacks  are  due  to  spasm  only  and  others,  in  young  infants  especially,  to 
muscular  spasm  secondary  to  swelling  of  the  mucosa. 

Symptoms. —  Catarrhal  asthma  differs  from  the  spasmodic  type  in  the 
amount  of  bronchial  secretion.  It  develops  during  or  after  an  attack  of 
nasal,  bronchial  or  pulmonary  catarrh,  broncho-pneumonia,  pertussis  and 
measles.  It  is  most  frequent  in  the  rachitic,  the  abnormally  fat  babies,  and 
those  with  adenoids  or  enlarged  tonsils.  The  catarrh  may  be  present  for  a. 
few  hours  or  days  before  the  attack.  Paroxysms  vary  in  frequency  and 
usually  come  on  at  night.  The  child  is  put  to  bed  apparently  well,  or 
perhaps  a  little  wheezy  and  coughing,  and  in  a  few  hours  develops  extreme 
dyspnoea,  with  anxious  face,  congested  eyes,  sweating  forehead,  pallor,, 
cold  extremities  and  restlessness.  On  examination  there  is  found  marked 
recession  of  the  soft  parts  and  lower  ribs,  absence  of  hyper-resonance,  and 
presence  of  sibilus  and  rhonchus,  with  fine  rales  at  the  bases.  There  may 
be  complete  apyrexia,  or  a  rise  of  temperature  2°or3°F.  The  attacks  last. 
for  some  hours  or  days  and  gradually  subside.  After  2  or  3  days  the  child 
is  well,  except  for  a  few  rales  in  the  chest  and  a  little  cough.  Many  attacks- 
are  quite  mild. 

A  paroxysm  may  come  on  during  the  course  of  bronchitis  which  has. 
persisted  for  weeks  or  months.  It  is  indicated  by  an  increase  in  the  dyspnoea,. 
a  respiration  rate  of  40-90,  a  feeble  pulse,  dry  rales,  and  a  little  fever.  The 
dyspnoea  varies  in  intensity,  is  worse  at  night  and  in  damp  weather,  and  is- 
increased  by  gastric  disturbance.  Occasionally  it  is  almost  of  a  chronic- 
type.  It  may  even  develop  if  the  temperature  falls.  The  characteristic- 
feature  is  that  the  amount  of  dyspnoea  is  out  of  all  proportion  to  the  state-. 
of  the  pulmonary  signs.    The  symptoms  may  last  for  weeks. 

Spasmodic  asthma  is  a  periodic  urgent  dyspnoea,  more  or  less  sudden 
in  onset,  which  usually  comes  on  during  the  night  at  about  12-3  a.m.,  and, 
sometimes  in  the  day  during  sleep.  It  is  preceded  by  no  catarrhal  symp- 
toms  and  lasts  for  1-6  hours,  occasionally  for  days,  without  any  rise  of- 
temperature.  It  is  ushered  in  with  a  feeling  of  tightness  or  oppression  of  the 
chest,  air-hunger  and  a  sense  of  suffocation.     The  inspiratory  efforts  are; 


Asthma.  403 

violent  and  expiration  is  much  prolonged,  cough  is  short  and  dry,  and  the 
attack  may  cease  abruptly,  sometimes  with  a  fit  of  coughing.  Infantile 
asthma  is  often  diurnal,  occurring  at  the  same  hour  on  successive  days. 
Sometimes  the  paroxysms  are  typical  in  duration  and  severity,  whereas  at 
others  they  are  characterised  by  periodical  attacks  of  musical  sonorous 
rales,  without  dyspnoea,  for  a  couple  of  days  or  so  at  a  time.  During  the 
attack  the  face  is  pale,  anxious,  and  becomes  more  or  less  cyanotic.  The 
chest  is  hyper-resonant,  in  a  position  of  full  inspiration  with  contracted 
inspiratory  muscles,  flaccid  expiratory  muscles  and  depressed  diaphragm. 
Recession  is  slight  or  absent.  Breathing  is  slow  and  laboured  ;  inspiration 
is  shallow  and  followed  by  a  pause  ;  expiration  is  prolonged.  The  cough 
is  short  and  dry.  As  the  attack  gets  worse,  the  head  is  thrown  back, 
shoulders  raised,  hands  clenched,  eyes  suffused  and  staring,  mouth  open, 
lips  livid,  skin  sweating  and  extremities  cold.  The  child  is  restless  or  rigid 
in  a  position  of  orthopnoea.  The  pulse  is  small,  frequent,  feeble  and  often 
irregular.  On  listening  to  the  chest  loud  inspiratory  and  expiratory 
wheezing,  sibilus  and  rhonchus  are  heard,  but  no  vesicular  murmur.  Pro- 
longed cases  have  emphysematous  lungs  and  possibly  some  dilatation  of 
the  right  side  of  the  heart.  The  dyspnoea  is  less  paroxysmal,  less  severe 
and  of  longer  duration  than  in  adults.  Minor  paroxysms  are  not  uncommon. 
The  attacks  subside  slowly,  or  may  terminate  in  a  fit  of  vomiting.  Pearly 
white  pellets  are  coughed  up. 

Diagnosis. — Asthma  is  liable  to  be  mistaken  for  sudden  acute  bron- 
chitis, but  in  this  the  dyspnoea  varies  in  severity  whereas  in  asthma  it 
maintains  the  same  degree  of  intensity  for  some  time.  The  diagnostic 
features  are  the  more  or  less  sudden  onset,  the  presence  of  .dyspnoea  out  of 
all  proportion  to  the  physical  signs,  the  absence  of  fever,  the  recurrent 
paroxysms,  the  almost  sudden  recovery  when  apparently  likely  to  prove 
fatal,  and  an  appropriate  family  history.  Care  must  be  taken  to  exclude 
cardiac  and  renal  dyspnoea,  and  that  due  to  diabetes  ;  the  pressure  of  a 
retro- oesophageal  abscess,  enlarged  thymus  or  bronchial  glands  ;  dyspnoea 
from  laryngeal  affections  and  foreign  bodies  in  the  air  passages.  In  laryn- 
geal obstruction  the  dyspnoea  is  inspiratory  and  in  spasmodic  asthma  it  is 
expiratory.  In  catarrhal  asthma  it  is  more  rapid,  less  laboured,  and  less 
expiratory.  The  spasmodic  type  is  differentiated  by  the  absence  of  catarrh, 
recession  and  fever  ;  hyper-resonance  ;  pronounced  expiratory  dyspnoea, 
with  slow  and  laboured  breathing  ;  freedom  from  catarrh  between  the 
attacks,  and  emphysema.  Hysterical  dyspnoea  may  be  paroxysmal  but 
is  not  accompanied  by  distress. 

Prognosis. — Attacks  arc  rarely  fatal  but  may  prove  so  in  infants. 
Death  results  from  suffocation,  cyanosis  and  prostration.  Much  emphy- 
sema is  found  after  death.  Recurrent  attacks  are  more  probable  in  the 
spasmodic  than  in  the  catarrhal  type  or  in  those  cases  in  which  a  definite 
exciting  cause  can  be  found. 


404  Chapter  XXXVI. 

The  prospects  of  recurrence  and  ultimate  cure  depend  on  the  family 
history,  the  social  position,  the  liability  to  catarrh,  and  the  presence  of  a 
definite  exciting  cause.  Most  children  recover,  the  attacks  subsiding  at  or 
before  puberty.  Cases  due  to  special  odours  or  foods  are  usually  persistent. 
Recurrence  is  often  periodic.  Unfavourable  signs  are  prolonged  and 
frequent  attacks,  with  incomplete  recovery  between  the  paroxysms,  emphy- 
sema and  dilatation  of  the  right  ventricle.  The  greater  the  freedom  from 
respiratory  catarrh  between  the  attacks,  the  better  is  the  outlook,  for  the 
less  is  the  damage  done  to  the  lungs. 

Treatment. — Keep  the  child  in  as  good  health  as  possible,  devoting 
attention  to  rendering  it  insusceptible  to  dyspepsia  and  catarrhal  affections, 
and  to  increasing  the  stability  of  the  respiratory  centre.  The  diet  should 
be  simple,  nutritious,  and  consist  of  small  regular  meals,  avoiding  meat 
extracts  and  excess  of  carbohydrates,  and  not  allowing  much  meat  or 
vegetables.  Fruit  can  usually  be  given.  An  anti-diabetic  diet  has  in  my 
experience  proved  absolutely  useless.  Exclude  foods  which  definitely  cause 
an  attack.  Attend  to  idiosyncrasies  in  climate,  altitudes,  town  or  country. 
High  altitudes  are  unsuitable  for  emphysema,  but  are  beneficial  in  the 
early  spasmodic  cases.  Choose  for  these  places  such  as  Mont-Dore-les-Bains 
in  France,  the  Engadine  or  Colorado.  If  there  is  much  catarrh,  choose  a 
warm  dry  climate  or  seaside  air  and  sandy  soil,  e.g.,  Bournemouth, 
Hastings  and  the  Ascot  district.  Attend  to  all  sources  of  nasal  irritation 
and  local  obstruction  ;  remove  adenoids  and  enlarged  tonsils.  An  emetic 
may  cut  short  an  attack,  e.g.,  injec.  apomorph.  m.  1-5,  up  to  the  age  of 
1  year.    Give  a  purge,  if  it  is  due  to  intestinal  irritation. 

During  the  paroxysm  of  spasmodic  asthma  keep  the  child  in  a  warm 
bed  in  a  room  with  the  windows  open.  General  vaso-dilatation  is  induced 
by  hot  water  or  vapour  bath  ;  hot  fomentations  or  turpentine  stupes  to  the 
chest ;  trinitrin  or  nitrites  internally,  chloral  by  mouth  or  rectum,  or 
alcohol.  Constriction  of  the  respiratory  mucosa  is  encouraged  by  inhalation 
to  cold  air  from  ice  in  a  jug  or  inhaler,  adrenalin  1  in  1000,  or  the  fumes  of 
brown  paper,  nitre  paper,  the  leaves  of  stramonium,  belladonna  or  hyos- 
cyamus,  or  Himrod's  powder.  Grindelia  robusta  is  occasionally  beneficial. 
Anything  which  increases  the  action  of  the  heart  increases  the  dyspnoea, 
unless  the  blood  pressure  also  falls.  Many  cardiac  depressants  such  as  tartar 
emetic,  lobelia  and  tobacco  do  no  good  until  they  produce  nausea,  faintncss 
or  collapse.  In  catarrhal  asthma  of  infants  give  inhalations  of  terebene, 
pine  oil  or  creosote  m.  20  to  the  pint ;  and  tartar  emetic  gr.  t-1q,  trinitrin 
gr.  -gi^,  pulv.  ipecac,  gr.  -J^  hourly  until  relief  is  obtained.  Atropin 
gr.  3^0^  to  y^o  subcutaneously  is  sometimes  useful.  Morphia  stops  an 
attack  but  should  rarely  be  employed. 

Between  the  attacks  give  a  course  of  pot.  iod.  or  syr.  f er.  iod.  and  cod- 
liver  oil.  Arsenic,  strychnia  and  cinchona  are  useful  tonics.  Cauterisation 
of  the  nose  may  be  tried.     The  general  treatment  includes  respiratory 


Asthma.  405 

exercises,  hill  climbing,  cycling  and  swimming  ;  suitable  diet  and  elimina- 
tion ;  Spa  treatment  and  Turkish  baths.  It  is  infinitely  more  important 
to  attend  to  the  general  health  of  the  child,  to  prevent  erroneous  methods 
of  feeding,  to  remove  local  sources  of  irritation  and  to  cure  the  catarrhal 
tendency,  than  to  rely  upon  measures  for  relieving  or  cutting  short  the 
paroxysms. 


CHAPTER    XXXVII 

BKONCHITIS    AND    BRONCHO-PNEUMONIA. 

Acute    Bronchitis  —  Plastic    Bronchitis  —  Chronic    Bronchitis  —  Capillary 
Bronchitis  or  Broncho- Pneumonia. 

Catarrhal  affections  of  the  bronchial  tubes  are  very  common  in  infants, 
and,  to  a  much  less  extent,  after  infancy.  They  are  dangerous  because  the 
young  cannot  cough  and  expectorate,  and  portions  of  the  respiratory  area 
become  useless  from  atelectasis.  They  are  subdivisible  into  groups  accord- 
ing to  the  degree  of  extension  of  inflammation  down  the  respiratory  passages. 
All  these  affections  are  infrequent  after  the  third  year,  except  as  complica- 
tions of  other  diseases. 

The  main  predisposing  causes  are  rickets  and  impaired  vitality.  Hence 
the  lack  of  maternal  nursing  is  a  potent  factor.  The  chief  exciting  causes 
are  chill,  rapid  changes  in  temperature,  wet  and  exposure,  and  cold  baths. 
A  few  cases  are  due  to  direct  inhalation  of  irritants,  such  as  steam  from  a 
kettle.  Many  are  secondary  to  extension  of  catarrh  from  the  throat,  naso- 
pharynx or  larynx.  They  are  common  complications  of  measles,  whooping 
•cough  and  influenza,  and  frequent  in  typhoid  fever,  diphtheria  and  other 
infectious  diseases.  Many  are  due  to  tuberculosis,  or  a  terminal  infection  of 
ileo-colitis  and  summer  diarrhoea.  Pathologically  they  may  be  ascribed  to 
infection,  the  bactericidal  action  of  the  mucosa  being  reduced  by  congestion. 

Acute  Bronchitis. —  Tracheo-bronchitis  is  limited  to  congestion  of  the 
mucosa  of  the  trachea  and  large  bronchi,  with  desquamation  of  epithelium 
and  exudation  of  mucus  and  muco-pus.  As  the  inflammation  spreads 
downward  it  involves  the  smaller  tubes  on  both  sides,  affecting  the  whole 
thickness  of  the  walls  of  the  bronchioles  and  the  peribronchial  tissues.  Pus 
and  mucus  can  be  squeezed  out  of  the  smaller  tubes  after  death.  It  next 
spreads  to  the  minute  tubes  and  alveoli,  causing  broncho-pneumonia.  In 
fatal  cases  of  capillary  bronchitis  there  is  more  or  less  atelectasis.  In  the 
other  varieties  emphysema  is  more  common.  The  mediastinal  glands  are 
enlarged. 

Symptoms. — Tracheo-bronchitis  and  bronchitis  of  the  large  and 
median  tubes  are  comparatively  mild  affections.  They  are  rarely  fatal, 
except  in  the  very  weakly  or  in  the  presence  of  acute  infectious  disease. 
Attacks  last  for  about  a  week  or  10  days.  General  malaise  is  slight  and 
may  be  quite  absent  in  mild  cases. 


Bronchitis  and  Broncho- Pneumonia.  407 

In  primary  cases  the  onset  is  more  or  less  acute.  In  a  secondary 
spread  downward  the  symptoms  are  usually  limited  to  hoarseness  and 
frequent  cough,  with  substernal  pain  and  perhaps  spasmodic.  On 
auscultation  there  may  be  no  abnormal  sounds  ;  a  little  roughness  of  the 
respiratory  murmur  ;  or  rhonchus  and  sibilus,  especially  in  the  subclavicular 
and  interscapular  regions,  according  to  the  degree  of  extension.  The 
breathing  is  weak  and  more  frequent,  wheezing  may  be  felt,  and  the  note  is 
resonant.  Older  children  may  complain  of  a  feeling  of  tightness  or  con- 
striction across  the  chest.  Respiration  is  increased  in  proportion  to  the 
fever,  mucosal  swelling  and  secretion.  The  cough  varies  in  severity  ;  at 
first  dry  and  hard,  later  loose  and  moist.  Rales  may  be  heard  in  the 
chest.  Typical  bronchitic  sputa,  occasionally  blood-stained  at  the  onset, 
may  be  expectorated  by  older  children.  Those  under  6  years  of  age  gener- 
ally cough  the  sputum  into  the  throat  and  swallow  it.  Anorexia,  dyspepsia, 
and  constipation  or  diarrhoea,  are  often  present.  Vomiting  maybe  induced 
by  coughing  or  the  irritation  of  sputum  in  the  throat.  The  temperature 
runs  up  to  101-103°  F.  in  generalised  cases  of  medium  severity,  depending 
on  the  nature  of  the  infection  rather  than  the  actual  pathological  changes. 
It  comes  down  gradually  in  a  few  days. 

Treatment. — Delicate  and  tuberculous  children  must  be  protected 
from  attacks  by  careful  feeding  and  general  hygiene.  It  is  a  mistake  to 
coddle  infants  in  hot  stuffy  nurseries.  They  should  be  gradually  inured  to 
free  exposure  to  fresh  air  and  all  changes  in  temperature,  provided  they  are 
properly  clad  and  not  exposed  to  strong  cold  wind.  At  night  they  should 
sleep  in  a  large  airy  room  with  the  window  open.  The  bed  must  be  screened 
from  direct  draught  and  a  fire  lighted  in  the  room,  if  the  weather  is  cold. 
The  temperature  of  the  room  should  not  exceed  65°  F.  in  the  first  year, 
60°  F.  in  the  second,  and  may  be  permitted  to  fall  to  50°  F.  in  later  years. 
The  child  should  wear  a  flannel  or  Jaeger  nightdress,  be  well  covered  with 
clothes  and  allowed  a  hot  water  bottle.  Up  to  the  fifth  year  of  life  children 
must  be  guarded  from  exposure  to  measles,  whooping  cough  or  influenza, 
for  the  bronchial  catarrh  common  in  these  diseases  is  liable  to  end  in  fatal 
broncho-pneumonia.  Delicate  infants  must  be  protected  from  the  risk 
of  catching  the  ordinary  infectious  cold.  If  the  child  develops  catarrh  of 
the  upper  respiratory  passages  whether  in  the  nose,  naso-pharynx,  tonsils, 
pharynx  or  larynx,  it  must  be  kept  in  bed  as  long  as  there  is  fever  and 
indoors  until  practically  well.  The  temperature  of  the  room  should  be 
kept  at  about  65°  F.  While  in  bed  the  position  should  be  often  changed. 
Debilitated  infants  must  not  be  allowed  to  lie  on  their  backs  all  day.  They 
should  be  nursed  at  intervals  or  put  in  the  prone  position. 

An  attack  may  be  cut  short  by  a  hot  bath,  diaphoretics,  a  dose  of 
calomel  or  castor  oil,  and  a  small  dose  of  Dover's  powder.  Phenacetin  and 
aspirin  are  sometimes  useful.  If  the  mischief  progresses,  apply  stimulating 
counter-irritants  to  the  chest  and  put  on  a  pneumonia  jacket  of  cotton  wool. 


408  Chapter   XXXVII. 

Poultices  are  better  avoided.  If  there  is  much  fever,  compresses  at  the 
room  temperature  can  be  applied  to  the  chest  every  £-2  hours.  Emetics 
and  expectorants  do  more  harm  than  good  in  the  first  year  of  life.  They  are 
liable  to  upset  the  stomach  and  depress  the  child.  Vinum  ipecac,  may  be 
given  in  drachm  doses  every  J-l  hour  until  it  acts  as  an  emetic  on  strong 
healthy  children  whose  tubes  are  blocked  with  secretion. 

Inhalations  of  simple  or  medicated  steam  relieve  the  feeling  of  tightness 
and  induce  secretion.  Later  on  turpentine,  creosote  and  the  oil  of  pine  or 
eucalyptus  can  be  given,  sprinkled  on  cardboard  or  lint,  for  10-15  minutes 
at  a  time  t.d.s.  In  early  stages  a  mixture  of  vin.  ipecac  (or  vin.  antimon.), 
pot.  citrat.  and  syr.  tolu  in  small  doses  is  unlikely  to  do  harm.  Ammonium 
chloride  and  potassium  iodide  can  be  given  in  a  day  or  two  to  render  the 
secretion  more  liquid,  and  later  on  drugs  such  as  squills,  creosote  and 
terebene.  Cardiac  and  respiratory  stimulants,  as  in  broncho-pneumonia, 
may  be  needed. 

As  a  general  principle  mild  cases  require  little  treatment  except  careful 
feeding  and  nursing,  and  more  severe  ones  are  treated  on  the  same  lines  as 
broncho-pneumonia.  In  older  children  minute  doses  of  opium  may  be 
given  at  the  onset  and  then  ammonium  chloride,  or  terebene  m.  2-5  on 
sugar,  and  inhalations  of  creosote  or  turpentine.  Phenacetin  and  Dover's 
powder  are  useful  if  the  cough  is  troublesome  and  secretion  scanty. 

Plastic  Bronchitis. — A  fibrinous  or  membranous  secretion  is  commonly 
due  to  extension  of  diphtheritic  membrane  from  the  larynx.  Sometimes 
it  is  primary,  acute  or  chronic,  and  of  doubtful  causation.  Such  cases  may 
be  due  to  the  pneumococcus  or  to  the  diphtheria  organism.  The  membrane 
may  be  limited  or  extend  widely,  even  to  the  minutest  tubes.  It  is  partially 
loose  where  it  is  becoming  separated,  previous  to  being  coughed  up. 
Patches  of  collapse,  broncho-pneumonia  and  emphysema  are  often 
present. 

Cases  are  ushered  in  with  headache,  cough,  vomiting,  and  the  feeling  of 
a  lump  in  the  chest.  The  aspect  is  dusky  and  the  sputum  blood-stained. 
The  symptoms  are  those  of  bronchitis  of  a  severity  varying  with  the 
degree  of  extension  of  the  membrane.  The  chronic  form  is  preceded  by 
several  attacks  of  prolonged  bronchitis  and  is  characterised  by  severe 
dyspnoea,  coughing  fits,  often  paroxysmal  and  associated  with  suffocation, 
and  the  expectoration  of  membrane.  In  prolonged  cases  anorexia,  pallor 
and  wasting  may  be  present.  Examination  of  the  chest  yields  signs  of 
bronchitis  and  secondary  infection.  If  the  mischief  is  unilateral  or  unilobar 
there  may  be  impairment  of  resonance,  large  rales,  and  bronchial  breathing. 
S.  West  (1908)  reported  a  case  of  a  girl,  11  years  of  age,  who  had  7  attacks 
in  4  years,  in  which  were  found  absent  breath  sounds  and  vocal  resonance, 
and  stony  dulness  due  to  collapse  of  the  lung,  with  extreme  displacement  of 
the  heart  and  mediastinum.  These  physical  signs  disappeared  when  the 
cast  was  coughed  up.    . 


Bronchitis  and  Broncho- Pneumonia.  409 

The  diagnosis  depends  on  the  expectoration  of  the  membrane.  It 
is  often  coughed  up  in  balls  and  is  not  recognised  as  membrane  unless 
floated  out  in  water.  That  from  the  trachea  and  larger  bronchi  looks 
somewhat  like  cooked  macaroni  and  from  the  smaller  tubes  like  vermicelli. 
It  may  form  an  arborescent  mould  of  the  whole  bronchial  tree  or  the 
branches  of  one  lobe.  A  central  cavity  is  exceptional.  The  membrane  is 
composed  of  fibrin,  leucocytes  and  epithelial  cells,  possibly  ciliated  ones  from 
the  trachea.    It  is  soluble  in  lime  water  and  alkalies. 

Acute  cases  last  a  few  weeks  but  are  usually  fatal.  Chronic  cases  may 
continue  for  months  or  years,  with  intervals  of  days  or  weeks  between 
the  attacks.  The  temperature  is  generally  raised  and  at  its  maximum  just 
before  the  cast  is  coughed  up.  Afterwards  the  child  improves  and  may  be 
apparently  well  till  membrane  forms  again  and  gives  rise  to  dyspnoea. 

These  cases  are  treated  by  inhalation  of  alkalies,  creosote,  terebene  or 
turpentine  ;  potassium  iodide  and  pilocarpin  internally  ;  and  residence 
in  a  warm  dry  climate. 

Chronic  Bronchitis. — Chronic  bronchitis  is  uncommon  in  children.  It 
may  be  a  sequel  of  an  acute  or  sub-acute  attack  in  a  delicate  child  or  one 
living  in  bad  hygienic  surroundings.  Predisposing  factors  are  deformity 
of  the  chest  from  rickets  and  spinal  curvature,  congenital  heart  disease, 
mitral  stenosis  and  regurgitation,  tuberculosis  and  bronchiectasis.  A  few 
cases  possibly  are  due  to  congenital  syphilis. 

Cough  is  the  main  symptom.  It  is  more  or  less  chronic,  worse  in  cold 
weather  and  winter,  worse  in  the  early  morning  from  accumulation  of 
secretion  in  the  tubes  during  sleep,  and  often  paroxysmal  from  bronchial 
spasm  and  suggestive  of  whooping  cough.  Expectoration  is  usually  scanty. 
The  general  health  is  little  or  not  at  all  affected.  Vomiting  may  be  induced 
by  cough,  especially  in  the  morning  after  breakfast.  Bronchitic  rales 
may  be  present  in  the  morning  and  during  exacerbations.  The  chest 
becomes  emphysematous. 

The  diagnosis  is  based  on  the  history,  emphysema,  bilateral  physical 
signs,  and  the  absence  of  signs  of  tuberculosis  such  as  nocturnal  fever, 
wasting,  and  tubercle  bacilli.  Pertussis  must  be  excluded.  The  duration 
of  the  disease  is  indefinite  and  there  is  great  liability  to  attacks  of  acute 
or  sub-acute  bronchitis. 

These  patients  are  treated  by  climate,  clothing,  food  and  cod-liver  oil. 
Terebene  or  hydrate  of  terpene,  m.  2-5  on  sugar  quartis  horis,  relieves  bron- 
chial spasm,  lessens  dyspncea  and  makes  the  secretion  less  and  thinner.  Pot. 
iod.  and  ammon.  chlor.,  cieosote  and  expectorants,  and  alkalies  are  also 
useful ;   and  digitalis  in  cardiac  cases. 

Broncho-Pneumonia. — Syn.  :  Capillary  Bronchitis — Catarrhal  or 
Lobular  Pneumonia — Acute  Infantile  Broncho- Pneumonia — Disseminated 
Patchy  Pneumonia — Broncho-pneumonitis.  Broncho-pneumonia  is  the 
best  name  for  this  disease  for  it  is  a  catarrhal  inflammation  of  the  respiratory 


410  Ckapter  XXXVII. 

tract  which  extends  to  the  minutest  bronchioles  and  to  the  adjacent  alveoli 
of  the  lungs.  It  causes  peribronchitis,  inflammation  of  the  interstitial 
tissue  of  the  lungs,  frequently  of  the  pleura,  as  well  as  patches  of  pneumonia. 
The  name  "  catarrhal  "  suggests  the  common  mode  of  production  and 
"  lobular  "  distinguishes  it  from  lobar  pneumonia,  while  "  capillary  bron- 
chitis "  indicates  that  the  minute  tubes  are  affected. 

The  affection  is  essentially  one  of  infancy  and  is  rare  after  the 
fourth  year.  Quite  half  the  cases  occur  in  the  first  year  of  life,  one-third 
in  the  second  year  of  life,  and  one-tenth  in  the  third  year.  During  the 
first  year  the  cases  are  equally  distributed  in  each  quarter.  After  infancy 
it  is  rarely  seen  except  as  a  complication  of  other  diseases.  In  addition 
to  being  one  of  the  most  common,  it  is  one  of  the  most  serious  diseases  of 
infancy.  Its  gravity  is  increased  in  the  very  young,  the  badly  nourished, 
and  those  weakened  by  grave  illness.  Two-thirds  of  the  cases  occur  in  the 
winter  and  spring.  It  is  both  more  frequent  and  more  serious  among  the 
poor  because  of  debility  and  lack  of  care. 

The  general  etiology  is  that  of  bronchitis.  About  one-third  of  the 
cases  are  primary  and  the  remainder  secondary  to  bronchial  catarrh.  The 
susceptibility  of  infants  to  this  form  of  lung  disease  is  due  to  the  incomplete 
development  of  the  alveoli  during  the  early  years  of  life,  for  they  are  not 
fully  developed  till  the  third  or  fourth  year.  Primary  broncho-pneumonia 
may  result  from  chill,  but  is  most  commonly  a  pneumococcal  infection,  such 
as  would  have  induced  pneumonia  in  older  children. 

Bacteriology. — The  majority  of  the  primary  cases  are  due  to  the 
pneumococcus  alone,  and  the  rest  to  the  pneumococcus  in  conjunction 
with  other  organisms,  especially  the  streptococcus.  In  secondary  cases 
the  streptococcus  is  the  most  common,  alone  or  with  the  pneumococcus. 
The  influenza  bacillus,  diphtheria  bacillus  and  B.  coli  have  also  been  found. 

Classification. — On  grounds  of  severity  there  are  four  groups.  The 
first  is  fatal  in  12-36  hours.  The  second  group  lasts  for  6-10  days.  The 
third  is  prolonged  for  3  or  4  weeks,  occasionally  6  or  8  weeks.  The  fourth 
is  cachectic  in  character,  with  little  or  no  fever  and  often  evidence  of  little 
or  no  disease  during  life.  S.  West  divides  cases  into  three  types  : — (1)  A 
secondary  broncho-pneumonia  of  gradual  onset  with  hectic  temperature, 
prolonged  course,  relapses,  and  termination  by  lysis  ;  (2)  Cases  of  sudden 
onset  but  otherwise  resembling  the  first  group  ;  (3)  A  primary  variety  with 
no  antecedent  affection  of  the  bronchi.  This  is  characterised  by  sudden 
onset,  short  duration,  persistently  high  temperature,  no  relapses,  and 
termination  by  crisis.  It  is  usually  pneumococcal  and  clinically  identical 
with  lobar  pneumonia  of  adults  from  which  it  only  differs  in  extent  of 
physical  signs.  According  to  West  it  is  really  a  patchy,  pneumococcal 
pneumonia.  On  anatomical  grounds  we  may  speak  of  a  "  capillary  bron- 
chitis," with  no  physical  signs  of  consolidation  during  life,  though  small 
patches  are  found  after  death  ;    "  lobular  pneumonia,"  in  which  there  are 


Bronchitis  and  Broncho- Pneumonia.  411 

definite  small  patches  of  bronchial  breathing,  possibly  aggregated  into  a 
sufficiently  large  mass  to  cause  a  local  area  of  dulness  ;  and  a  "  lobar  " 
form,  in  which  the  patches  are  so  large  and  confluent  as  to  closely  resemble 
lobar  pneumonia. 

Some  cases  are  characterised  by  intense  pulmonary  congestion,  or  by 
rapid  dilatation  and  failure  of  the  heart,  or  by  high  temperature  and  acute 
delirium,  or  by  asthenia  or  toxaemia.  Thus  we  may  speak  of  congestive, 
cardiac,  nervous,  asthenic  and  toxoemic  types.  On  the  whole  it  is  advisable 
to  recognise  these  different  clinical  groups  and  that  they  may  occur  in 
primary  or  secondary  varieties,  and  in  any  type  of  anatomical  distribution. 

Morbid  Anatomy. — In  capillary  bronchitis  the  lung  is  vesicular  through- 
out and  engorged  at  the  onset,  and  shows  patches  of  collapse.  In  broncho- 
pneumonia irregular  areas  of  consolidation  are  present.  The  pneumonic 
condition  may  be  peribronchial,  limited  to  the  air  cells  round  the  smaller 
tubes  ;  bronchial  and  vesicular  simultaneously  ;  or  in  the  form  of  irregular 
lobular  pneumonia  with  no  definite  relation  to  the  bronchioles.  Isolated 
lobules  or  groups  of  lobules  appear  as  prominent  purplish  patches  on  the 
surface.  These  patches  are  more  or  less  grey  and  give  the  lung  a  granular 
feel,  like  "  frog's  spawn,"  on  passing  the  finger  over  the  cut  surface.  Exuded 
fluid  can  be  squeezed  out  of  the  bronchi  and  inflamed  lobules.  Isolated 
patches  on  the  surface  are  surrounded  by  emphysema.  In  the  lobar  type 
the  consolidated  area  is  not  as  sharply  defined  as  in  true  pneumonia,  and 
portions  of  the  lobe  escape.  Thus  the  different  stages  are  acute  congestion, 
commencing  consolidation,  patchy  red  and  grey  hepatisation,  and  general 
grey  hepatisation.  In  the  last  stage  isolated  pneumonic  patches  break 
down  and  form  small  cavities  containing  pus  ;  the  vesicles  are  full  of 
leucocytes  and  the  alveolar  septa  much  thickened  ;  vesicular  and  inter- 
stitial emphysema  are  present. 

Broncho-pneumonia  is  generally  bilateral,  in  the  posterior  parts  of  the 
lower  lobes,  especially  in  infants  under  one  year  kept  constantly  on  the 
back.  Often  it  has  a  paravertebral  distribution  up  to  the  middle  of  the 
scapula.  It  rarely  extends  beyond  the  axilla.  Both  lungs  are  affected  in 
over  half  the  cases  and  the  base  five  or  six  times  as  often  as  the  rest  of  the 
lung.  It  may  be  unilateral  and  affect  any  part,  notably  that  portion  of  the 
left  upper  lobe  in  front  of  the  pericardium. 

Symptoms. — In  the  primary  cases  the  onset  is  sudden  and  acute  with  a 
rise  of  temperature  to  103-105°  F.,  severe  dyspnoea,  great  prostration  and 
occasionally  convulsions.  Vomiting  occurs  in  two-thirds  of  the  cases  and 
there  is  often  pain  in  the  side.  The  fever  shows  remissions  of  2-3°  F.  every 
morning  but  is  sometimes  higher  in  the  morning  than  at  night.  The  course 
is  that  of  true  pneumonia  ending  by  crisis  and  it  is  rarely  fatal.  In  the 
secondary  type  the  onset  is  often  sudden  but  generally  more  insidious.  Many 
attacks  are  ushered  in,  or  preceded  for  a  day  or  two,  by  diarrhoea  and 
vomiting.     Usually  after  a  variable  period  of  slight  bronchial  catarrh  the 


412  Chapter   XXXVII. 

child  becomes  rapidly  and  seriously  ill  with  cough,  fever  and  respiratory 
distress.  The  temperature  rises  to  about  104°  F.,  and  ranges  irregularly 
between  that  and  102°  F.  A  mild  attack  lasts  3-5  days  and  subsides  by 
a  fairly  rapid  lysis.  In  10  per  cent,  the  fall  of  temperature  is  so  rapid  as  to 
deserve  the  name  of  crisis.  Often  a  pseudo-crisis  and  secondary  rise 
occur.  In  asthenic  cases  there  may  be  little  fever  and  even  a  subnormal 
temperature  throughout,  although  lung  consolidation  is  extensive.  Eelapses 
are  apt  to  occur  in  the  secondary  variety  and  may  be  similar  in  character 
and  course  to  that  of  the  primary  type.  Remissions  and  exacerbations  are 
common,  and  fever  may  continue  for  several  weeks  and  subside  gradually. 

An  Acute  Congestion  of  the  Lungs  sometimes  occurs  in  }roung  infants. 
The  onset  is  sudden  with  high  temperature,  dyspnoea,  shallow  breathing,, 
cyanosis  and  prostration.  The  symptoms  indicate  severe  toxaemia  and  no 
suggestive  lung  signs  may  be  found.  The  babe  is  listless  and  apathetic.  The 
fever  and  symptoms  may  abate  in  2  or  3  days,  or  clear  up  entirely  within 
a  week. 

The  general  symptoms  of  broncho-pneumonia  are  very  variable. 
In  a  well-marked  case  the  facial  aspect  is  anxious,  of  a  livid  pallor  or 
cyanosed,  with  injected  eyes.  The  nails  are  bluish  and  the  skin  a  dull 
leaden  hue  in  bad  cases.  The  child  is  restless  and  the  cry  short  and 
suppressed.  Respiration  is  hurried  and  laborious,  60-90  per  minute,  or 
more  when  the  small  bronchi  are  invaded.  The  early  alteration  in  the 
ratio  of  respiration  to  pulse  rate  is  a  valuable  sign.  The  alae  nasi  dilate  and 
the  respiratory  obstruction  causes  exaggerated  movements  of  the  chest, 
with  considerable  recession  of  the  soft  parts  and  especially  of  the  lower  ribs 
in  the  lateral  regions.  The  child  is  greatly  distressed  by  the  difficulty 
in  breathing.  This  distress  is  an  important  feature  for  it  is  absent  in 
pneumonia,  although  respirations  may  be  as  frequent,  but  in  pneumonia 
there  is  not  the  same  obstruction  in  the  air  passages.  The  pulse  rate  ranges 
from  140-200.  It  is  decreased  in  volume  and  often  irregular.  The  tongue 
is  furred,  appetite  lost,  abdomen  often  distended  from  tympanites,  and 
diarrhoea  or  constipation  present.  The  child  is  irritable,  listless  and 
drowsy,  or  languidly  restless.  Prostration  increases  with  toxaemia  and 
greater  involvement  of  the  lung,  and  may  pass  into  the  typhoid  state. 

In  the  very  malignant  type,  most  frequent  in  young  infants,  the 
mechanical  congestion  is  general,  obstruction  complete,  and  toxaemia 
marked.  The  temperature  is  over  104°  F.,  breathing  hurried,  pulse  rapid 
and  weak,  prostration  grave,  'and  cough  often  absent.  There  may  be  no 
physical  signs  ;  sometimes  vesicular  breath  sounds  are  absent  or  exag- 
gerated. Death  may  result  from  asphyxia  or  from  toxaemia.  In  the  latter 
case  there  is  much  collapse  and  a  temperature  of  only  100-101°  F.,  or  dulness 
and  apathy  pass  on  into  stupor  and  convulsions.  These  cases  may  be 
spoken  of  as  acute  congestion  of  the  lung,  acute  capillary  bronchitis,  or 
possibly  la  maladie  cle  Woillez  (p.  420). 


Bronchitis  and  Broncho- Pneumonia.  413 

In  the  next  most  serious  type  the  child  is  more  robust  or  the  fever, 
oppression,  asphyxia  and  signs  of  toxaemia  are  less  marked  and  of  more 
gradual  development.  It  may  be  a  sequel  of  the  previous  variety.  It  may 
clear  up  in  about  a  week,  pass  on  into  the  next  variety  or  increase  in 
severity  with  constant  cough,  hyperpyrexia,  and  death  in  a  few  days  from 
asphyxia,  respiratory  or  cardiac  failure.  In  the  more  favourable  cases 
the  onset  is  less  abrupt  and  the  physical  signs  those  of  bronchitis  until  the 
mischief  extends  downward.  Then  the  temperature  rises  to  102-104°  F., 
the  pulse  to  140-160,  respirations  to  60-90,  and  the  child  is  restless  and 
more  ill.  Cough  is  at  first  less  hard,  but  then  becomes  incessant,  hard, 
painful,  and  perhaps  paroxysmal.  Mucus  is  coughed  up  into  the  pharynx 
and  swallowed,  or  only  into  the  larynx  and  is  then  sucked  back  into  the  lung ; 
it  often  causes  vomiting.  The  alae  nasi  dilate,  the  face  is  pale  and  the 
lips  blue,  and  the  inspiratory  muscles  are  strongly  exerted.  The  expiratory 
grunting  of  pneumonia  is  heard.  On  the  third  to  the  fifth  day  the  symptoms 
subside  to  a  great  extent.  Pulse  rate,  respirations  and  fever  are  less.  The 
paroxysms  of  cough  and  restlessness  are  less  severe  and  everything  seems 
favourable  to  ultimate  recovery.  The  prognosis  may  be  satisfactory,  but 
frequently  exacerbation  ensues  in  one  or  more  days,  from  the  development 
of  a  fresh  patch  of  consolidation.  And  so  the  disease  may  run  on  for 
weeks  at  a  time,  the  inflammation  subsiding  in  one  place  and  breaking  out 
in  another  a  few  days  later. 

The  breathing  is  most  frequent  in  capillary  bronchitis.  Its  rhythm  is 
altered  in  all  varieties,  it  is  often  typically  Cheyne-Stokes.  As  the  child  gets 
worse  it  becomes  more  frequent,  shallow  and  irregular,  all  the  accessory 
muscles  are  brought  into  action,  recession  is  great  and  cyanosis  extreme. 
The  eyes  are  glazed  and  half-closed,  the  head  often  retracted,  the  pulse 
small  and  running,  and  the  extremities  cold  and  livid.  The  facial  aspect 
exhibits  ominous  pallor,  cold  sweats,  and  moaning  apathy.  Cough  and 
crying  cease,  meteorism  is  often  troublesome,  mucus  collects  in  the  throat 
and  death  results  from  convulsions  or  asthenia.  The  temperature  is  often 
low  and  breathing  very  feeble  towards  the  end. 

Cyanosis  is  a  grave  and  important  symptom  and  often  associated  with 
dilatation  of  the  right  side  of  the  heart.  Convulsions  are  uncommon  at  the 
onset  but  apt  to  occur  and  prove  fatal  in  whooping  cough  cases.  Inability 
to  recognise  parents,  excitement  and  delirium  occur  in  bad  cases.  Occasion- 
ally symptoms  such  as  head  retraction,  drowsiness,  torpor  and  vomiting, 
suggest  meningitis.  Intestinal  catarrh  or  ileo-colitis  is  often  troublesome 
and  intractable,  the  stools  containing  mucus  and  undigested  food.  It  is 
due  to  overfeeding,  impaired  digestion,  fever  and  toxaemia.  The  urine 
is  febrile  in  character,  contains  albumin  in  high  fever,  and  sometimes 
acetone. 

The  physical  signs  of  capillary  bronchitis  are  limited  to  weak  breathing 
and    fine    rales    scattered    all    over    the    lungs ;     perhaps    more    marked 


414  Chapter  XXXVII. 

in  some  parts  than  in  others  and  associated  with  impaired  resonance. 
Often  only  bronchitic  signs  are  present  though  multiple  minute  areas  of  con- 
solidation are  found  after  death.  Patchy  consolidation  is  indicated  by  the 
tympanitic  note,  local  aggregation  of  sharp  rales,  and  harsh  breath  sounds, 
usually  over  the  lower  lobe  and  near  the  spine.  Bronchial  breathing  and 
bronchophony  afford  definite  confirmation.  Bronchophony  is  more  easily 
heard  than  bronchial  breathing.  The  heart  sounds  may  be  unduly  well 
conducted  to  the  back.  Dulness  is  not  a  reliable  or  constant  sign ;  it  may  be 
absent  or  obscured  by  surrounding  emphysema.  The  cardiac  dulness  may  be 
diminished  by  emphysema  of  the  anterior  borders  of  the  lungs.  Extensive 
consolidation  gives  rise  to  the  same  signs  as  lobar  pneumonia,  but  the 
dulness  is  less  definitely  circumscribed  and  often  not  limited  to  one  lobe. 
It  is  less  marked  because  more  superficial,  and  less  complete  because  of 
intervening  areas  of  healthy  or  emphysematous  lung.  Usually  crepitations 
are  present  throughout  for  air  enters  more  or  less  into  the  bronchioles  and 
the  air  cells,  except  in  collapsed  lobules,  whereas  in  true  pneumonia  the 
cells  are  apt  to  be  completely  bunged  up  with,  exudation.  Bronchial  catarrh 
is  found  in  the  rest  of  the  lung.  In  protracted  cases  the  breathing  may 
become  cavernous  and  the  signs  of  consolidation  are  more  complete. 
It  is  often  necessary  to  make  the  child  cry  during  auscultation,  in  order  to 
get  it  to  breathe  deeply  and  for  the  sake  of  estimating  the  voice  resonance. 
Physical  signs  are  generally  present  in  a  week. 

Diagnosis. — Primary  broncho-pneumonia  closely  resembles  pneumonia 
in  its  onset  and  course.  Usually  it  is  of  shorter  duration,  if  limited  and 
localised.  Frequently  there  is  more  cyanosis  and  dyspnoea,  more  trouble- 
some cough,  more  laboured  breathing,  greater  remissions  of  temperature, 
and  disseminated  lesions.  Sometimes  differential  diagnosis  is  impossible. 
Acute  malignant  capillary  bronchitis  may  be  mistaken  for  cerebrospinal 
meningitis  or  a  specific  fever  with  suppressed  eruption.  Symptoms  are  often 
more  reliable  than  physical  signs,  and  the  diagnosis  has  to  be  based  on 
the  rapid  breathing,  high  temperature,  prostration,  cough  and  cyanosis. 
Examination  of  the  chest  may  prove  useless,  unless  secondary  pneumonia 
has  developed.  The  disease  is  often  unrecognised  in  the  first  few  months  of 
life,  for  it  may  occur  with  little  cough,  dyspnoea,  cyanosis  or  fever.  Locali- 
sation is  a  very  important  sign.  Limitation  of  catarrh  to  one  lobe  or  lung 
indicates  broncho-pneumonia  or  tuberculosis.  In  bronchitis  the  patient 
is  less  languid  and  ill,  cough  more  forcible  and  paroxysmal,  rales  coarse  and 
dulness  absent.  Friction  and  rales  are  much  alike  in  many  cases  and 
both  may  be  present.  Pain  is  a  sign  of  pleurisy.  The  signs  of  effusion 
must  be  looked  for,  if  the  symptoms  do  not  abate  in  a  week  or  two  and  the 
dulness  persists  or  increases.  In  the  first  three  months  of  life  atelectasis 
is  often  associated  with  broncho-pneumonia,  but  atelectasis  alone  is 
rare  after  this  age.  Some  of  the  apyrexial  cases  in  the  first  year  of  life 
simulate  asthma  but  the  latter  disease  is  rare  and,  though  the  breathing  is 
rapid,  there  is  little  distress.     Tuberculous  broncho-pneumonia  cannot  be 


Bronchitis  and  Broncho- Pneumonia.  415 

distinguished  by  either  symptoms  or  physical  signs.  Many  cases  run  an 
acute  course  and  are  only  recognised  after  death.  It  should  not  be 
diagnosed  hurriedly  for  simple  broncho-pneumonia  may  run  a  prolonged 
course  of  3  months  and  yet  end  in  recovery.  In  many  instances  unsuspected 
miliary  tuberculosis  is  found  in  fatal  cases  of  supposed  capillary 
bronchitis. 

Prognosis. — The  mortality  of  hospital  cases  is  very  high,  from  30-75 
per  cent,  according  to  the  severity  of  the  cases  admitted.  Compared  with 
pneumonia  it  is  a  most  deadly  disease.  On  the  other  hand  the  mortality 
in  private  practice  ranges  from  10-30  per  cent.,  according  to  the  social  class 
of  the  patient.  The  younger  the  child  the  worse  is  the  prognosis,  and  the 
mortality  is  increased  by  rickets,  deformity  of  the  chest,  debility,  diarrhoea 
and  vomiting.  It  is  bad  in  diphtheria  and  scarlet  fever,  less  dangerous  in 
measles  unless  it  occurs  before  the  rash,  less  in  pertussis,  and  good  after 
simple  bronchitis.  Primary  cases  are  not  so  fatal  as  secondary  ones. 
Streptococcal  infections  are  worse  than  pneumococcal  ones  and  are  usually 
associated  with  a  more  hectic  type  of  temperature,  which  is  consequently 
rather  a  bad  sign.  The  percentage  mortality  increases  with  the  rise  of 
temperature  above  104°  F.  The  disease  is  more  serious  if  the  pulse  rate  is 
over  180,  and  if  the  ratio  of  respiration  to  pulse  is  1-2,  or  2-3.  It  increases 
with  the  amount  of  lung  involved,  but  the  less  definite  the  area  of  consoli- 
dation the  worse  is  the  prognosis,  for  the  disease  is  less  fatal  in  the  lobar 
pneumonic  type.  Late  convulsions  are  almost  invariably  of  fatal  signifi- 
cance or  may  be  the  terminal  event.  Death  is  usually  due  to  asthenia, 
asphyxia,  and  sudden  or  gradual  failure  of  the  heart.  A  few  die  from 
hyperpyrexia  or  meningitis,  and  come  from  secondary  empyema.  The 
chief  bad  signs  are  increasing  restlessness,  distress,  cyanosis  and  dilatation 
of  the  right  side  of  the  heart ;  the  child  ceasing  to  shed  tears,  becoming 
drowsy  and  lethargic  ;  the  pulse  faster  and  weaker  ;  increasing  dyspnoea 
and  recession  ;  tympanites,  vomiting  and  diarrhoea.  A  suppressed  and 
inefficient  cough  and  an  unusually  low  temperature  are  signs  of  debility 
and  deficient  reflex  sensibility.  As  long  as  food  is  taken  and  digested 
well,  the  child  is  likely  to  recover.  Four-fifths  of  the  cases  recover  or  die 
within  3  weeks  and  after  4  weeks  the  outlook  is  bad.  Sometimes  the 
disease  may  continue  for  6-12  weeks  with  continued  fever,  or  irregular 
pyrexia  and  exacerbations  ;  wasting,  anaemia  and  debility  ;  anorexia, 
vomiting  and  ill-digested  stools  ;  dry  inelastic  skin,  bed  sores  and  punctate 
haBmorrhages.  Such  cases  simulate  phthisis.  The  general  state  is  of  more 
value  than  the  physical  signs  as  regards  the  immediate  prognosis  ;  but 
the  duration  of  the  illness  is  greater,  the  greater  the  extent  of  the  con- 
solidation. Death  may  occur  within  12  hours.  A  child  of  8  months, 
became  blue  and  short  of  breath  in  the  morning,  had  convulsions  at  raid-day,, 
was  collapsed  at  4  p.m.  and  died  at  6  p.m.  Relapses  and  recurrent  attacks 
may  produce  chronic  interstitial  pneumonia.  These  children  are  liable  to 
recurrent  attacks. 


416  Chapter   XXXVII. 

Complications  and  Sequela?. — Vomiting  a"nd  diarrhoea  are  common, 
especially  in  the  summer,  and  very  fatal  in  infancy.  Collapse  of  the  lung 
is  frequent  in  the  weakly  and  almost  invariably  present  in  fatal  cases. 
It  produces  increased  dyspnoea,  sometimes  sudden  and  fatal,  increasing 
cyanosis,  and  dulness.  Periods  of  great  depression,  sudden  in  onset  and 
disappearance,  may  possibly  be  due  to  this  cause.  Fibrinous  pleurisy  and 
serous  or  purulent  effusions,  often  bilateral,  are  not  uncommon.  Emphy- 
sema is  constant ;  minute  abscesses,  due  to  necrosis  of  pneumonic  patches, 
frequent ;  and  gangrene  occasional.  Other  complications  are  otitis 
media,  purulent  meningitis,  peritonitis,  purulent  arthritis,  acute  periostitis, 
and  pyEeniia.  It  is  not  always  easy  to  be  certain  which  is  the  primary 
disease.  Otitis  media  may  give  rise  to  the  usual  symptoms  or  only  be 
recognised  by  the  appearance  of  otorrhcea. 

In  all  varieties  of  bronchitis  and  broncho-pneumonia  the  mediastinal 
glands  are  engorged  and  rendered  susceptible  to  tuberculous  infection. 
Many  cases  of  tuberculosis  can  be  traced  to  an  attack  of  this  kind.  General 
tuberculosis  is  a  rare  complication,  but  both  it  and  chronic  tuberculosis 
are  not  uncommon  sequels.  It  is  difficult  to  distinguish  chronic  broncho- 
pneumonia of  an  upper  lobe  from  phthisis.  Eecovery  may  be  prolonged  on 
account  of  anaemia,  severe  dyspepsia,  or  dilatation  of  the  heart.  For  some 
months  these  children  are  liable  to  catch  cold  and  get  recurrent  attacks  of 
bronchitis,  finally  developing  chronic  bronchitis  and  emphysema. 

Treatment. — The  prophylaxis  is  that  of  bronchitis  generally.  During 
an  attack  the  child  must  be  kept  in  a  well  ventilated  room  at  60-65°  F., 
or  5°  F.  higher  if  very  weak.  Open  air  treatment  is  very  beneficial  in  secondary 
cases,  when  the  attack  is  not  due  to  exposure  to  cold.  By  this  is  meant  a 
free  supply  of  pure  air  and  not  reckless  exposure  to  damp  and  fog.  The 
good  effects  are  produced  very  quickly.  The  child  becomes  less  restless  and 
irritable,  the  face  less  flushed,  the  lips  less  blue  ;  the  pulse  and  respiration 
rates  fall ;  the  appetite  improves,  the  child  sleeps  better  and  the  strength 
is  well  maintained.    It  is  contra-indicated  by  convulsions  and  laryngitis. 

The  diet  must  be  liberal,  nutritious,  easily  digested,  and  given  in  small 
quantities.  It  is  of  the  utmost  importance  to  guard  against  tympanites. 
In  the  first  year  of  life  breast  milk  is  the  best.  If  that  is  not  available  give 
diluted  or  peptonised  milk,  sweetened  with  milk  sugar  and  strengthened 
with  plasmon  or  other  form  of  dried  casein.  Whey,  albumin  water,  veal 
or  chicken  broth  and  a  liberal  supply  of  water  can  be  given. 

Emetics  are  only  justifiable  in  the  case  of  robust  infants  with  excessive 
bronchial  secretion  and  respiratory  obstruction.  At  the  onset  of  an  acute 
attack  with  fever  give  a  bath  at  90-95°  F.,  reduced  to  80°  F.  or  75°  F.,  for  5 
minutes.  First  give  the  child  a  stimulant,  then  sit  it  in  the  water,  support- 
ing the  back  with  the  hand,  and  do  not  let  the  water  rise  above  the  level 
of  the  lower  ribs.  Sponge  it  freely,  wrap  it  up  in  a  warm  blanket  and  put  it 
back  to  bed.    A  warm  bath  night  and  morning  can  be  given  if  the  temperature 


Bronchitis  and  Broncho-Pneumonia.  417 

is  over  102°  F.  At  the  onset  a  poultice  of  linseed,  one  part  of  mustard 
to  eight  of  linseed,  bread  or  bran,  can  be  used.  It  must  be  sufficiently  large 
to  cover  the  back  of  the  chest  and  not  extend  on  to  the  front  of  the  chest  or 
abdomen.  Apply  one  every  20  minutes  for  a  couple  of  hours,  but  be  sure 
that  the  temperature  is  not  too  high,  and  then  put  on  a  cotton  wool  jacket. 
The  ordinary  measures  of  counter-irritation  are  preferable  in  mild  cases. 

If  seen  in  the  early  stage  give  tr.  belladonnse  m.  4,  or  extract  gr.  £,  every 
3  or  4  hours.  It  reduces  the  bronchial  spasm,  diminishes  the  amount  of 
secretion  in  the  tubes,  and  is  both  a  cardiac  and  respiratory  stimulant. 
If  it  does  not  produce  a  definite  result  in  24  hours  it  should  be  discontinued. 
The  belladonna  should  be  combined  with  diuretics  and  diaphoretics.  If 
the  child  is  not  seen  for  12-24  hours  after  the  onset  give  a  mixture  of 
amnion,  carb.,  pot.  iod.  or  ammon.  chlor.,  tr.  nuc.  vom.,  syr.  tolu.  and 
chloroform  water.  Under  1  year  of  age  gr.  J-l  of  the  carbonate  can  be  given 
every  4-6  hours.  Later  on  stimulating  expectorants,  especially  squill  and 
senega,  are  required.  The  squill  is  also  a  cardiac  tonic.  Small  doses  of 
phenacetin  are  useful  in  nervous  cases,  severe  headache  and  high  fever. 
Keep  the  bowels  open  by  small  doses  of  calomel  or  grey  powder.  Strong 
purges  are  apt  to  set  up  fatal  ileo-colitis. 

The  bronchitis  kettle  can  be  used,  if  the  atmospheric  air  is  very  dry 
and  the  cough  dry  and  hard.  If  it  is  used,  the  child  must  be  put  in  a  half- 
tent  so  as  not  to  keep  out  too  much  fresh  air.  The  vapour  from  the  steam 
kettle  is  apt  to  condense  and  become  cold,  and  the  child  then  inhales  a 
vapour  which  is  more  likely  to  do  harm  than  good.  Inhalations  are  best 
given  by  sprinkling  turpentine,  eucalyptus,  etc.,  on  lint  or  flannel  and 
holding  it  in  front  of  the  child's  nose  and  mouth  for  5-10  minutes  every 
2  hours.  If  there  is  much  tympanites  starve  the  child  entirely,  unless  very 
weak,  giving  nothing  but  water  for  a  time.  Gastric  distension  is  relieved 
by  lavage,  and  intestinal  distension  by  the  passage  of  a  rectal  tube  or  an 
enema  of  asafoetida  and  water.  Nux  vomica  or  strychnia  can  be  given  in 
large  doses.  Severe  diarrhoea  is  treated  on  dietetic  lines,  and  occasionally 
it  is  necessary  to  take  the  grave  responsibility  of  giving  minute  doses  of 
opium  to  check  excessive  peristalsis. 

High  fever  is  treated  by  hydrotherapeutic  measures  (p.  90).  For  ner- 
vous symptoms  associated  with  moderate  fever,  a  hot  bath  gives  more 
relief  than  a  cold  one,  but  cold  is  necessary  if  the  temperature  is  high. 

For  sudden  collapse  due  to  rapid  distension  of  the  heart  from  toxaemia 
or  mechanical  obstruction  of  the  lungs,  or  due  to  atelectasis,  give  a  mustard 
pack  or  bath,  and  inhalations  of  oxygen  or  amyl  nitrite,  and  stimulants 
freely.  Oxygen  cylinders  must  be  at  hand  in  every  bad  case.  The  most 
useful  stimulants  are  brandy,  strychnia,  nitroglycerin,  camphor  and  cafTein. 
If  the  collapse  is  definitely  due  to  cardiac  failure,  large  doses  of  carbonate 
of  ammonia,  sal  volatile  or  ether  should  be  given.  Strophanthus  and 
digitalis  help  to  prevent  dilatation  of  the  heart  but  are,  I  think,  dangerous 

2   E 


418  Chapter   XXXVII. 

if  it  is  already  present.  Dilatation  of  the  right  side  of  the  heart,  sufficient  to 
cause  dyspnoea  and  cyanosis,  is  best  relieved  by  applying  1-3  leeches  about 
the  level  of  the  right  nipple. 

For  failure  of  respiration  give  an  injection  of  atropin  gr.  Tcrocrslso* 
strychnia  gr.  ±tre-  xihy,  and  cafiein  gr.  ^.  Such  cases  should  be  encouraged 
to  breathe  deeply  by  making  them  cry,  and  by  alternate  hot  and  cold 
douching  of  the  chest.  For  passive  congestion  at  the  bases  of  the  lungs 
dry  cupping  is  of  great  use.  An  important  point  in  the  nursing  of  these 
babies  is  not  to  allow  them  to  lie  on  their  backs  all  day  long. 

In  the  convalescent  stage,  all  the  hygienic  precautions  suitable  for 
incipient  tuberculosis  should  be  adopted.  The  dilatation  of  the  right  side 
of  the  heart,  especially  after  whooping  cough,  requires  treatment  by  tonics 
and  moderate  exercise.  For  chronic  cough  give  terebene  or  creosote 
preparations.  The  ordinary  convalescent  requires  cod-liver  oil,  iron  pre- 
parations, arsenic  and  small  doses  of  quinine.  Choose  for  these  patients 
a  warm  and  dry  climate,  and  a  high  altitude  in  hot  weather. 

Mild  cases,  especially  primary  ones,  recover  under  the  simplest 
methods  of  feeding  and  nursing.  In  those  with  marked  mechanical 
obstruction,  pay  chief  attention  to  relieving  the  congestion  of  the  lungs 
by  drugs  and  counter-irritation  to  the  chest.  If  the  toxsemic  symptoms  are 
pronounced,  rely  upon  alcohol,  strychnia  and  elimination. 


CHAPTER    XXXVIII. 

PNEUMONIA. 

■Syn.  :    Pneumonic  or  Pneumococcal  Fever — Pneumococcal  Infection  of  the 
Lungs — Croupous  or  Fibrinous  Pneumonia — Pleuro- Pneumonia. 

Pneumonia  is  an  acute  infective  disease,  characterised  by  a  definite 
course  and  type  of  lung  inflammation.  It  is  a  general  pneumococcal  infec- 
tion for  the  organisms  and  toxin  are  present  in  the  blood.  Death  is  usually 
due  to  toxaemia  and  heart  failure.  It  affects  healthy  children,  is  almost 
always  primary,  of  sudden  onset,  typical  course,  ends  by  crisis,  and  is 
lobar  and  sharply  denned  in  distribution. 

Its  causation  is  the  same  as  in  adults  and  its  infective  character  is 
■clearly  established.  Groups  of  cases  are  sometimes  seen  in  hospital  practice, 
showing  a  certain  amount  of  epidemicity.  Two-thirds  of  the  cases  occur  in 
the  winter  and  spring  months,  either  because  of  the  changes  in  temperature 
•or  lowered  resistance  due  to  indoor  life  and  winter  catarrhs. 

Ante-natal  pneumonia  has  been  reported.  A  child,  born  36  hours  before 
the  death  of  the  mother  from  double  pneumonia,  lived  2  days.  Lobar 
pneumonia  was  present  and  diplococci  were  very  numerous  (Levy,  1890). 
Other  cases  of  ante-natal  pneumonia  may  be  syphilitic  in  origin.  True 
pneumonia  in  the  newborn  has  been  reported  at  8  days  of  age ;  the  whole  of  the 
left  lower  lobe  showing  red  hepatisation  (Townsend,  1889).  Pneumonic 
affections  in  the  newborn  are  usually  of  the  nature  of  broncho-pneumonia, 
due  to  inspiration  of  discharges,  cold,  etc.  Pneumonia  was  regarded  as 
-exceptional  under  2  years  of  age  and  Parrot  went  so  far  as  to  deny  its 
•existence.  Now  it  is  recognised  to  be  quite  frequent  and  even  more  common 
at  this  period  than  later  in  life.  Out  of  147  cases,  45  were  under  2  years 
■(Dunlop,  1908).  Other  observers  have  found  it  almost  as  frequent.  Riviere 
•collected  154  cases  under  10  years  of  age  :  20  in  the  first,  46  in  the  second, 
38  in  the  third,  27  in  the  fourth,  18  in  the  fifth,  and  5  in  the  ninth  year. 
These  figures  suggest  that  cases  of  primary  broncho-pneumonia  may  have 
been  included.  They  are  not  confirmed  by  post-mortem  evidence  and 
diagnosis  may  be  erroneous.  Pneumonic  affections  in  infancy  were  formerly 
regarded  as  due  to  broncho-pneumonia  ;  now  there  is  an  undue  tendency  to 
regard  broncho-pneumonia  as  pneumonia.  The  sex  incidence  is  3  boys 
to  2  girls. 


420  Chapter   XXXVIII. 

Bacteriology. — The  pneumococcus  is  a  normal  inhabitant  of  the  naso- 
pharynx and  adjacent  parts,  and  is  found  in  the  saliva  and  lungs  of  healthy 
children.  It  sets  up  disease  when  the  vital  resistance  is  lowered,  and  is 
found  in  the  blood  in  pathological  states.  In  certain  conditions  it  is  highly 
resistant  and  it  lives  for  a  long  time  in  sputum.  It  is  easily  killed  by  chemical 
agents  and  moist  heat.  As  an  infective  agent  it  has  a  short  life  history,  and 
the  rapid  development  of  an  antitoxin  leads  to  a  short  acute  illness  and 
well  marked  crisis.  It  forms  little  or  no  soluble  toxin.  It  may  produce  a 
general  pyaemic  state  giving  rise  to  broncho-pneumonia,  empyema,  arthritis,, 
peritonitis,  pericarditis,  infective  endocarditis,  abscess  of  the  lung,  throm- 
bosis of  the  lateral  sinus,  meningitis,  otitis  media,  etc.  Davies  and  Langdon 
Brown  collected  39  such  cases,  of  which  21  were  under  12  years  of  age  and 
none  of  these  due  to  pneumonia.  The  presence  of  the  organism  in  the  blood 
is  of  grave  prognostic  significance. 

Morbid  Anatomy. — The  anatomical  changes  are  the  same  as  in  adults,, 
but  the  line  of  demarcation  from  the  unaffected  tissue  is  less  well  defined 
and  the  cut  section  looks  less  granular.  No  intervening  unaffected  lobules, 
are  found  as  in  broncho-pneumonia,  but  broncho-pneumonia  may  occur 
round  pneumonic  patches  or  may  affect  the  opposite  lung,  especially  under 
2  years  of  age.  In  other  words  the  pneumococcus  may  produce  both 
broncho-pneumonia  and  true  pneumonia  at  this  age  and  even  simul- 
taneously. Pleurisy  of  all  grades  is  associated  with  it.  In  pleuro-pneumonia 
the  affected  lung  is  covered  with  a  thick  layer  of  lymph.  The  left  lower 
lobe  is  involved  in  about  one-third  of  the  cases,  and  the  right  lower  lobe  in 
about  half  that  number.  The  right  upper  lobe  is  as  susceptible  as  the 
right  lower  lobe,  and  the  left  upper  lobe  much  less  often  involved.  The 
disease  may  involve  the  whole  lung,  both  apices  or  portions  of  both  lungs> 
or  be  limited  to  one  lobe,  part  of  a  lobe  or  a  single  central  area.  The  pro- 
portion of  cases  on  the  right  side  to  those  on  the  left  is  9-8. 

Symptoms. — An  acute  idiopathic  congestion  of  the  lungs,  probably 
a  degree  of  acute  pneumonia  or  acute  capillary  bronchitis  (p.  412),  is  known 
as  la  maladie  de  Woillez.  Pne.umococci  alone,  or  associated  with  stapylococci 
or  streptococci,  were  found  in  9  out  of  14  cases  by  Carriere,  and  the 
pneumococcus  was  found  in  the  blood  in  7  out  of  10.  Leucocytosis  was. 
present.  .  The  attack  is  ushered  in  by  chilliness  or  rigor,  pain  in  the  side,, 
rapid  and  shallow  breathing,  a  moderate  degree  of  fever,  and  cough.  The 
physical  signs  are  impaired  resonance,  feeble  and  sometimes  bronchial 
breath  sounds,  and  fine  crepitations. 

The  clinical  picture  of  pneumonia  in  the  young  differs  from  that  in 
adults  because  of  the  impressibility  of  the  nervous  tissues.  After  thc 
seventh  year  it  more  closely  resembles  the  adult  type.  In  infancy  the- 
symptoms  may  be  very  alarming  and  the  cause  obscure.  Occasionally 
cough  is  slight  and  respiration  is  little  accelerated.     The  constitutional 


Pneumonia.  121 

■symptoms  depend  on  the  toxaemia  and  often  bear  no  proportion  to  the 
severity  or  extent  of  the  local  inflammation. 

The  onset  is  sudden  with  vomiting,  malaise,  pallor,  and  shivering  or  a 
feeling  of  cold.  Vomiting  occurs  in  two-thirds  of  the  cases.  It  may  be 
single  or  repeated  for  one  or  two  days  and  may  be  very  violent.  Occasion- 
ally convulsions  or  a  rigor  occur  ;  sometimes  severe  headache  and  epistaxis. 
Pain  in  the  belly  is  not  uncommon  and  is  more  frequent  in  young  children 
than  pain  in  the  chest.  It  may  be  referred  to  the  right  iliac  region. 
Probably  pleural  pain  is  rare,  for  dyspnoea  is  much  more  marked  in 
adults  than  in  children  under  5  years  of  age.  Diarrhoea  is  not  infrequent ; 
sometimes  there  is  abdominal  distension  and  constipation.  Cough  is 
slight  and  may  be  absent  for  2  or  3  days  or  throughout.  At  the  onset  it  may 
be  painful,  short  and  suppressed,  and  induce  crying.  It  is  most  marked  in 
defervescence. 

In  a  few  hours  the  face  is  flushed,  the  eyes  brilliant,  the  temperature 
raised,  the  breathing  rapid,  pulse  full  and  frequent,  and  skin  pungently  hot. 
The  child  passes  into  a  state  of  drowsiness  or  stupor ;  or  less  often  becomes 
restless  and  delirious. 

The  breathing  is  frequent  from  the  onset  but  there  is  no  true  dyspnoea. 
It  is.  increased  out  of  proportion  to  the  fever  and  pulse,  ranges  from  40-60 
or  more  per  minute,  is  shallow  or  superficial,  and  mainly  abdominal.  The 
accessory  muscles  are  not  brought  into  action  and  there  is  no  recession  of 
the  lower  ribs,  for  there  is  no  mechanical  interference  with  the  entrance  of 
air  into  the  chest.  Usually  breathing  is  quiet,  but  it  may  exhibit  a  curious 
■expiratory  moan,  grunt  or  pant,  possibly  due  to  the  pleura  being  affected. 
An  inverted  type  of  breathing  may  be  seen  in  infants  and  young  children  for 
hours  or  days.  The  pause  takes  place  after  inspiration  instead  of  after 
expiration  and  the  air  is  momentarily  retained  in  the  chest.  Sometimes  the 
breathing  is  of  a  cerebral  type,  irregular,  cyclical  in  character,  with  a 
temporary  slowing  or  actual  pause,  somewhat  like  Cheyne-Stokes  breathing. 
These  peculiarities  in  respiration  are  perhaps  due  to  disturbance  of  the 
respiratory  centre  in  the  medulla  from  stimulation  of  the  peripheral  ends 
of  the  vagus.  Possibly  this  also  accounts  for  the  initial  vomiting  and  the 
fact  that  the  heart  is  not  increased  in  frequency  in  proportion  to  the 
respiration.  If  the  vagus  is  cut  and  its  central  end  stimulated,  the  respira- 
tions are  accelerated  and  the  heart  is  slowed.  This  increased  frequency  of 
breathing  is  present  from  the  onset,  is  out  of  proportion  to  the  rise  of 
temperature,  and  does  not  vary  directly  as  the  extent  of  lung  involved. 
The  rate  falls  with  the  crisis,  still  further  in  another  2-1  days  and  finally  to 
normal  7-10  days  after  the  crisis.  An  increase  in  respirations  with  a  fall  or 
no  rise  of  temperature  may  indicate  cardiac  failure  or  muscular  exhaustion. 
If  the  temperature  rises  without  any  increase  in  respirations,  the  fever  is 
not  due  to  extension  of  lung  mischief. 


422  Chapter   XXXVIII. 

The  ratio  of  pulse  to  respiration  is  not  as  reliable  as  in  adults, 
for  the  pulse  is  so  easily  accelerated  in  infants.  It  ranges  from 
140-180,  and  a  high  rate  is  not  of  itself  unfavourable.  At  first  the  tension 
is  raised. 

During  the  progress  of  the  disease  the  facial  aspect  is  generally  placid, 
neither  anxious  nor  distressed,  in  spite  of  the  rapid  breathing,  unless  there 
is  pain.  Flushed  cheeks  are  common,  but  sometimes  there  is  marked  pallor 
and  depression.  The  alae  nasi  dilate,  usually  during  expiration.  This 
expiratory  dilatation  is  associated  with  the  inverted  type  of  respiration  and 
due  to  forcible  expiration.  Active  dilatation  during  inspiration  is  commonly 
a  sign  of  inspiratory  obstruction.  Herpes  labialis  is  present  on  the  second 
to  the  fourth  day,  though  frequently  absent  in  infants,  especially  in  the 
first  year. 

Pain  is  usually  absent.  If  it  is  abdominal  it  is  generally  situated  in  the 
epigastrium  or  at  the  navel,  occasionally  in  the  right  iliac  fossa  and 
associated  with  muscular  rigidity.  Cough  is  short  and  suppressed  and 
may  induce  crying  because  of  pain.  Sputum  can  be  collected  by  inserting 
a  tongue  depressor  to  the  back  of  the  throat,  causing  cough  and  collecting  the 
mucus  on  a  swab.  Gastro-intestinal  symptoms  are  common.  Anorexia, 
diarrhoea  or  constipation,  sometimes  vomiting,  and  distension  may  be 
present  throughout.  Jaundice,  high  temperature  and  vomiting  may  be 
early  symptoms.  Tympanites  is  frequent  and  serious.  The  knee-jerks- 
may  be  diminished  or  absent,  but  this  does  not  influence  prognosis  or 
assist  in  diagnosis. 

The  temperature  chart  is  often  as  typical  as  in  adults.  In  infants  it  is 
frequently  irregular,  showing  diurnal  variations  of  1-3°  F.,  or  even  more 
marked  oscillations,  especially  towards  the  end  of  the  process.  In  rare  cases 
oscillations  of  3-10°  are  present  throughout.  The  inflammation  of  the  lungs 
is  not  the  cause  of  the  fever,  for  the  temperature  is  often  at  its  highest 
before  any  such  inflammation  is  evident.  The  temperature  falls  suddenly, 
though  no  change  can  be  traced  in  the  condition  of  the  lung,  and  its  height 
is  not  proportionate  to  the  amount  of  lung  involved.  The  fever  ends  by 
crisis  on  the  fifth  to  the  ninth  day,  most  frequently  on  the  seventh.  Abortive 
cases  may  terminate  on  the  second  or  third  day.  A  temporary  fall  of  several 
degrees  of  temperature,  sometimes  to  normal  or  even  below,  for  a  few  hours 
is  called  a  pseudo-crisis.  It  occurs  more  frequently  in  the  young  than  in 
older  subjects,  usually  on  the  third  to  the  fifth  day,  and  is  a  good  sign. 
The  symptoms  are  temporarily  relieved  but  become  worse  with  a  further 
rise,  which  lasts  for  24-48  hours  and  is  not  a  sign  of  extension.  Crisis  is  least 
common  in  infants.  Sometimes  it  does  not  occur  until  the  fourteenth  day 
or  later,  because  of  extension  to  another  lobe,  pleurisy  or  bronchitis.  Pro- 
longed cases  are  more  likely  to  end  by  lysis.  A  crisis  is  generally  accom- 
panied by  considerable  prostration,  but  rarely  by  the  collapse  sometimes 
seen  in  adults.     The  critical  discharge  is  commonly  profuse  sweat  and 


Pneumonia.  423 

the  child  drops  into  a  quiet  sleep.    A  post-critical  fever  may  last  for  a  few 
hours.     If  prolonged,  it  indicates  spread  of  mischief  or  a  complication. 

Up  to  the  time  of  the  crisis  the  patient  steadily  gets  worse.  The  tongue 
is  thickly  coated  and  dry,  and  in  5  or  6  days  the  mental  condition  one  of 
apathy,  somnolence  or  delirium.  The  urine  is  febrile  in  character,  deficient 
in  chlorides,  contains  an  excess  of  urates  and  urea,  and  sometimes  albumin. 
The  patient  is  generally  worst  just  before  the  crisis,  but  afterwards  is  soon 
bright  and  well,  or  in  2  or  3  days  if  the  attack  is  severe. 

Physical  Signs. — Examination  is  often  difficult  because  of  restlessness 
and  irritability.  Definite  physical  signs  may  be  slight,  delayed  until  the 
fourth  or  fifth  day,  not  present  until  after  the  crisis,  absent  throughout,  or 
missed  because  they  are  so  deeply  seated.  Central  pneumonia  is  frequent 
in  children,  especially  in  the  upper  lobe,  and  the  physical  signs  may  be 
limited  to  persistent  rapid  breathing  and  high  fever. 

In  basal  pneumonia  expansion  is  deficient  in  the  subclavicular  region 
on  the  affected  side.  Generally  speaking  the  early  signs  are  distant,  faint 
or  absent  breath  sounds  with  a  tympanitic  note  due  to  vicarious  emphy- 
sema, and  harsh  puerile  breathing  on  the  opposite  side.  Consequently  the 
sound  side  seems  more  dull  and  the  breathing  may  be  mistaken  for  bronchial 
breathing.  Crepitations  are  more  often  absent  than  present.  They  may  be 
only  heard  when  the  child  cries.  Vocal  vibrations  afford  no  assistance  in 
young  children.  Bronchial  breathing  and  bronchophony,  especially  the 
latter,  are  most  valuable  signs  and  may  be  heard  on  crying  or  coughing,  even 
on  the  second  day  in  basal  pneumonia.  In  apical  pneumonia  they  are 
generally  heard  over  the  spine  of  the  scapula  on  the  fourth  to  the  sixth  day. 
Inspiration  may  be  mistaken  for  expiration  in  the  inverted  type  of  breathing, 
and  bronchial  breathing  will  then  seem  louder  on  inspiration  instead  of,  as 
normal,  in  expiration.  Always  examine  high  up  in  the  axilla,  for  consoli- 
dation here  is  often  overlooked.  The  physical  signs  clear  up  with  remarkable 
rapidity,  often  within  2  or  3  days  of  the  crisis  and  almost  invariably  within 
a  week. 

Clinical  varieties. — Certain  types  are  described  in  accordance  with  the 
predominance  of  particular  symptoms — 

1.  Cerebral  Pneumonia,  sometimes  called  eclamptic,  if  fits 
predominate  ;  meningeal,  if  coma  and  delirium.  It  may  begin  with 
convulsions.  Headache,  vomiting,  delirium  or  drowsiness,  and  some- 
times retraction  of  the  head  may  be  conspicuous  features  in  the  early 
stages  and  before  physical  signs  can  be  found  in  the  chest.  This 
type  is  the  "  brain  fever  "  of  the  novelist.  Active  delirium  is  rare  under 
3  years  and  generally  present  after  the  fourth  year.  It  may  be  wild 
or  muttering  and  is  worst  at  night.  It  is  generally  associated  with 
tremor  of  the  tongue  and  hands,  muscular  twitching  of  the  face  and 
limbs,  retraction  of  the  head,  opisthotonos,  general  rigidity,  intolerance 


424  Chapter  XXXVIII. 

of  li<*ht,  screaming  and  crying  when  disturbed,  sometimes  unilateral 
contractures  and  fits.  The  child  is  completely  unconscious  and  the 
pupils  contracted.  In  other  cases  the  cerebral  condition  is  one  of 
drowsiness  as  in  the  typhoid  state.  Cerebral  symptoms  are  more 
frequent  in  apical  than  in  basal  pneumonia.  They  are  due  to  toxsemia, 
or  to  hyperemia,  congestion  and  oedema  of  the  nervous  tissues,  or  may 
depend  on  a  high  temperature.  They  may  be  so  marked  that  the 
chest  is  not  even  examined.  The  physical  signs  precede,  accompany 
or  follow  the  cerebral  ones. 

A  true  meningoencephalitis  may  occur  as  part  of  the  pneu- 
mococcal infection  and  develop  at  the  height  of  the  fever  or  not 
until  later.  It  cannot  be  diagnosed  unless  the  base  of  the  brain  is 
involved.  The  pneumococcus  has  been  found  in  the  exudate.  Some- 
times the  cerebral  symptoms  depend  on  acute  otitis. 

2.  Pleuro- pneumonia. — In  these  cases  the  pleurisy  is  prominent 
and  masks  the  pneumonia.  The  physical  signs  depend  on  the  amount 
of  exudation.  If  there  is  much,  the  breath  sounds  are  less  distinct, 
dulness  persists  long  after  the  crisis,  or  the  case  runs  a  chronic  course 
and  ends  by  lysis. 

3.  G 'astro-intestinal  Pneumonia. — These  cases  present  the  aspect 
of  typhoid  fever.  The  tongue  becomes  inflamed,  anorexia  and  vomiting 
are  marked,  diarrhoea  is  sometimes  severe  and  intractable,  slight  jaun- 
dice may  be  present,  and  the  abdomen  is  distended,  hard,  and  may  be 
tender.  Abdominal  pain  and  constipation  are  more  frequent  than 
diarrhoea.  Cough  may  be  absent.  There  may  be  no  physical  signs  for 
some  days,  perhaps  not  until  after  the  crisis,  and  in  infants  even  absent 
throughout.  Some  of  these  cases  are  instances  of  pneumococcal 
pysemia  or  direct  infection  of  the  alimentary  tract. 

4.  Nephritic  Pneumonia. — In  rare  instances  there  is  an  acute 
hasmorrhagic  nephritis  with  general  anasarca  from  the  onset.  It  is 
difficult  to  be  certain  whether  this  or  the  pneumonia  is  the  primary 
disease.  An  acute  onset  with  vomiting,  rapid  breathing,  and  high 
fever  is  improbable  in  acute  nephritis.  The  renal  symptoms  subside 
rapidly  after  the  crisis,  not  lasting  more  than  2  weeks  and  ending  in 
complete  recovery.  Nephritis  may  be  distinctly  secondary  and 
become  subacute,  persisting  for  weeks  after  defervescence.  The  true 
nephritic  pneumonia  must  be  regarded  as  part  of  the  general  pneu- 
mococcal infection. 

5.  Pneumonic  or  Pneumoccal  Fever. — Cases  often  occur  which 
would  be  diagnosed  by  the  symptoms  and  course  as  pneumonia  if  the 
chest  were  not  examined.     Physical  signs  are  absent  throughout. 

6.  Abortive  Pneumonia. — In  these  cases  the  fever  lasts  only  a  few 
days,  even  one  or  two,  but  the  signs  of  consolidation  appear  later. 


Pneumonia.  425 

Diagnosis. — The  chief  difficulties  arise  from  the  absence  of  a  charac- 
teristic onset  or  symptoms,  and  of  sputum,  and  the  presence  of  abnormal 
types  of  disease.  The  main  features  are  the  vomiting  at  the  onset,  rapid 
breathing,  high  fever,  flushed  cheeks,  dilating  nostrils,  expiratory  grunting, 
inverted  respiratory  or  cerebral  rhythm,  short  course  and  critical  fall. 
Intractable  vomiting  (pneumonie  emetisante)  simulates  peritonitis  if  asso- 
ciated with  high  fever,  abdominal  pains  and  rigidity.  Cases  with  vomiting, 
pain  in  the  right  iliac  fossa  and  rigidity  may  be  mistaken  for  appendicitis, 
but  the  abdomen  is  not  tender  and  respiration  is  unduly  frequent.  The 
association  of  fever,  gastro-intestinal  and  nervous  symptoms  may  suggest 
acute  ileo-colitis  or  enteric  fever.  Even  in  the  pronounced  meningitic  type 
the  ratio  of  pulse  to  respiration,  rapid  breathing,  high  temperature  and 
flushed  cheeks  enable  a  diagnosis  to  be  made.  Central  pneumonia  with 
gastric  symptoms  simulates  acute  meningitis.  Occasionally  cerebrospinal 
meningitis  is  ushered  in  by  fits,  high  fever  and  rapid  shallow  breathing- 
indicative  of  a  serious  toxsemia  impossible  of  diagnosis  from  pneumonia. 
So,  too,  acute  specific  fevers  cannot  always  be  differentiated  at  the  onset. 
The  differential  diagnosis  between  true  pneumonia  and  primary  broncho- 
pneumonia depends  on  a  careful  consideration  of  the  course  and  progress 
of  the  disease  and  is  often  impossible.  The  diagnosis  of  double  pneumonia 
from  bilateral  broncho-pneumonia  is  also  very  difficult.  Occasionally  acute 
•empyema  closely  simulates  pneumonia. 

Prognosis. — Cases  are  rarely  fatal  when  sthenic  and  uncomplicated. 
The  mortality  in  childhood  ranges  from  2-5  per  cent.,  and  is  extremely 
small  after  the  second  year  of  life.  Death  may  result  from  pneumococcal 
meningitis  ;  acute  otitis  and  secondary  thrombosis  of  the  lateral  sinus, 
meningitis  or  cerebral  abscess  ;  purulent  pericarditis  or  pleurisy ;  or 
from  toxsemia.  The  toxin  acts  upon  the  heart  muscle  and  causes  dilatation, 
■and  on  the  cardiac  or  vasomotor  centre  in  the  medulla.  Death  is  some- 
times sudden  and  due  to  one  or  both  of  these  causes.  The  heart  stands  the 
strain  well,  especially  in  infancy,  for  the  right  ventricle  is  strong  and 
•dilatation  is  uncommon.     Fatal  syncope  in  convalescence  is  very  rare. 

The  prognosis  varies  with  the  age  and  nutrition.  Wasted  infants  die. 
Girls  have  less  resisting  power  than  boys.  Rickets  and  pre-existing  heart 
lesions  or  lung  affections  increase  its  gravity.  The  nephritic  type  is  some- 
times fatal.  Convulsions  at  the  onset  are  of  no  prognostic  value.  They 
rarely  occur  after  the  second  year.  During  the  course  of  the  disease  they 
usually  indicate  a  fatal  issue.  The  sthenic  cases  show  the  most  extensive 
lesions  and  the  greatest  fever.  No  estimation  of  the  extent  of  the  lung 
involved  or  the  duration  of  the  illness  can  be  based  on  the  violence  of  the 
•onset,  the  height  of  the  fever,  or  the  severity  of  the  nervous  symptoms. 
The  greater  the  extent  of  the  lung  involved,  the  worse  is  the  prognosis. 
The  outlook  is  good  if  the  temperature  is  under  103°  F. ,  bad  if  it  is  over  106°  F. 
-and  serious  if  the  fever  is  prolonged  beyond  9  days.    It  is  very  fair  as  long 


426  Chapter   XXXVIII. 

as  the  pulse  remains  under  150  and  the  breathing  under  60  per  minute. 
Diarrhoea  and  pericarditis  are  serious  complications.  Tympanites  is  a 
bad  sign.  Acute  abdominal  distention  is  not  an  uncommon  precursor  of 
death.  A  high  leucocytosis  may  indicate  a  powerful  reaction  or  virulent 
infection. 

Complications  and  Sequels. — In  spite  of  the  blood  infection  compli- 
cations are  rare.  Dilatation  of  the  right  auricle  must  be  examined  for  daily. 
Empyema  is  the  most  important  sequel  and  gives  rise  to  the  usual  signs  of 
fluid  in  the  chest,  persistent  fever,  or  a  secondary  rise  shortly  after  the 
crisis.  Thick  creamy  pus  may  be  found  a  day  or  two  after  the  crisis,  although 
loud  bronchial  breathing  is  present.  Otitis  media  and  broncho-pneumonia 
are  quite  frequent.  Among  the  other  complications  may  be  mentioned 
hyperpyrexia,  endocarditis,  pericarditis,  peritonitis,  meningoencephalitis 
and  secondary  chronic  hydrocephalus,  post-pharyngeal  abscess,  jaundice,, 
acute  nephritis,  purulent  arthritis,  osteomyelitis,  abscess  in  the  lungr 
gangrene  due  to  food  aspiration,  and  subcutaneous  emphysema.  The 
pulse  during  convalescence  may  be  infrequent  and  very  irregular,  as  a 
sequel  of  the  action  of  the  toxin  on  the  cardiac  muscle. 

Treatment. — The  natural  tendency  of  pneumonia  is  to  recovery.  Keep 
the  child  in  bed,  lightly  clothed,  in  a  well  ventilated  room  with  open  windows- 
and  temperature  60°  F.  Have  an  oxygen  cylinder  handy  if  there  is  much 
cyanosis.  Tent  beds,  steam  and  antiseptic  vapours  are  rarely  advisable, 
but  towels  soaked  in  creosote  and  eucalyptus  may  be  hung  up  in  the  room. 

Give  water  freely,  especially  if  the  child  refuses  other  fluids  ;  or  a 
plentiful  supply  of  weak  nutritious  digestible  foods,  e.g.,  milk,  whey,  weak 
tea,  fruit  juice,  plasmon,  meat  juice,  broth  and  eggs.  A  healthy  well- 
nourished  child  can  do  quite  well  without  food  for  24-48  hours  during  the 
early  acute  stage.  Overfeeding  may  cause  acute  abdominal  distension, 
vomiting  and  diarrhoea.  Do  not  wake  the  child  for  food  unless  it  is  very 
weak.  It  must  be  fed  nasally  if  necessary.  Alcohol  is  rarely  needed  before 
the  crisis. 

Locally  apply  poultices,  mustard  leaf,  ice  bag  or  ice  poultices,  or  leeches. 
Heat  is  better  borne  than  cold  and  children  commonly  resent  ice  bags.  It 
is  not  always  clear  which  portion  of  lung  is  affected,  and  there  is  no  proof 
that  local  applications  of  cold  affect  the  underlying  lung  or  that  the 
treatment  is  beneficial,  even  if  it  does  affect  the  lung.  A  mustard  leaf  or 
intermittent  turpentine  stupes  relieve  the  pain.  Dry  cupping  and  leeches 
are  even  more  efficacious.    A  pneumonia  jacket  is  of  doubtful  advantage. 

In  an  ordinary  simple  case  give  an  initial  dose  of  calomel  or  saline 
cathartic,  and  a  mixture  of  citrate  and  acetate  of  potash,  spirit  of  nitrous 
ether  and  camphor  water  every  3  or  4  hours.  Tepid  sponging  of  the  skin 
is  comforting  to  the  child,  and  helps  to  reduce  the  fever.  If  there  is  much 
vomiting  and  constipation,  small  doses  of  calomel  can  be  given  frequently. 
The  mouth  and  teeth  must  be  kept  clean. 


Pneumonia.  427 

Antipyretic  measures  are  more  necessary  for  nervous  symptoms  than 
high  fever  only.  Apply  ice  to  the  head.  Treat  fever  and  hyperpyrexia 
according  to  the  measures  recommended  on  p.  90. 

Expectorants  do  more  harm  than  good.  Drugs  such  as  tr.  veratrise 
and  tr.  aconiti,  phenazone  and  other  coal  tar  derivatives  are  depressants. 
Small  doses  of  phenacetin  can  be  given  if  the  temperature  is  very  high,  and 
to  allay  headache,  restlessness  and  nervous  irritability.  Digitalis,  in  my 
opinion,  is  more  likely  to  do  harm  than  good,  unless  arterial  tension  is  very 
low  and  the  pulse  feeble  and  weak.  In  older  children,  and  to  a  less  extent 
in  the  very  young,  the  common  condition  in  pneumonia  is  one  of  high  arterial 
tension  \#th  a  feeble  and  distended  right  auricle  and  ventricle.  Heart 
failure  is  due  to  the  action  of  the  toxin  or  prolonged  high  temperature 
on  the  cardiac  muscle,  for  which  digitalis  is  not  advisable.  A  few  leeches 
over  the  liver  will  relieve  dyspnoea,  distress  and  insomnia  due  to  dilatation 
of  the  right  heart,  by  reducing  the  size  of  the  auricle.  It  affords  relief  for 
one  or  two  days,  can  be  repeated,  and  is  not  necessarily  contra-indicated 
by  pallor  of  the  face  and  smallness  of  the  pulse.  After  leeching  it  is  possible 
that  digitalis  or  strophanthus  may  be  useful,  but  it  is  better  to  rely  upon 
strychnia,  mix  vomica,  alcohol,  caffein,  ether  and  ammonium  carbonate. 
Strychnia  is  of  more  value  than  in  adults  to  counteract  the  easily  depressed 
nerve  tone,  and  it  must  be  given  freely  if  acute  tympanites  develops. 
Cardiac  tonics  are  often  wanted  before  the  crisis  and  quinine  is  one  of  the 
best. 

Severe  dyspnoea  and  cyanosis  are  treated  by  oxygen  inhalation  and 
mustard  poultices,  dry  cupping  of  the  bases  of  the  lungs  or  leeches.  The 
cyanosis  is  often  due  to  cardiac  dilatation,  but  bleeding  is  rarely  necessary, 
except  by  leeches  over  the  liver  in  childhood.  For  toxsemic  dyspnoea  give 
atropin  and  strychnia  subcutaneously.  For  convulsions  give  chloral  per 
rectum.  Troublesome  and  irritating  cough  is  treated  by  change  of  posture, 
inhalations,  small  doses  of  vinum  ipecac,  paregoric,  heroin,  oxymel  scillse, 
syr.  of  tolu,  and  such-like  remedies.  A  small  dose  of  chloral,  ammonium 
bromide,  or  urethane  may  be  added.  The  latter  drugs  are  useful  for  sleepless- 
ness and  delirium  and  preferable  to  Dover's  powder  or  morphia,  which  are 
sometimes  necessary.  These  symptoms  are  best  treated  by  cold  to  the 
head,  tepid  sponging,  food  and  alcohol,  rather  than  by  sedatives.  Sponging 
with  cold  water,  a  drink  of  milk,  and  a  dose  of  bromide  or  veronal  is 
generally  efficacious.  If  the  cerebral  symptoms  are  marked,  give  calomel 
freely.    Serum  treatment  is  of  little  value. 

Three  days  after  the  fall  in  temperature  the  child  may  be  allowed 
out  of  bed,  if  the  lung  signs  have  cleared  up  and  there  is  no  cardiac  dilata- 
tion. In  another  week  he  may  go  out.  Tonics,  liberal  diet  and  general  care 
are  required  during  convalescence. 

Chronic  Pneumonia. — Bronchiectasis. — Chronic  inflammation  of  the 
lung  is  generally  tuberculous.     It  may  occasionally   follow  pneumonia, 


428  Chapter  XX XV III. 

broncho-pneumonia,  pleurisy,  foreign  bodies  in  the  bronchus,  or  pressure  by 
intra-thoracic  glands.  It  is  especially  apt  to  follow  the  infective  diseases 
which  give  rise  to  broncho-pneumonia,  and  is  therefore  most  frequent  at 
2-3  years  of  age. 

The  affection  is  a  chronic  interstitial  fibrosis  of  varying  causation  and 
distribution.  There  may  be  a  general  firm  adhesion  of  the  lung,  one  lobe 
or  portion  of  a  lobe  to  the  chest  wall,  diaphragm  and  pericardium.  On 
section,  the  affected  lung  is  found  hard  and  fibrous,  with  more  or  less 
complete  disappearance  of  alveolar  structure,  and  traversed  by  dilated 
bronchi.  If  secondary  to  bronchitis  or  broncho-pneumonia  the  fibrous 
changes  are  more  patchy  in  distribution,  surrounded  by  emphysematous 
areas  ;  and  the  chronic  inflammatory  process  appears,  microscopically, 
to  have  started  and  to  be  most  advanced  round  the  dilated  small  bronchi 
and  bronchioles. 

Bronchiectasis  or  bronchiolectasis  is  a  dilatation  of  the  large  or  small 
bronchial  tubes,  the  result  of  atrophy  of  their  walls  and  subsequent  thicken- 
ing from  peribronchitis.  There  is  always  more  or  less  evidence  of  a  base- 
ment membrane.  It  may  follow  or  precede  chronic  pneumonia,  and  the 
two  affections  cannot  be  clearly  differentiated.  It  is  unilateral  or  bilateral. 
It  may  affect  both  lungs,  one  lobe  or  lung,  both  lower  lobes,  and  rarely  both 
upper  or  the  right  upper  and  middle  lobes.  Like  pneumonia  it  is  most 
frequent  in  the  left  lower  lobe.  Its  etiology  is  the  same  as  that  of  chronic 
pneumonia.  Sometimes  it  can  be  traced  to  a  chronic  cough  or  chronic 
pleurisy. 

Three  forms  have  been  described.  (1)  Simple,  cylindrical  or  spindle- 
shaped  ;  (2)  Saccular ;  (3)  False  or  trabecular  bronchiectasis.  The 
cylindrical  variety  is  an  acute  dilatation  of  the  tubes,  due  to  acute  bronchitis 
and  whooping  cough.  Chronic  bronchiectasis  is  partly  cylindrical  and 
partly  saccular,  and  shows  considerable  fibroid  thickening.  The  lung  is 
eventually  composed  of  fibroid  tissue  and  dilated  tubes.  Cystic  disease  of 
the  lung  is  a  congenital  variety  of  bronchiectasis,  usually  bilateral,  in  which 
the  lung  is  cystic  throughout. 

The  cavities  are  multiple,  more  or  less  spherical,  and  in  size  up  to  that 
of  a  pea.  Sometimes  they  are  larger  and  very  irregular  in  shape.  They  are 
empty  or  contain  purulent  secretion,  and  may  communicate  with  each  other. 
Their  walls  are  thickened  and  they  are  usually  separated  from  each  other  by 
bands  or  septa.  There  is  much  fibrosis  and  destruction  of  alveoli  round  the 
cavities  and  patches  of  consolidation.  The  adventitia  of  the  blood  vessels 
is  thickened. 

Some  are  undoubtedly  dilated  bronchioles,  for  they  are  lined  by 
columnar  epithelium  and  contain  muscle  and  elastic  fibres  in  their  walls. 
Others  are  dilated  infundibula  and  atria,  or  due  to  the  discharge  into 
bronchioles  of  softened  pneumonic  patches.  Some  of  these  may  project, 
as  bullae,  above  the  surface,  if  the  pleura  is  non-adherent. 


Pneumonia.  429 

Various  factors  are  concerned  in  their  production.  The  resistance  of 
the  walls  is  diminished  in  bronchitis  and  general  malnutrition.  A  distending 
force  is  exerted  from  within  by  violent  cough,  and  by  retained  secretion  in 
the  case  of  foreign  bodies.  Traction  on  the  walls  from  without  is  exerted 
by  contraction  of  fibrous  tissue  in  the  lungs  and  pleura.  According  to  the 
theories  of  their  formation,  some  of  the  cavities  are  due  to  necrosis  of  lung 
tissue,  forming  minute  abscesses  that  communicate  with  the  bronchioles. 
Others  are  due  to  a  true  bronchiolectasis  from  dilatation  of  the  terminal 
bronchioles  and  infundibula  ;  these  cavities  not  projecting  above  the 
surface  of  the  pleura.  In  a  third  type,  atriectasis,  the  atria  of  the  bron- 
chioles are  dilated  and  several  infundibula  open  into  one  atrium.  Probably 
all  three  forms  are  present  in  a  single  case,  except  in  the  acute  cylindrical 
type  of  the  disease. 

Symptoms. — Sometimes  there  are  no  signs  or  symptoms,  the  lung 
inflammation  has  subsided  and  death  is  due  to  intercurrent  disease ; 
or  the  symptoms  are  those  of  chronic  bronchitis.  Other  cases  present 
the  physical  signs  of  disseminated  broncho-pneumonia,  and  a  "  honey- 
comb "  lung  is  found  after  death.  In  a  fourth  type  the  cases  are 
of  prolonged  duration  and  give  rise  to  the  characteristic  signs  and 
symptoms. 

In  a  case  which  follows  lobar  pneumonia,  with  or  without  pleurisy,  the 
temperature  falls  by  crisis  and  remains  down,  or  comes  down  gradually  to 
about  the  normal  level  and  the  physical  signs  do  not  clear  up.  There 
remain  persistent  dulness,  rales  and  patchy  bronchial  breathing,  and 
general  feebleness  of  air  entry.  The  dulness  may  increase  and  the  signs 
of  bronchiectasis  develop.  This  condition  may  persist  for  months  with 
little  variation,  or  be  modified  by  recurrent  attacks  of  bronchitis  or  broncho- 
pneumonia,  each  attack  leaving  the  lung  a  little  worse  than  before.  The 
child  is  pale  and  wasted,  but  may  subsequently  gain  strength  and  flesh  and 
appear  robust,  although  the  physical  signs  do  not  disappear  and  a  variable 
degree  of  cough  persists. 

In  a  well-marked  case  the  face  is  pale  and  puffy,  sometimes  congested. 
Dyspnoea  is  present  on  exertion  and  may  be  obvious  even  at  rest.  Breathing 
is  rapid  and  shallow.  The  temperature  is  normal  or  raised,  nutrition  is 
well  maintained,  and  there  are  no  night  sweats  and  no  tubercle  bacilli  in 
the  sputum.  The  cough  is  troublesome  and  paroxysmal,  especially  in  the 
morning  and  at  bedtime,  and  often  induced  by  change  in  posture.  It  is 
aggravated  by  fresh  catarrh.  The  breath  is  offensive  and  expectoration 
copious.  The  sputum  consists  of  tenacious,  airless,  greenish  pus,  rarely 
f  cetid  in  children,  and  separates  into  three  layers  on  standing.  It  is  coughed 
or  vomited  up  in  considerable  quantity  once  or  twice  a  day.  Haemoptysis 
is  not  infrequent.  Old  standing  cases  exhibit  clubbing  of  the  fingers  and 
toes,  slight  cyanosis,  emphysema  of  the  opposite  lung,  and  displacement 
of  the  heart  to  the  affected  side. 


430  Chapter   XXXV 111. 

The  physical  signs  vary  with  the  amount  of  secretion  in  the  cavities. 
If  there  is  much  secretion,  the  breath  sounds  are  feeble  or  absent,  the  note 
dull,  the  vocal  vibrations  diminished,  and  the  vocal  resonance  indistinct. 
If  the  cavities  are  emptied  by  cough,  the  breath  sounds  are  louder,  the  note 
more  resonant,  vocal  vibrations  increased,  and  sharp  rales,  bronchial 
breathing,  bronchophony  and  pectoriloquy  are  present.  The  shadow  with 
X-rays  becomes  less  dense. 

Diagnosis. — It  is  most  difficult  to  exclude  tuberculosis.  Limitation 
to  an  upper  lobe  is  more  likely  to  be  tuberculous  than  if  the  disease  is  in 
the  lower  lobe.  Chief  stress  must  be  laid  upon  the  absence  of  tubercle 
bacilli,  the  good  general  nutrition,  the  very  slow  course  tending  to  improve- 
ment, the  absence  of  further  breaking  down  of  lung  tissue,  the  feeble  air 
entry  and  the  absence  of  fever.  Haemoptysis  may  occur  in  either  disease. 
A  more  common  error  is  to  mistake  an  empyema  discharging  through  the 
lungs  for  bronchiectasis,  or  simple  empyema  following  pneumonia  for 
chronic  pneumonia.  Some  cases  suggest  new  growth  ;  but  in  course  of  time 
this  can  be  excluded  by  the  absence  of  an  increase  in  the  area  of  dulness 
and  of  cardiac  displacement  to  the  opposite  side. 

Course  and  Prognosis. — Foetid  expectoration  and  fever  are  bad  signs 
and  indicative  of  constitutional  disturbance  due  to  toxic  absorption. 
Acute  bronchiectasis  from  bronchitis  or  pertussis  almost  invariably  gets 
well,  unless  death  results  from  the  primary  disease.  Chronic  cases  can  be 
■arrested,  improved  by  treatment  and  may  get  well.  Many  are  more  or  less 
progressive  and  incurable,  but  last  for  years.  The  prognosis  in  the  very 
young  is  better  than  generally  supposed.  It  depends  on  the  cause,  the 
state  of  the  surrounding  tissues  and  the  social  environment,  and  varies 
directly  as  the  extent.  A  limited  area  is  harmless.  A  more  extensive  one 
interferes  with  general  health,  and  causes  dyspnoea  on  exertion.  Many 
children  remain  permanently  delicate  and  phthisis  is  not  an  uncommon 
termination.  Some  die  from  broncho-pneumonia.  Nevertheless  a  severe 
case,  involving  a  whole  lower  lobe,  may  improve  to  such  an  extent  that 
there  is  little  evidence  of  mischief  in  a  year's  time. 

Complications. — Recurrent  inflammation,  bronchitis  and  broncho- 
pneumonia are  common.  Septic  absorption  leads  to  hectic  fever  and 
wasting.  Other  complications  are  haemoptysis,  phthisis,  enlarged  and 
perhaps  caseous  bronchial  glands,  fatty  and  amyloid  degeneration, pulmonary 
abscess,  gangrene,  pneumothorax,  subcutaneous  and  mediastinal  emphy- 
sema, suppurative  meningitis,  cerebral  abscess,  cardiac  failure,  nephritis, 
periostitis  and  arthritis. 

Treatment. — Prevention  consists  in  the  proper  treatment  of  the  initial 
disease,  notably  of  broncho-pneumonia  in  the  course  of  measles  and 
whooping  cough.  Subsequently  it  must  be  directed  to  emptying  the 
cavities,  relieving  foetor  and  encouraging  the  full  expansion  of  the  lungs. 
The  child's  general  health  must  be  maintained  and  guarded  against  catarrh. 


Pneumonia.  431 

The  cavities  can  be  emptied  by  inversion  of  the  body,  holding  the  child 
up  by  the  legs  and  compressing  the  chest  or  abdomen  during  expiration, 
or  by  leaning  the  body  over  the  side  of  the  bed  with  the  hands  on  the  floor. 
It  should  be  done  three  times  a  day.  Give  expectorant  mixtures  containing 
iodide  of  potassium,  and  an  emetic  of  vin.  ipecac,  every  fourth  day  if  the 
child  is  strong  enough. 

Prevention  of  fcetor  wards  off  septic  complications  for  it  is  due  to 
bacterial  decomposition  It  is  relieved  by  spray  producers,  atomisers  or 
inhalers  with  terebene,  ol.  pini.  sylvestris,  eucalyptus,  creosote,  iodine,  tar 
compounds,  carbolic  acid  or  thymol ;  by  creosote  vapour  baths  ;  by 
intra-tracheal  injections  of  izal,  5  per  cent,  in  glycerin,  or  guaiacol  1,  menthol 
5,  olive  oil  94  parts  ;  by  the  internal  use  of  deodorising  and  antiseptic 
drugs  given  in  capsules  after  food,  e.g.,  creosote,  oil  of  garlic,  syr.  allii 
U.S. P.  or  syr.  picis  liq.  U.S. P.  t.d.s.  A  suitable  mixture  consists  of  ol. 
tereb.  dr.  1,  mellis  oz.  -|,  pulv.  trag.  co.  oz.  -|,  aq.  menth.  pip.  ad  oz.  3,  in 
doses  of  1  dr.  t.d.s.  Balsams  and  sulphur  waters  are  also  useful.  Choose 
for  these  patients  a  dry,  warm,  equable  climate  such  as  Jamaica  (November 
to  April),  the  Mediterranean,  South  California,  South  Africa  and  the 
West  Indies.  The  general  treatment  is  that  of  phthisis  ;  good  hygiene, 
liberal  diet,  respiratory  exercises  and  tonics.  Operative  treatment  is 
inadvisable,  as  there  are  many  cavities,  duck's  operation,  extirpation  of 
part  of  the  lung,  was  first  done  in  1885.  The  middle  lobe  was  removed 
successfully  by  Korte  (1907)  in  a  boy  aged  13. 


CHAPTER    XXXIX. 

THE  PLEUEA  AND  PLEUEAL  CAVITY. 

Hydrothorax — Multiple  Serositis — Pleurisy — Pleural  Effusions — Empyema 

— Pneumothorax. 

There  is  a  continual  circulation  of  lymph  through  the  pleural  sac,  via 
the  stornata  and  lymphatics.  It  is  maintained  by  respiration,  and  absorption 
plays  a  very  small  part  in  the  process.  During  inspiration  fluid  is  sucked 
in  and  on  expiration  it  is  driven  out.  Just  enough  fluid  is  kept  in  the  sac 
to  prevent  friction.  In  hydrothorax  it  enters  more  rapidly  than  it  can  be 
removed.  In  inflammation,  exudation  is  increased  and  the  stomata  are 
blocked  by  congestion,  pressure  and  exudation,  thus  preventing  its  removal. 
With  increasing  effusion  the  respiratory  movements  become  more  limited 
and  the  effect  of  expiration  in  getting  rid  of  the  fluid  is  reduced.  In  large 
effusions  the  respiratory  movements  on  the  affected  side  may  be  entirely 
abolished  and  no  re-absorption  can  occur.  The  removal  of  a  small  portion 
of  the  fluid  sets  in  action  the  respiratory  movements  and  leads  to  dis- 
appearance of  the  fluid,  an  effect  not  infrequently  seen  in  practice.  Treat- 
ment by  limitation  of  fluid  ingesta,  purgation,  diuresis  and  diaphoresis  is. 
illogical  and  useless  for  it  cannot  affect  the  mechanical  state  of  affairs  in  the 
chest.    It  may  prove  of  some  value  in  hydrothorax  from  nutritional  changes. 

Hydrothorax  is  due  to  mechanical  causes,  nutritional  changes  in  the 
endothelium  and  altered  conditions  of  the  blood.  It  is  not  common  in 
children  but  is  occasionally  met  with  in  obstructive  heart  or  lung  disease,. 
renal  affections,  new  growths  and  blood  states  such  as  leukaemia. 

Multiple  Serositis,  also  called  polyserositis,  polyorrhomenitis  or  Concato's 
disease. — This  is  a  general  inflammation  of  the  serous  membranes,  with 
effusion  into  the  pericardial,  pleural  and  peritonealcavities.  Strictly  speak- 
ing it  is  not  due  to  tubercle  or  new  growth.  Some  of  the  cases  described 
under  this  heading  are  tuberculous  in  origin  ;  a  few  possibly  of  rheumatic, 
origin  ;  and  others  are  associated  with  hepatic  cirrhosis,  chronic  interstitial 
nephritis  or  indurative  mediastinitis.  Occasionally  the  effusion  is  purulent,. 
and  there  may  be  a  collection  of  pus  behind  the  parietal  pleura,  adjacent, 
to  the  spine,  due  to  extension  of  the  mischief  along  the  lymphatics. 

Pleurisy  is  divisible  into  the  dry  or  fibrinous  variety,  and  pleurisy  with, 
effusion  which  may  be  serous  or  serofibrinous,  seropurulent  or  purulent. 


The  Pleura  and  Pleural  Cavity.  433 

(empyema),  or  hemorrhagic.     Hemorrhagic  effusions  in  children  are  not 
necessarily  due  to  tubercle  or  new  growth. 

Apart  from  this  last  variety  the  etiology  of  these  affections  may  be 
considered  together.  They  may  occur  at  any  age.  In  the  newborn  they  are 
commonly  due  to  sepsis.  In  a  stillborn  infant,  born  at  full  time  without 
difficulty,  I  found  recent  dry  pleurisy  with  no  other  pathological  lesion. 
In  early  life  inflammatory  effusions  are  commonly  secondary  to  inflam- 
matory or  zymotic  disease  and  have  a  marked  tendency  to  be  purulent. 
Most  of  them  are  secondary  to  pneumonia,  broncho-pneumonia,  tuber- 
culosis and  hemorrhagic  infarction  of  the  lung  ;  to  infectious  diseases 
such  as  measles,  scarlet  fever,  typhoid  fever,  diphtheria  and  influenza, 
usually  secondary  to  lung  mischief ;  to  pyemic  affections  such  as  sepsis, 
appendicitis  and  osteomyelitis  ;  to  rheumatism  ;  to  extension  from  adjacent 
organs  and  to  new  growth.  The  disease  almost  always  is  a  sign  of  a  general 
morbid  state  and  not  merely  a  local  affection.  It  generally  indicates  lung 
mischief  and  is  due  to  the  pneumococcus  or  the  tubercle  bacillus.  Of  these 
the  pneumococcus  is  far  the  more  prevalent  in  early  life,  and  consequently 
pleural  effusions  in  the  young  are  generally  purulent.  About  90  per  cent,  of 
cases  of  empyema  are  secondary  to  lung  mischief.  A  few  are  primary  or 
synchronous  with  pneumonia.  All  varieties  of  effusion  are  more  frequent 
in  the  spring  months,  and  rather  more  common  in  boys  because  of  their 
greater  liability  to  pneumonia.  Practically  two-thirds  of  300  collected 
cases  of  empyema  occurred  under  5  years  of  age,  and  one-third  between 
5-10  years. 

Morbid  Anatomy. — In  dry  pleurisy  the  amount  of  lymph  varies  from 
merely  enough  to  cause  pain  and  friction  to  a  thick  layer  covering  an 
extensive  area  of  lung.  Its  appearance  varies  with  the  number  of  pus  cells. 
There  may  be  only  a  few  fibrinous  adhesions,  loss  of  lustre,  and  roughening 
of  the  pleural  surface  ;  or  a  thick  yellowish  or  yellowish  green  layer  of 
lymph.  The  latter  is  present  in  pleuro-pneumonia.  In  tuberculous 
pleurisy  grey  or  yellow  tubercles  are  present  and  a  moderate  exudation  of 
serum  and  lymph,  except  in  those  cases  which  have  become  purulent  from 
secondary  infection  with  the  pneumococcus  or  pyogenic  organisms.  In 
empyema  the  exudation  of  pus  is  preceded  by  that  of  lymph  and  the 
consistency  of  the  fluid  depends  on  the  relative  proportions  of  the  serum 
and  pus  cells.  The  extent  of  the  fibrinous  exudation  is  generally  greatest  in 
pneumococcal  infections  and  large  masses  of  lymph  are  found  covering 
the  pleural  surfaces.  Thin  yellowish  seropurulent  effusions  are  often 
due  to  a  streptococcus,  and  thick  pale  green  ones  to  the  pneumococcus,  but 
the  naked-eye  appearances  are  unreliable  evidence  of  the  type  of  organism 
present.  Empyemata  are  primary  effusions.  Occasionally  a  serous 
effusion  becomes  purulent  in  course  of  time.  It  is  sometimes  unfairly 
stated  that  serous  effusions  do  not  become  purulent  except  from  lack  of 
care  in  exploration.    There  is  no  doubt  that  this  is  untrue  and  that  secondary 

2   F 


1 34  Chapter  XXXIX. 

infection  with  the  pneumococcus  or  pyogenic  organisms  does  occur.  In 
pneumonia  the  effusion  may  be  serous  at  the  onset  and  purulent  at  a  later 
date.  Sometimes  a  bilateral  effusion  is  serous  on  one  side  and  purulent  on 
the  other,  and  a  multilocular  unilateral  empyema  may  contain  some 
loculi  filled  with  serum. 

Both  serous  and  purulent  effusions  may  be  localised,  shut  off  by 
adhesions  ;  or  sacculated,  in  several  pockets  ;  or  general,  due  to  adhesions 
being  broken  down  by  the  accumulated  fluid.  They  may  be  situated  in 
any  part  of  the  chest,  most  often  posteriorly  at  the  base.  A  localised 
serofibrinous  effusion  after  infancy  is  usually  over  the  right  middle  lobe. 
Localised  empyemata  are  found  in  the  large  fissure  of  the  lung,  between 
the  base  and  the  diaphragm,  or  between  the  vertebral  column  and  the 
lung,  and  are  very  rarely  apical.  In  pneumonia  it  is  by  no  means  un- 
common to  find  a  small  localised  effusion  of  thick  creamy  inoffensive  pus, 
perhaps  amounting  to  barely  1  dr.  of  fluid  and  hardly  deserving  the  name 
of  empyema. 

Examination  of  the  Fluid. — Withdraw  some  of  the  fluid  from  the  chest, 
centrifugalise  it  gently  and  examine  the  deposit  under  the  microscope 
(Cyto-diagnosis).  In  hydrothorax  only  a  few  flat  endothelial  cells  are 
found.  In  recent  tuberctdous  pleurisy  the  cells  are  almost  entirely  small, 
mononuclear  lymphocytes.  Sometimes  in  early  stages  of  tuberculous 
pleurisy  there  is  an  excess  of  polymorphs.  This  probably  means  primary 
pleurisy  and  secondary  tuberculous  infection,  or  a  secondary  infection  of  a 
tuberculous  one.  In  tuberculous  cases  of  long  standing,  in  non-tuberculous 
infective  pleurisy,  and  in  cases  becoming  purulent  or  complicated  by 
pneumonia,  the  polymorphs  are  much  increased  in  number  and  are  in 
great  excess. 

Joussefs  Method  is  used  for  finding  tubercle  bacilli.  Draw  off  a 
few  ounces  of  fluid  and  allow  it  to  clot.  Digest  the  clot  with  artificial 
gastric  juice,  again  centrifugalise  and  stain  the  precipitate.  The  tubercle 
bacilli  are  entangled  in  the  clot,  unaffected  by  the  digestion,  and  are 
precipitated. 

Cultural  and  inoculation  methods  afford  positive  results  in  many 
tuberculous  cases,  but  leave  others  doubtful  and  take  a  long  time.  The 
tuberculin  test  is  available  in  apyrexial  cases  and  only  indicates  a  tuber- 
culous process  somewhere.    Eosinophilia  is  of  no  diagnostic  importance. 

Bacteriology. — Serous  effusions  are  commonly  due  to  the  pneumococcus, 
especially  in  nurslings,  the  streptococcus,  staphylococcus  and  tubercle 
bacillus.  Idiopathic  pleurisy  with  effusion  is  more  often  tubercidous  than 
commonly  supposed.  Empyemata  are  due  to  the  pneumococcus  alone  in 
60-90  per  cent.,  the  streptococcus  alone  in  5-15  per  cent.,  the  tubercle 
bacillus  in  about  5  per  cent.,  while  the  remainder  are  due  to  mixed  infections. 
Widal  and  Philibert(  1907)  have  shown  that  some  pleural  effusions,  in  which 
the  pus  is  microscopically  like  that  of  pneumococcal  pyaemia,  may  be  sterile 


The  Pleura  and  Pleural  Cavity.  435 

and  contain  intact  polymorphs.     It  is  much  more  difficult  to  determine  the 
responsible  organism  in  serous  than  in  purulent  effusions. 

The  general  conclusions  are  that  the  pneumococcus  is  the  most  common 
■cause  of  empyema,  especially  in  infants ;  that  the  disease  is  usually 
secondary  to  lobar  pneumonia  ;  that  pyogenic  germs  may  be  found 
associated  together,  or  with  the  pneumococcus,  and  are  chiefly  present  in 
•cases  of  pyaemic  origin  and  infective  disease  ;  and  that  in  tuberculosis  there 
is  usually  a  secondary  infection.  A  sterile  empyema  is  almost  certainly 
tuberculous. 

Symptoms. — Pleurisy  gives  rise  to  pain  in  the  side,  worse  on  drawing 
.a  deep  breath  and  on  cough.  The  pain  may  be  severe  and  is  sometimes 
referred  to  the  umbilicus  or  the  right  iliac  region.  Except  in  tuberculous 
cases  the  onset  is  sudden,  but  rarely  as  acute  as  in  pneumonia.  The  disease 
is  ushered  in  with  fever  and  chilliness,  headache  and  general  malaise,  some- 
times vomiting.  The  temperature  rises  to  101-103°  F.,  occasionally  higher  ; 
pulse  100-150  ;  and  the  breathing  is  frequent  and  shallow,  with  short, 
hacking,  dry,  restrained  cough.  There  is  no  dyspnoea  or  cyanosis.  The 
affected  side  may  be  tender.  Usually  the  child  lies  on  its  back  or,  if  there, 
is  no  local  tenderness,  on  the  affected  side,  so  as  to  limit  the  respiratory 
movement  on  that  side  and  allow  free  expansion  of  the  opposite  lung. 
Friction  and  perhaps  a  little  impairment  of  resonance  are  found  on 
•examination.  If  there  is  much  lymph  it  gives  rise  to  marked  dulness,  weak 
breathing,  and  deficient  vocal  vibrations  and  vocal  resonance. 

A  baby  with  pleurisy  is  very  ill  and  looks  still  more  so.  The  eyes  are 
sunken,  the  aspect  suffering,  and  the  skin  somewhat  bluish.  The  tempera- 
ture may  suggest  pneumonia.  Breathing  is  shallow  and  consequently  there 
may  be  no  friction  sounds.  Sometimes  there  is  impaired  air  entry  and 
distress  on  movement.  If  the  pleurisy  is  diaphragmatic  the  attack  may 
suggest  peritonitis,  for  the  legs  are  drawn  up  and  the  upper  half  of  the 
abdomen  is  immobile.  Breathing  is  still  more  shallow,  frequent,  and  often 
irregular  and  apparently  painful.  Should  the  attack  be  on  the  right  side 
pain  is  caused  by  pushing  the  liver  upward.  A  little  impairment  of 
resonance  is  found  at  the  base  and  in  the  axilla. 

The  course  of  dry  pleurisy  is  either  that  of  the  disease  with  which  it  is 
associated  or  is  quite  short,  lasting  only  a  few  days  to  a  week.  Some 
adhesions  are  left.  In  severe  cases  with  extensive  thick  exudation  the 
whole  pleural  cavity  may  be  obliterated  and  the  lungs  become  universally 
adherent  to  the  chest  wall.  A  thickened  pleura  may  be  left,  causing 
impaired  resonance  and  deficient  expansion  of  the  lung. 

Simple  pleurisy  is  rare  in  early  life  except  as  a  complication,  generally 
of  bronchitis,  pneumonia  or  broncho-pneumonia.  Herpes  zoster,  myalgia, 
neuralgia,  and  local  inflammatory  affections  may  cause  similar  pain.  True 
pneumonia  must  not  be  overlooked.  Weak  breath  sounds  and  absence  of 
bronchial  breathing  are  more  valuable  signs  than  the  degree  of  dulness  and 
.alterations  in  vocal  vibrations  and  vocal  resonance. 


436  Chapter   XXXIX. 

By  the  efficient  treatment  of  pleurisy  it  is  possible  to  prevent  the  effusion 
of  fluid.  Keep  the  patient  in  bed  and  adopt  the  ordinary  treatment  of 
febrile  states  until  the  local  signs  have  cleared  up. 

Severe  pain  is  relieved  by  counter-irritation,  mustard  leaves,  hot 
fomentations,  etc.,  or  strapping  with  adhesive  plaster.  Leeches  are  useful 
in  older  children.  In  babies  the  pain  is  best  relieved  by  opium.  The 
general  treatment  is  that  of  fever.  Absorption  of  thickened  pleura  may  be 
aided  by  painting  with  tincture  of  iodine  and  pot.  iod.  internally. 

Pleural  Effusion. — There  is  generally  a  history  of  pain  in  the  side  or 
some  lung  trouble  followed  by  gradually  increasing  shortness  of  breath, 
varying  in  degree  with  the  amount  of  fluid  present  and  increased  on 
exertion.  Sometimes  there  is  an  intervening  period  of  a  few  days  of 
apparent  health.  Both  in  pleurisy  and  pleural  effusion  the  pupils  are  not 
infrequently  unequal,  the  one  on  the  affected  side  being  a  little  dilated 
and  sluggish  in  reaction  to  light.  This  is  probably  due  to  peripheral  irritation 
of  the  sympathetic. 

The  fluid  exerts  mechanical  effects  on  the  heart,  mediastinum,  lungs 
and  diaphragm.  Consequently  the  symptoms  are  increasing  dyspnoea 
and  frequency  of  the  pulse,  with  a  variable  amount  of  general  malaise  and 
perhaps  fever.  The  physical  signs  are  those  of  cardiac  displacement, 
collapse  of  the  lung  and  the  presence  of  fluid. 

As  the  fluid  increases  in  quantity  the  lung  becomes  more  and  more 
compressed,  until  it  is  eventually  quite  collapsed  and  airless  and  is  with- 
drawn into  the  angle  formed  by  the  ribs  and  the  vertebral  column.  Its 
elastic  traction  is  reduced  and  then  abolished,  so  that  it  cannot  counteract 
the  elastic  traction  of  opposite  lung.  Hence  the  mediastinum  and  heart  are 
drawn  over  to  the  opposite  side,  the  cardiac  apex  is  displaced  and  the  area 
of  dumess  altered  ;  and  the  diaphragm  is  depressed.  These  effects  are  most 
marked  in  left-sided  effusions.  Dulness  and  pulsation  are  found  to  the 
right  of  the  sternum,  pulsation  is  present  in  the  epigastrium,  and  the 
heart  may  be  felt  beating  beneath  the  right  nipple.  The  position  of  the 
apex  must  be  carefully  located  with  the  child  lying  on  the  back,  and  any 
alteration  from  day  to  day  must  be  noted.  An  apparent  initial  displacement 
to  the  left  is  of  little  value,  for  it  may  be  due  to  cardiac  dilatation  or  be- 
the  normal  position  in  infancy  and  early  childhood.  Alteration  in  the 
position  of  the  heart,  occasionally  so  marked  as  to  suggest  transposition,, 
causes  breathlessness,  often  a  systolic  displacement  murmur,  and  a  liability 
to  syncopal  attacks. 

The  more  the  lung  is  compressed  the  greater  is  the  dyspnoea,  but  the 
child  quickly  accommodates  itself  to  altered  conditions  if  the  fluid  effuses 
slowly.  In  rapid  effusions  the  distress  is  very  great,  while  in  slow  ones  it 
may  be  so  slight  as  to  attract  no  attention.  The  amount  of  fluid  varies 
with  the  age,  size  of  the  child,  and  the  duration  and  character  of  the; 


The  Pleura  and  Pleural  Cavity.  437 

effusion.     It  is  greater  if  the  fluid  is  thin.     Under  3  years  of  age  there 
is  about  J-l  pint,  in  older  children  up  to  3  or  4  pints. 

In  early  stages  there  may  be  some  narrowing  of  the  intercostal  spaces, 
from  reflex  contraction  of  the  intercostal  muscles.  Later  these  spaces  bulge 
and  the  affected  side  as  a  whole  is  expanded,  assumes  the  position  of 
complete  inspiration  and  measures  more  by  cyrtometer.  Its  movements  are 
deficient.  The  degree  of  dulness  depends  on  the  amount  of  fluid  and 
fibrinous  exudate.  It  may  be  limited  to  one  base,  or  reach  the  second 
rib  or  higher.  It  then  extends  on  to  the  sternum  and  perhaps  f-1  inch 
to  the  opposite  side  of  the  manubrium,  from  distension  of  the  pleural  sac. 
The  dulness  is  more  wooden  and  more  superficial  than  in  pneumonia.  It 
varies  with  the  size  of  the  effusion  and  the  position  of  the  patient.  A  small 
effusion  occupies  the  lateral  costo-diaphragmatic  furrow  if  the  patient 
sits  up,  and  gives  rise  to  dulness  in  the  axillary  line  in  the  lower  part  of  the 
•chest,  with  an  almost  horizontal  upper  border  and  a  lower  border  convex 
upwards.  In  the  dorsal  decubitus  the  fluid  occupies  the  costo-vertebral 
furrow  and  the  lateral  dulness  disappears.  Larger  effusions  extend  laterally 
and  anteriorly.  In  the  seated  position  the  upper  limit  in  the  anterior  and 
lateral  regions  is  horizontal.  Behind,  at  a  distance  of  1-3  ins.  from  the 
vertebral  column,  the  line  of  dulness  falls  abruptly,  forming  a  triangle  in 
which  resonance  persists  below  the  general  level  of  dulness.  Sometimes  a 
semilunar  zone  of  impaired  resonance,  known  as  "the  Hat,"  is  found  above 
the  level  of  dulness,  and  is  due  to  partial  collapse  of  the  lung  from  pressure. 
In  moderate  effusions  the  anterior  level  of  dulness  becomes  lower,  sometimes 
higher,  in  the  horizontal  posture.  In  large  effusions  there  is  no  change  with 
alteration  in  posture. 

Grocco's  Triangle  (1902),  or  the  paravertebral  basic  triangle  of  dulness, 
is  a  patch  of  partial  dulness  adjacent  to  the  spine  on  the  side  opposite  the 
effusion.  It  is  not  invariably  present.  The  triangle  is  formed  by  the  vertical 
line  of  the  spinal  processes,  the  lower  limit  of  pulmonary  resonance,  and  a 
hypothenuse  which  may  show  a  slight  outward  convexity.  The  apex  of  the 
triangle  is  rather  below  the  level  of  the  upper  limit  of  effusion.  It  is  absent 
when  the  patient  lies  on  the  affected  side,  unless  the  effusion  is  very  large, 
and  present  both  in  the  upright  posture  and  when  lying  on  the  sound  side. 
This  patch  of  impaired  resonance  is  due  to  displacement  of  the  mediastinum, 
conduction  of  dulness  from  the  opposite  side,  or  to  the  fluid  against  the 
bodies  of  the  vertebrae  suppressing  bone  vibration.  It  is  most  marked  in 
xight-sided  effusions  and  it  is  absent  in  pneumonia  or,  if  present,  it  does  not 
vary  in  position. 

Dulness  may  assume  abnormal  forms  as  the  result  of  adhesions.  Vocal 
vibrations  are  diminished  or  absent,  but  the  sign  is  difficult  to  elicit  in 
children  because  of  the  character  of  the  voice.  Breath  sounds  are  weak 
and  distant,  or  occasionally  absent.  Distant  bronchial  breathing  and 
bronchophony  are  common,  but  sometimes  the  sounds  are  as  loud  as  over 


I .  | s  Chapter   X  X  X I X. 

solid  lung,  especially  near  the  spine.  Nasal  voice  sounds  and  segophony  may 
be  heard  at  the  upper  limit  of  dulness.  Friction  may  be  heard  above  the 
fluid  and  during  absorption.  The  weakness  or  absence  of  breath  sounds 
and  vocal  resonance  are  better  guides  than  dulness  to  the  amount  of 
effusion,  for  dulness  may  be  due  to  fibrinous  exudation.  At  the  apex  of 
the  lung  the  note  is  impaired,  boxy  or  tympanitic,  and  bronchial  breathing 
may  be  present,  if  there  is  a  great  amount  of  collapse. 

Examination  by  the  X-ray  screen  is  not  reliable  for  small  effusions  at 
the  base  of  the  lung.  In  larger  ones  it  may  reveal  a  dark  shadow  with  a 
straight  upper  border,  flattening  of  the  diaphragm,  and  exaggerated 
movement  on  the  opposite  side.  The  dome  shape  of  the  diaphragm  is  due 
to  the  elastic  traction  of  the  lungs.  In  most  effusions  the  amount  of  fluid 
is  not  enough  to  create  a  positive  pressure  within  the  pleural  cavity.  During 
the  process  of  syphonage  to  evacuate  the  fluid,  as  soon  as  the  opening  of  the 
tube  is  held  at  the  same  level  or  even  a  little  below  that  in  the  thorax,  the 
flow  is  stopped  or  reversed.  In  large  effusions  there  may  be  positive 
pressure  with  accentuation  of  the  displacement  of  various  organs. 
The  liver  and  spleen  may  be  felt  per  abdomen,  through  flattening  of 
the  diaphragm,  and  in  cases  of  positive  pressure  may  be  actually 
pushed  down. 

Empyema. — The  past  history  of  a  case  of  empyema  is  that  of  an  acute 
illness  with  consolidation  of  the  lung  and  effusion  of  fluid.  Often  the 
antecedent  illness  is  vaguely  described  and  has  not  been  followed  by  com- 
plete convalescence  ;  or  an  attack  of  pneumonia  is  followed  by  a  fall  of 
temperature  to  normal  or  nearly  so,  and  a  gradual  rise  with  increasing, 
symptoms  instead  of  convalescence.  The  lung  may  not  have  resolved.  In 
other  cases  the  lung  undergoes  resolution  and  apparent  convalescence  is 
followed  by  a  gradual  development  of  empyema  3-5  weeks  later.  Broncho- 
pneumonia is  a  more  common  antecedent  than  lobar  pneumonia.  Some- 
times the  history  is  limited  to  increasing  anaemia,  debility,  breathlessness 
and  perhaps  cough. 

Acute  primary  empyema  simulates  pneumonia.  The  onset  is  sudden 
and  symptoms  are  severe,  fever  high,  and  in  a  few  days  the  side  is  full 
of  pus,  sometimes  mixed  with  blood.  There  is  much  dyspnoea.  Delirium 
is  earlier  in  onset  and  more  marked  than  in  pneumonia.  It  is  generally 
pneumococcal. 

Latent  empyema  in  infants  is  often  overlooked,  because  of  the  small 
size  and  slight  pulmonary  symptoms.  Occasionally  one  cavity  is  opened 
but  a  second  one  is  shut  off  by  adhesions.  A  small  empyema  leads  to  pro- 
gressive wasting  and  ansemia  with  irregular  fever  and  few  respiratory 
symptoms.  It  is  gradual  in  onset  and  prolonged  in  duration.  The  physical 
signs  may  be  limited  to  slight  impairment  of  resonance,  generally  at  the 
extreme  base  near  the  spine  and  modified  in  character  by  the  stomach  and 
liver.    The  signs  may   vary   from  day  to    day.      It   may    give   rise    to 


The  Pleura  and  Pleural  Cavity.  439 

broncho-pneumonia,  purulent  pericarditis,  meningitis,  peritonitis,  arthritis 
and  pysemia.     Cases  are  usually  mistaken  for  tuberculosis  or  marasmus. 

Interlobar  empyema  may  consist  simply  of  a  layer  of  pus  between  the 
two  lobes.  Pulsating  empyema  is  almost  always  on  the  left  side,  the 
pulsation  being  transmitted  from  the  heart  or  aorta.  An  empyema  may 
point  within  a  few  days  or  not  for  weeks  ;  generally  in  the  fifth  space  in  the 
neighbourhood  of  the  posterior  or  anterior  intercostal  membrane,  most  often 
in  front. 

After  a  purulent  effusion  has  existed  for  some  time  it  produces  certain 
signs  of  the  presence  of  pus.  The  child  becomes  more  and  more  anaemic, 
wastes,  loses  appetite  and  strength,  perhaps  sweats  profusely,  and  may  have 
an  irregular  or  hectic  temperature.  The  temperature  chart  is  unreliable  and 
variable.  Usually  the  fever  ranges  from  100-102°  F.,  and  it  may  be  hectic 
or  absent  entirely.  In  still  more  prolonged  cases  the  clinical  picture  suggests 
tuberculosis  because  of  emaciation,  fever,  clubbing  of  the  fingers,  diarrhoea, 
albuminuria  and  even  general  oedema.  The  abscess  may  point  through  the 
chest  wall ;  burst  through  the  lung,  oesophagus  or  bronchus  ;  or  track  in 
various  directions,  e.g.,  through  the  diaphragm  and  among  the  abdominal 
mxiscles,  between  the  external  and  internal  oblique,  or  down  the  spine  and 
simulate  psoas  abscess. 

Diagnosis. — We  have  to  determine  the  presence  of  fluid,  its  situation 
and  physical  effects,  its  characters  and  its  causation.  The  diagnosis  of 
fluid  depends  on  the  displacement  of  the  heart,  the  descent  of  the  diaphragm, 
the  area  of  dulness,  the  wooden  percussion  note  and  sense  of  resistance, 
weak  breath  sounds,  distant  bronchial  breathing  and  bronchophony. 
Grocco's  sign,  when  present,  is  of  much  value.  The  absence  of  rales  and  the 
presence  of  friction  and  nasal  voice  sounds  at  the  upper  level  of  dulness  are 
important  signs.  The  more  extensive  the  dulness,  the  greater  is  the  prob- 
ability of  fluid,  and  its  extension  on  to  or  beyond  the  sternum  is  practically 
diagnostic.  The  presence  of  fluid  can  generally  be  determined  without 
having  recourse  to  exploration.    This  should  be  the  last  measure  adopted. 

In  infants  and  the  very  young  it  may  be  impossible  to  make  a  diagnosis 
from  the  physical  signs.  They  were  completely  absent  in  a  baby  although 
pus  was  found  on  exploration,  carried  out  because  of  the  dyspnoea  and 
general  symptoms,  and  several  ounces  were  evacuated.  Occasionally 
bronchial  breathing  may  be  very  loud  and  the  signs  may  be  those  of  the 
consolidation  with  which  it  is  often  synchronous.  Effusion  has  chiefly  to  be 
distinguished  from  pneumonia,  broncho-pneumonia,  tuberculosis,  fibrinous, 
pleurisy,  pericardial  effusion,  bronchiectasis,  subphrenic  abscess  and  new? 
growth.  The  disappearance  of  a  paravertebral  triangle  of  dulness  indicates; 
that  persistent  dulness  is  due  to  thickened  pleura  rather  than  continued 
effusion.     Diaphragmatic  hernia  may  give  rise  to  similar  physical  signs. 

Differential  Diagnosis  between  Serum  and  Pus. — A  certain  amount  of 
importance  can  be  attached  to  the  age  of  the  child,  the  causation,  the 


440  Chapter   XXXIX. 

mode  of  onset,  duration  and  degree  of  illness.  Serous  effusions  are  much 
less  frequent  than  purulent  ones  in  the  first  three  years  of  life.  After  that 
age  the  serous  effusion  rather  preponderates.  An  acute  onset  is  in  favour  of 
serum,  while  empyema  comes  on  more  gradually  as  a  complication  of 
pneumonia.  Some  acute  pleural  effusions  are  purulent  from  the  start,  and 
in  tuberculous  pleurisy  the  onset  is  frequently  insidious.  If  due  to  simple 
chill  or  rheumatism,  and  in  the  absence  of  pulmonary  disease,  the  effusion 
is  probably  serous.  The  longer  the  duration  of  the  illness  and  the  greater 
the  effect  on  the  general  health,  the  greater  is  the  probability  of  pus.  Rigors 
and  sweating  are  more  frequent  in  purulent  than  in  serous  effusions.  The 
physical  signs  are  of  little  value  unless  there  are  bulging,  redness,  tenderness 
and  oedema.  The  temperature  affords  no  reliable  evidence.  It  may  be 
strongly  suggestive  of  pus  although  the  effusion  is  serous.  Empyema  must 
be  suspected  in  cases  diagnosed  as  unresolved  pneumonia  ;  in  pneumonia 
followed  by  a  rise  of  temperature,  pulse  and  respiration  after  an  apparent 
crisis  or  if  they  do  not  fall  within  a  reasonable  time  ;  if  there  is  undue 
delirium  on  the  second  or  third  day,  great  oscillations  of  temperature,  and 
tenderness  in  the  affected  side. 

Small  loculated  collections  can  only  be  differentiated  by  exploration 
and  the  general  character  of  the  symptoms.  A  local  collection  of  serum 
gives  rise  to  physical  signs  but  no  general  malaise. 

Frequently  the  differential  diagnosis  can  only  be  made  by  exploration. 
Though  almost  invariably  harmless  it  is  not  devoid  of  risk.  Strict  aseptic 
precautions  must  be  adopted.  Use  a  syringe  about  the  size  of  an  ether 
syringe  with  a  needle  of  medium  calibre  2-3  ins.  long.  Choose  a  dull  area 
and  insert  the  needle  vertically  to  the  chest  wall  through  the  lower  part 
-of  the  intercostal  space,  first  drawing  the  skin  a  little  upward.  The  child 
should  be  on  its  back,  close  to  the  edge  of  the  bed  or  table,  with  the  arm 
-elevated.  Be  careful  that  the  needle  enters  the  pleural  cavity  and  does  not 
penetrate  the  lung.  With  a  little  suction  enough  fluid  can  be  obtained  for 
examination.  Withdraw  the  needle  sharply  and  cover  the  puncture  with  a 
pad  of  gauze  and  collodion. 

I  have  never  seen  any  evil  effect  from  exploration.  It  may  cause 
puncture  of  the  intercostal  artery  and  hemorrhage  into  the  pleural  cavity  ; 
puncture  of  the  lung  and  haemorrhage  or  pneumothorax  ;  puncture  of  the 
heart  or  pericardium,  if  too  long  a  needle  is  used  for  exploring  the  left  side, 
and  if  empyema  has  been  diagnosed  instead  of  purulent  pericarditis  or 
pneumonia  with  dilated  heart.  A  few  cases  have  been  recorded  of  death 
occurring  very  rapidly  after  puncture  of  the  lung  in  cases  of  chronic  fibroid 
disease  explored  for  supposed  pus.  In  some  of  these  haemorrhage  has  been 
profuse  and  in  others  slight  or  absent.  Sometimes  much  frothy  mucus  is 
expectorated.  Death  is  due  to  inhibition  of  the  cardiac  and  respiratory 
centres,  cardiac  inhibition  by  vagus  irritation,  or  suffocation  through 
bleeding  into  the  air  passages.  Dangerous  symptoms  have  been  followed  by 
recovery  at  the  time  and  death  a  few  hours  later. 


The  Pleura  and  Pleural   Cavity.  441 

Course  and  Prognosis. — Acute  serous  pleurisy  is  rarely  fatal.  It  runs 
a  fairly  definite  course.  For  a  few  days  the  child  is  ill  and  feverish.  The 
amount  of  fluid  increases  with  variable  rapidity,  then  remains  stationary 
and  finally  disappears.  The  duration  is  about  3  weeks.  If  fluid  is  left  after 
that,  it  is  a  residual  effect  rather  than  a  continuance  of  the  disease.  In 
secondary  cases  the  duration  is  more  uncertain.  "When  left  alone  a  serous 
effusion  generally  clears  up,  but  it  may  be  long  before  the  breath  sounds  and 
percussion  note  become  normal.  This  is  due  to  the  slow  absorption  of 
fibrinous  exudation,  adhesions  interfering  with  full  expansion,  and  partial 
collapse  of  the  lung.  A  tuberculous  effusion  may  be  very  chronic,  quite 
temporary,  or  become  infected  with  organisms  causing  empyema.  Earely 
it  is  purulent  from  the  onset,  perhaps  due  to  rupture  or  extension  from  a 
caseous  gland  or  a  caseous  focus  near  the  surface  of  the  lung.  Such  a  case 
occurred  in  a  girl  aged  4  years.  The  dulness  began  over  the  manubrium  and 
gradually  extended  to  the  right.  Thick  caseous  pus  was  eventually 
evacuated  through  the  axilla  and  the  child  slowly  recovered. 

Sudden  death  may  occur  from  cardiac  inhibition  in  large  effusions, 
especially  when  there  is  much  displacement  of  the  mediastinum.  It  may  be 
caused  by  sudden  changes  in  intra-pleural  pressure  or  vascular  intra- 
thoracic conditions  ;  the  result  of  cough,  movement,  sudden  change  of 
position,  rapid  removal  of  fluid  and  irrigation.  Occasionally  it  is  due  to 
pulmonary  embolism  or  thrombosis,  myocardial  degeneration  or  rupture  of 
an  empyema. 

A  small  purulent  effusion  can  be  re-absorbed,  the  fluid  parts  being  first 
absorbed  and  then  the  solid  parts  undergoing  fatty  degeneration  and 
necrosis  ;  or  a  caseous  mass  may  be  left  behind,  a  potent  source  of  future 
mischief.  Ordinarily  it  goes  on  increasing  in  size  and  eventually  ruptures, 
leaving  a  permanent  sinus  and  perhaps  finally  ending  in  death  from 
amyloid  disease. 

Thus  the  prognosis  of  serous  effusions  is  good,  unless  the  lung  is  per- 
manently bound  down  by  adhesions,  a  rare  event  in  children.  The  duration 
is  not  a  certain  guide  for  in  some  long  standing  cases  expansion  occurs  at 
once,  while  in  others  of  much  shorter  duration  permanent  collapse  may 
be  present.  In  tuberculous  disease  the  prognosis  is  that  of  tuberculosis. 
The  prognosis  of  empyema  is  bad  in  the  acute  primary  cases.  In  the  other 
forms  it  depends  on  the  age  of  the  patient,  the  complications  and  causation 
•of  effusion,  early  diagnosis,  and  to  a  slight  extent  on  the  methods  of  treat- 
ment. In  the  first  and  second  year  the  mortality  is  very  high,  but  few 
cases  die  subsequently  to  this  age.  Speaking  generally,  the  percentage 
mortality  of  children  under  5  years  of  age  is  about  the  same  in  each  year  of 
life  in  cases  treated  by  incision,  and  is  rather  higher  in  the  first  two  years 
in  cases  treated  by  resection.  The  prognosis  is  particularly  bad  in  the  first 
year.  The  causes  of  death  have  apparently  little  to  do  with  the  nature  of 
the  operation  and  include  bronchitis,  pericarditis,  broncho-pneumonia, 
•oedema    of    the    lungs,    general    tuberculosis,    purulent    meningitis,    and 


442  Chapter   XXXIX. 

occasionally  syncope  during  irrigation  or  erysipelas  starting  from  the- 
wound.  There  is  a  certain  amount  of  evidence  that  the  prognosis  is  worse 
in  mixed  than  in  pure  infections,  and  in  streptococcal  than  in  pneumococcal 
cases,  unless  there  is  a  polyserositis  or  a  general  pneumococcal  blood 
infection.  It  is  especially  bad  in  bilateral  cases  and  those  secondary  to 
tuberculosis.  It  is  better,  if  the  organisms  stain  feebly  and  grow  badly 
(Bythell).  If  they  are  of  high  vitilaty,  the  prognosis  varies  as  the  degree 
of  leucocytosis.  Deficient  leucocytosis  is  a  bad  sign.  If  the  empyema  is 
left  alone,  death  may  result  from  pressure  on  the  heart,  acute  toxaemia  or 
some  complication.  The  patient  may  recover  by  absorption  of  the  pus 
or  rupture  of  the  abscess  and  discharge  through  the  lung  or  chest  wall.  In 
such  an  event  the  illness  is  prolonged,  its  course  uncertain  and  the  risks- 
jrrave.  Even  if  recovery  does  result,  there  is  usually  a  deformed  chest,, 
shrunken  side,  approximated  ribs,  depressed  shoulder,  curvature  of  the  spine,, 
diminished  movement  of  the  chest,  displaced  heart,  fibroid  change  in  the 
lung,  and  secondary  tuberculosis  or  lardaceous  disease.  The  lung  is  small, 
solid,  carnified,  retracted  and  covered  by  a  dense  layer  of  thickened  pleura. 
Similar  results  may  follow  approved  methods  of  treatment  in  old  standing 
cases.  In  some  of  these  re-expansion  of  lung  is  complete.  Untreated  cases- 
commonly  die  from  asthenia,  amyloid  disease  due  to  chronic  discharge,  or 
some  complication.  In  purulent  pleurisy,  differing  from  empyema  merely 
in  degree,  absorption  does  take  place  and  may  leave  no  ill  effects.  The  lung 
re-expands  more  readily  in  children  than  in  adults,  but  there  is  greater- 
liability  to  complications. 

Treatment. — Acute  serous  effusion  is  treated  during  the  febrile  stage  on 
the  same  principles  as  dry  pleurisy.  It  may  be  necessary  to  evacuate  a. 
large  and  rapidly  increasing  effusion.  Generally  the  child  is  kept  in  bed  until 
the  fluid  is  re-absorbed ;  and  is  not  allowed  to  sit  up  or  make  any  exertion 
if  there  is  much  effusion.  Absorption  is  apt  to  be  slow,  and  possibly  can  be 
hastened  by  counter-irritants  and  mercurial  applications.  Thiosinarnin  and 
fibrolysin  injections  have  been  recommended.  Special  care  is  necessary 
during  convalescence  because  of  the  possibility  of  tuberculosis.  Breathing 
exercises  encourage  the  expansion  of  the  lung. 

A  serous  effusion  must  be  evacuated  if  dyspnoea  is  excessive  ;  if  there 
is  mischief  in  the  opposite  lung,  indicated  by  wheezing,  rales,  and  bron- 
chitic  or  blood-stained  expectoration  ;  if  there  are  attacks  of  faintness  or 
syncope  ;  if  the  patient  is  restless,  unable  to  take  food  properly  and  unable 
to  sleep,  or  develops  nausea,  vomiting  or  diarrhoea  ;  if  the  fluid  has  existed 
for  more  than  3  weeks  and  is  not  commencing  to  subside.  Early  tapping  is- 
only  necessary  if  there  is  serious  dyspnoea  from  rapid  and  excessive  effusion. 
It  neither  reduces  the  fever  nor  shortens  the  duration  of  inflammatory 
process.  The  fluid  very  soon  re-accumulates  and  often  to  as  great  an  extent- 
It  may  remain  stationary  for  a  long  time  and  then  clear  up  in  the  course  of 
a  few  days.   I  have  never  come  across  a  case  of  persistent  effusion  in  a  child 


The  Pleura  and  Pleural  Cavity.  443 

untreated  by  paracentesis,  so  this  operation  is  probably  rarely  necessary 
except  with  the  object  of  hastening  recovery. 

The  risks  of  paracentesis  or  tapping  are  those  of  exploration,  plus 
certain  dangers  due  to  the  particular  method  adopted.  Syphonage  is 
much  safer  than  aspiration.  The  apparatus  consists  of  a  small  trocar 
and  cannula,  2-3  ins.  long,  3  feet  of  rubber  tubing  with  a  short  piece  of 
glass  tubing  interrupting  its  continuity  about  4  ins.  from  the  end,  a 
test  tube,  bull-dog  forceps,  thread  and  a  large  beaker  or  basin.  The  tubing 
is  tied  on  to  the  canula  with  thread  and  the  trocar  is  pushed  through  the 
stretched  rubber  into  the  cannula.  The  other  end  of  the  tubing  is  tied  so 
that  it  rests  in  the  test  tube,  reaching  the  bottom.  Both  tube  and  test 
tube  are  filled  with  sterile  water  or  salt  solution  and  clamps  put  on.  The 
trocar  and  cannula  are  plunged  into  the  chest  and  the  trocar  removed,  the 
clamps  are  taken  off  and  syphon  action  is  at  once  set  up.  With  the 
patient  on  the  back  in  bed  and  the  receiver  on  the  floor  a  suction  action 
is  exerted  equal  to  that  of  a  column  of  water  about  2  feet  high,  and  it  can 
be  at  once  stopped  by  raising  the  test  tube  to  a  level  with  the  hole  in  the 
chest.  This  pressure  is  sufficient  to  remove  all  fluid  which  can  be  taken 
away  with  safety.  As  the  fluid  flows  out  the  lung  re-expands  and  the 
heart  slowly  returns  to  its  normal  position.  Cough,  perhaps  paroxysmal, 
may  be  induced  by  irritation  of  the  lung  by  the  cannula,  or  depend  on 
expansion  of  the  lung.  Occasionally  dyspnoea,  pain,  faintness  and  general 
discomfort  ensue.  If  they  are  severe,  they  may  necessitate  temporary  or 
complete  cessation  of  the  operation.  Withdraw  the  cannula  if  the  fluid 
becomes  blood-stained.  The  glass  tube  enables  one  at  once  to  note  any 
change  in  the  character  of  the  fluid. 

An  aspiration  bottle  can  be  used  by  exhausting  the  air  slowly  and  with 
extreme  care  after  the  cannula  has  been  inserted  into  the  chest,  stopping  at 
once  if  cough,  pain  or  discomfort  is  induced.  The  rapid  removal  of  fluid 
may  cause  sudden  and  fatal  syncope  ;  rapid  transudation  of  a  serous  fluid 
into  the  lungs,  leading  to  an  alarming  profuse  expectoration  and  signs  of 
suffocation  ;  or  pneumothorax  and  subsequent  pyo-pneumothorax  from 
rupture  of  a  lung  bound  by  adhesions  or  unable  to  expand.  Treatment  by 
incision  and  drainage  is  justifiable  in  a  case  which  does  not  clear  up  after 
repeated  tapping. 

Empyema. — As  soon  as  the  presence  of  pus  in  the  pleural  cavity  has 
been  diagnosed  measures  should  be  taken  for  its  free  evacuation.  Although 
cases  have  got  well  if  left  alone,  and  after  tapping,  the  prospect  of  cure 
is  so  small  and  uncertain  and  the  risks  are  so  great  that  free  drainage  should 
be  adopted.  Paracentesis  is  useful  to  reduce  the  size  of  a  large  effusion 
and  ward  off  temporarily  acute  distress,  and  for  an  empyema  on  one  side 
while  that  on  the  other  is  drained.  Babies  are  liable  to  collapse  if  a  large 
effusion  is  evacuated  rapidly.  Gentle  aspiration  is  preferable  to  syphonage, 
for  the  pus  may  be  thick.    Both  methods  are  unsatisfactory  and  incomplete. 


444  Chapter   XXXI X. 

The  notion  that  a  successful  result  is  based  on  the  filling  up  of  the 
cavity  and  sinus,  bv  granulation  tissue  and  adhesion  of  the  visceral  and 
parietal  pleura,  leads  to  bad  methods  of  treatment.  Such  a  course  is 
extremely  slow  and  fidl  expansion  of  the  lung  can  only  take  place  subse- 
quently. Cure  is  effected  by  expansion  of  the  lung,  elevation  of  the 
diaphragm,  and  falling  in  of  the  chest  walls.  If  the  lung  expands  quickly, 
adhesions  form  and  the  sinus  rapidly  closes.  The  cavity  is  drained  by 
simple  incision,  or  resection  of  a  portion  of  one  or  more  ribs.  The  presence 
of  pus  is  first  located  by  exploration  and  the  incision  is  made  with  the 
exploring  needle  in  position.  Without  this  precaution  the  operation  may 
be  done  in  the  absence  of  pus  or  a  localised  empyema  may  be  missed. 
Valvular  drainage,  intermittent  drainage,  drainage  by  continuous,  negative, 
hydrostatic  pressure,  and  the  removal  of  fluid  and  injection  of  air  have  all 
been  tried. 

It  is  claimed  for  resection  that  better  drainage  is  secured  ;  that 
masses  of  fibrin  can  be  more  easily  removed  ;  that  the  boundaries  of  the 
cavity  can  be  explored  and  all  loose  adhesions  broken  down,  not  an 
unmixed  advantage  for  it  may  convert  a  local  empyema  into  a  general  one  ; 
that  there  is  less  danger  of  haemorrhage,  and  that  recovery  is  more  rapid. 
It  is  a  more  serious  operation  ;  the  medullary  cavity  of  the  rib  is  exposed 
and  forms  an  absorbing  surface  ;  and  the  rapid  growth  of  callus  soon 
diminishes  the  orifice. 

The  advocates  of  simple  incision  point  out  that  the  operation  is  simpler 
and  more  quickly  performed,  that  the  shock  and  the  anaesthetic  danger  are 
less,  and  that  the  risk  of  pyeemia  is  smaller  ;  that  a  large  oval  opening  is 
easily  made  and  drainage  is  quite  efficient.  These  arguments  are  par- 
ticularly applicable  for  babies  under  2  years.  The  risk  of  haemorrhage  is 
infinitesimal,  if  it  is  remembered  that  the  artery  runs  along  the  under 
border  of  the  rib.  The  assertion  that  resection  is  usually  a  quicker  and 
more  certain  cure  than  simple  incision  is  not  borne  out  by  clinical  exper- 
ience. Post-mortem  evidence  proves  that  drainage  is  quite  efficient  in  the 
simpler  operation.  If  at  the  time  of  operation  the  ribs  are  too  close  together 
to  get  in  a  good  sized  tube,  two  smaller  ones  can  be  put  in  side  by  side. 
Next  day  it  will  be  found  that  the  ribs  are  more  widely  separated  and  a 
larger  tube  can  be  inserted.  Eesection  should  be  reserved  for  those  cases, 
rare  in  children,  in  which  the  ribs  are  so  close  together  that  good  drainage 
cannot  be  secured  without ;  for  those  in  which  a  high  temperature  and 
offensive  discharge,  subsequent  to  the  simpler  operation,  indicate  insuffi- 
cient drainage  ;  for  those  in  which  partial  re-expansion  of  the  lung  and 
falling-in  of  the  chest  wall  have  been  insufficient  to  close  the  sinus.  In 
the  primary  operation  an  inch  or  more  of  the  rib  is  removed  and  the 
periosteum  left.  For  the  closure  of  a  sinus  it  may  be  necessary  to  remove 
portions  of  several  ribs  or  Estlander's  operation,  a  dangerous  and 
unsatisfactory  mode  of  procedure,  may  be  requisite.  If  not  fatal,  it  results 
in  fearful  deformity. 


The  Pleura  and  Pleural  Cavity.  445 

General  anaesthesia  is  preferable  to  local,  when  exploratory  punctures 
are  necessary  as  a  preliminary.  Chloroform  or  ethyl  chloride  is  used. 
Light  anaesthesia  is  sufficient  and  may  be  stopped  as  soon  as  the  pleura  is 
opened.  The  child  will  then  cough  and  assist  expulsion  of  fluid.  The 
anaesthetic  is  given  with  the  patient  on  the  back  near  the  side  of  the 
operating  table  and  the  operation  completed  without  altering  the  child's 
position.  Alarming  or  fatal  collapse  may  result  from  turning  the  patient 
over  on  to  the  unaffected  side.  Local  anaesthesia  is  advisable  in  large 
effusions  on  the  left  side  and  in  bilateral  cases. 

The  incision  should  be  made  in  the  fifth  or  sixth  space  in  the  mid- 
axillary  line  or  just  behind  it.  This  is  the  most  satisfactory  place  for 
drainage  of  a  general  empyema,  for  the  comfort  of  the  patient  and  the 
convenience  of  the  surgeon.  If  the  opening  is  made  behind,  the  patient  is 
apt  to  lie  on  the  unaffected  side  and  the  action  of  gravity  is  opposed  to 
effective  drainage.  If  the  opening  is  made  lower  down,  the  diaphragm 
may  ascend  and  partially  close  it ;  or  the  diaphragm  may  be  injured  should 
the  opening  be  lower  than  the  seventh  space  on  the  right  side  and  the  eighth 
on  the  left.  The  diaphragm  rises  higher  in  the  chest  than  in  adults.  In  a 
child  on  its  back  the  most  dependent  part  of  the  pleural  cavity  is  in  the 
posterior  axillary  line  or  just  anterior  to  it. 

The  incision  is  made  in  the  middle  of  a  space,  1J-2  ins.  long,  and  the 
hole  is  kept  open  with  dilators  to  allow  masses  of  fibrin  to  escape.  Do  not 
be  anxious  to  empty  the  cavity.  If  the  patient  shows  any  bad  sign,  insert 
a  tube  and  put  the  dressings  on  quickly.  Evacuate  large  effusions  slowly. 
Do  not  use  a  long  tube,  one  about  2  ins.  long  and  of  as  large  a  calibre  as- 
convenient  is  big  enough.  The  origin  of  the  use  of  a  long  tube  is  the 
erroneous  belief  that  the  cavity  heals  by  granulation  from  the  bottom. 
Holes  in  the  side  of  the  tube  are  of  little  value  for  assisting  drainage,  which 
takes  place  chiefly  by  the  sides,  and  the  tube  is  merely  a  temporary 
expedient  for  maintaining  the  opening.  Use  a  flanged  rubber  tube  or  a 
straight  one  transfixed  with  a  large  safety  pin  to  which  tapes  are  tied  to 
go  round  the  chest.  Put  antiseptic  gauze  under  and  over  the  safety  pin,, 
cover  with  a  large  pad  of  cotton  wool  and  dress  twice  daily  at  first.  At 
each  dressing  the  tube  is  removed  and  washed.  A  new  tube  may  cause- 
increased  discharge,  perhaps  because  of  the  sulphur  in  its  substance. 

The  removal  of  the  tube  depends  upon  the  state  of  expansion  of  the 
lung,  the  duration  and  the  size  of  the  empyema,  the  character  of  the  pus 
and  the  organisms  present,  and  the  condition  of  the  patient.  It  is  usually 
left  in  too  long  and  acts  as  a  foreign  body  creating  a  permanent  sinus, 
maintaining  the  discharge,  and  possibly  causing  necrosis  of  a  rib.  It  is 
generally  removed  in  2  or  3  weeks  but  in  many  cases  it  can  be  left  out  in  a 
few  days,  if  the  discharge  is  scanty  and  serous.  The  wound  closes  in 
another  few  days  and  a  rapid  and  perfect  cure  ensues.  The  chief  risk  of 
early  removal  is  the  accumulation  of  a  small  amount  of  pus  or  sero-pus 
beneath   the  scar.     Such   a   collection  is  treated  as    a    simple   abscess- 


446  Chapter   XXXIX. 

Occasionally  the  use  of  a  short  tube,  or  even  a  long  one,  allows  a  pocket 
of  pus  to  be  shut  off  by  adhesion,  keeping  up  the  temperature  and  malaise. 
It  can  generally  be  found  on  exploration  with  a  probe.  After  either 
incision  or  resection  the  sinus  heals  in  3-7  weeks,  sometimes  more  and 
occasionally  less  rapidly. 

Exploration  -with  the  finger  is  of  doubtful  value.  There  is  no  advantage 
in  scraping  away  thick  adherent  lymph.  Only  detachable  flakes  and 
masses,  which  would  come  away  in  the  course  of  a  day  or  two,  can  be 
removed  with  safety  by  this  method.  Scraping  may  produce  raw  bleeding 
surfaces  for  the  absorption  of  septic  products.  Irrigation  is  necessary  in 
putrid  effusions  but  the  utmost  care  must  be  taken  to  permit  the  free  escape 
of  the  fluid.  It  may  cause  fatal  syncope,  said  by  some  writers  to  be  due 
to  the  use  of  irritant  injections.  It  is  best  to  use  saline  lotions  or  the  iodine 
bath. 

The  after-treatment  consists  of  frequent  dressings  and  antiseptics  if 
there  is  much  discharge.  The  tube  is  removed  and  cleaned,  the  child  is 
turned  on  the  side  and  drainage  assisted  by  judicious  compression  of  the 
chest.  Drainage  may  not  be  perfect  after  either  incision  or  resection.  Some- 
times a  second  or  so-called  counter- opening  is  needed. 

In  order  to  induce  re-expansion  of  the  lung  after  the  sinus  is  closed  the 
child  can  be  taught  to  blow  soap  bubbles,  trumpets,  or  fluids  from  one 
bottle  to  another,  breathing  exercises  and  the  use  of  dumb-bells.  These 
methods  are  applicable  with  the  sinus  still  open  and  can  be  assisted  by  an 
apparatus  to  create  negative  pressure  in  the  pleura.  There  is  no  immediate 
necessity  for  this  treatment  as  extraordinary  improvement  occurs  in  time. 
Whooping  cough  is  sometimes  markedly  beneficial. 

The  causes  of  failure  after  operation  are  too  small  an  opening,  inefficient 
drainage  and  accumulation  of  pus  ;  thick  pleural  adhesions,  defective 
breathing  and  weak  respiratory  muscles  ;  and  complications.  A  persistent 
sinus  is  due  to  imperfect  drainage,  non-expansion  of  the  lung,  dead  bone, 
tuberculous  pleurisy  or  caries  of  the  spine.  Occasionally  adjacent  ribs 
become  united  by  bony  bridges  and  help  to  keep  up  the  fistula.  Bier's 
suction  cups  applied  several  times  daily  are  useful  for  encouraging  contrac- 
tion of  the  sinus. 

A  localised  empyema  is  treated  on  similar  principles.  If  an  empyema 
is  due  to  tuberculosis,  operate  unless  the  condition  was  hopeless  before  the 
empyema  formed.  Eemove  the  fluid  by  gentle  aspiration.  If  the  lung 
seems  not  much  diseased  and  able  to  expand,  incise  and  drain.  In  chronic 
cases  in  which  the  lung  has  little  power  of  expansion  and  the  effusion  is 
only  producing  symptoms  by  mechanical  interference  with  the  heart  and 
lungs,  an  occasional  partial  aspiration  is  sufficient.  Should  the  case  go  on 
well  an  incision  should  be  made  in  the  hope  that  the  chest  wall  will  fall  in 
and  the  cavity  granulate  up. 


The  Pleura  and  Pleural  Cavity.  447 

Bilateral  Empyemata  are  treated  on  similar  lines.  If  there  is  general 
■effusion  on  both  sides,  remove  some  of  the  fluid  by  aspiration  to  relieve  the 
heart  and  lungs.  On  the  next  day  drain  the  left  side,  and  operate  on  the 
right  side  a  few  days  to  a  week  later.  If  the  effusion  is  general  on  one  side 
^tnd  localised  on  the  other,  drain  the  general  effusion  first.  Bilateral 
localised  effusions  can  be  drained  simultaneously. 

The  successful  treatment  of  empyema  depends  on  early  diagnosis, 
early  and  efficient  drainage,  removal  of  the  tube  as  soon  as  the  discharge 
becomes  scanty  and  serous,  and  the  absence  of  the  various  complications 
on  which  fatal  results  usually  depend.  Many  cases  go  wrong  through 
mismanagement.  It  is  advisable  that  the  treatment  of  these  cases  should  be 
left  entirely  in  the  hands  of  the  physician,  at  any  rate  after  the  drainage 
tube  has  been  first  inserted. 

Pneumothorax. — Pneumothorax  is  rare  and  almost  invariably  due  to 
tuberculous  disease  of  the  lung,  injury  or  rupture  of  an  empyema  ;  rarely 
to  emphysema,  pulmonary  abscess,  gangrene  or  hydatid.  The  symptoms 
are  the  same  as  in  adults.  An  acute  effusion  of  air  is  ushered  in  with  pain, 
alarming  dyspnoea,  cyanosis,  rapid  fall  of  temperature,  and  all  the  signs 
•of  severe  collapse.  More  often  there  is  a  slowly  increasing  shortness  of 
breath.  The  chest  is  in  a  position  of  inspiration,  immobile  and  hyper- 
resonant,  and  the  heart  is  much  displaced.  The  opening  varies  in  size 
and  shape,  and  may  be  multiple  in  caseous  phthisis.  If  there  is  fluid, 
splashing,  metallic  tinkling  and  bell  sound  may  be  obtained.  The  breathing 
is  amphoric  if  the  opening  is  large  and  tinkling  may  be  heard,  due  to  fluid 
dropping  from  the  aperture  into  the  cavity  on  coughing. 

It  may  be  necessary  to  relieve  urgent  symptoms  at  the  onset  by 
syphonage.  Later  on,  tapping  is  required  to  get  rid  of  the  fluid  which  is 
poured  out.  Sometimes  the  air  is  absorbed  and  then  the  fluid,  but  often  it  is 
necessary  to  evacuate  the  fluid  by  syphonage  if  it  is  serous,  and  by  incision 
and  drainage  if  it  is  purulent.  In  syphonage  it  is  important  to  keep  the 
mouth  of  the  cannula  below  the  level  of  the  fluid  ;  it  will  not  create  enough 
pressure  to  cause  the  weak  place  in  the  lung  to  give  way.  The  prognosis 
is  bad  in  hydro-pneumothorax  due  to  tuberculosis  and  still  worse  in 
pyo-pneumothorax. 


CHAPTER    XL. 

THE  HEAET  AND   CIRCULATION. 

The  Heart  at  Birth — Examination  of  the  Heart — The  Pulse — Functional 
Heart  Murmurs — Functional  Disorders — Diseases  of  Blood  Vessels — 
(Edema  and  allied  conditions. 

At  birth  the  heart  weighs  from  |-1  oz.  ;  varying  with  the  bulk  of  the 
body,  though  relatively  greater  than  in  adults.  It  is  equal  to  one-seventh 
that  of  the  liver,  and  doubles  its  weight  in  about  2  years.  Up  to  this  time 
its  ratio  to  the  body  weight  decreases  and  after  that  it  increases.  At  puberty 
there  is  considerable  increase  in  size.  The  walls  of  the  ventricles  are  at 
birth  almost  equal  in  thickness  but  at  the  end  of  the  second  year  the  left 
ventricle  is  double  the  thickness  of  the  right.  It  is  situated  more  to  the 
left  than  to  the  right,  rather  more  horizontally  and  higher  up  than  in  the 
adult,  and  the  apex  is  consequently  higher  up  and  further  to  the  left.  The 
apex  is  the  lowest  and  most  external  point  at  which  the  cardiac  impulse 
can  be  felt.  It  varies  greatly  with  the  position  of  the  child  and  should  be 
noted  in  the  dorsal  decubitus  at  the  beginning  of  any  illness.  Up  to  the 
end  of  the  third  year  the  apex  may  be  as  much  as  -J  in.  outside  the 
nipple  line  in  the  fourth  space.  It  is  then  felt  in  or  near  the  nipple  line,  and 
after  the  seventh  year  is  from  \-\  in.  within  the  nipple  line  in  the  fifth  space ; 
before  that  it  may  be  either  in  the  fourth  or  the  fifth.  The  position  is 
modified  by  deformities,  cardiac,  pulmonary  and  pleural  affections,  and 
other  causes.  Pericardial  fat  is  absent  at  birth  and  remains  scanty  during 
childhood.  A  murmur  may  be  present  during  the  first  few  days,  due  to  an 
open  ductus  arteriosus. 

Examination  of  the  Heart. — In  every  patient  the  heart  should  be 
examined  with  the  chest  bare,  for  heart  affections  are  common  in  early 
life  and  their  onset  is  often  overlooked.  Examination  is  easy  since  it  is 
rarely  interfered  with  by  emphysema,  adiposity,  great  muscular  develop- 
ment or  pendulous  breasts.    Be  careful  that  the  hands  are  warm. 

First  localise  the  apex.  Dilatation  of  the  right  ventricle  pushes  the 
apex  upward  and  outward,  along  the  arc  of  a  circle  with  its  centre  at  the 
aortic  valve  and  a  radius  from  this  point  to  the  apex.  The  aortic  valves 
are  the  most  fixed  point  and  are  situated  under  the  middle  of  the  left  third 
chondro-sternal  juncture.  In  dilatation  of  both  ventricles  the  apex  is 
displaced  outward  only,  and  in  dilatation  of  the  left  ventricle  downward. 


The   Heart  and  Circulation.  449 

Note  the  character  of  the  impulse  and  any  precordial  prominence.  Pay 
special  attention  to  evidence  of  dilatation  or  hypertrophy.  The  heart  of  the 
child  is  precocious  in  its  development  and  relatively  hypertrophied, 
especially  in  active  boys.  Unless  there  is  evidence  of  dilatation,  such  as 
increased  dulness  along  the  left  border  of  the  heart  and  epigastric  pulsation, 
this  condition  is  unimportant.  Palpate  gently  and  percuss  lightly,  without 
using  a  pleximeter.  Pulsation  and  dulness  to  the  right  of  the  sternum 
are  important  facts.  Dulness  in  the  fourth  right  intercostal  space  is  normal 
and  due  to  the  auricle.  If  it  is  increased,  it  may  extend  J-l  in.  from  the 
sternum  and  about  half  this  distance  in  the  third  space.  In  great  dilatation 
there  may  be  even  dulness  in  the  second  space.  The  presence  of  this 
dulness  is  often  of  grave  importance  and  indicative  of  the  necessity  for 
leeches.  The  normal  limit  of  cardiac  dulness  to  the  left  is  one  finger-breadth 
inside  the  nipple  line,  sometimes  it  reaches  the  nipple  line  and  occasionally 
extends  a  finger-breadth  beyond  it.  After  infancy,  dulness  beyond  the 
nipple  line  is  pathological. 

For  auscultation  use  a  binaural  stethoscope,  unless  thoroughly  com- 
petent to  use  a  wooden  one  without  undue  pressure  on  the  chest.  The  pulse 
and  general  appearance  of  the  patient  may  give  more  valuable  evidence  than 
auscultation.  It  is  excellent  practice  to  make  a  provisional  diagnosis  before 
using  the  stethoscope.  By  such  a  method  the  doctor  gets  into  the  habit  of 
properly  appreciating  the  effects  of  disease  on  the  heart  and  not  merely 
on  the  characters  revealed  by  auscultation.  The  pulmonary  second  sound 
is  increased  in  mitral  stenosis,  mitral  regurgitation  and  generally  in 
congenital  morbus  cordis.  This  is  a  striking  feature  for  on  account  of  low 
blood  pressure  the  aortic  second  sound  is  feeble.  If  a  murmur  is  present,  note 
the  time,  quality,  distribution  and  point  of  maximum  intensity  ;  so  too  in 
the  case  of  thrills.    Above  all  do  not  confuse  facts  with  inferences. 

The  Pulse  is  not  felt  during  the  first  quarter  of  a  minute  after  birth. 
The  heart  then  begins  to  beat  slowly  at  the  rate  of  10-12  beats  per  minute. 
In  the  second  half  minute  the  child  usually  cries  and  the  pulse  rate  goes  up 
to  160.  After  that  it  falls  to  130-140.  Both  the  pulse  and  respiration  rate 
are  normally  higher  in  infancy  and  early  life  than  in  adults.  Both  are 
increased  in  fever  but  the  relative  increase  in  the  pulse  rate  is  less  than  in 
the  adult.  In  the  infant  for  each  rise  of  a  degree  in  temperature  the  pulse 
rate  increases  5  beats  per  minute  ;  in  early  childhood  7  ;  and  in  the  adult  10. 
The  infant's  pulse  would  become  dangerously  rapid  if  it  increased  10  beats 
with  every  rise  of  1  degree  in  temperature.  Anything  over  160-180  beats 
per  minute  is  bad.  The  respiration  rate  increases  more  than  in  adults 
rising  3  in  infants,  2-2|  in  early  childhood,  and  2  in  adults  for  each  degree 
of  temperature.  The  pulse  rate  is  four  times  as  frequent  as  the  respiration 
rate,  but  with  rise  of  temperature  the  ratio  decreases  down  to  3-1  at  105°  F. 
The  pulse  rate  is  roughly  in  the  first  year  100-130  ;  second  year  110-125  ; 
at  2-5  years  100-115  ;   at  5-10  about  100,  and  up  to  13  years,  80-90.    The 

2  G 


450  Chapter  XL. 

blood  pressure  is  low  for  the  lumen  of  the  vessels  is  relatively  greater.  The 
pressure  in  infancy  is  80-85  ;  up  to  7  years  85-95  ;  up  to  10  years  95-100  ; 
and  up  to  13  years  100-110.  All  these  figures  may  be  modified  by  disease 
of  the  heart,  lungs  or  brain,  and  typhoid  fever,  etc. 

An  intermittent  pulse  is  frequent  during  sleep  and  under  chloroform. 
Irregularity  is  present  in  nervousness,  tuberculous  meningitis,  organic 
heart  disease,  gastro-intestinal  troubles,  appendicitis;  anaemia,  chorea, 
during  convalescence,  and  from  the  effects  of  toxins  and  drugs.  Irregularity 
in  rate  or  rhythm  is  much  less  important  than  in  adults.  Increased  pulse 
rate  occurs  in  fevers,  toxaemia,  pericarditis  and  effusion,  and  nervousness. 
In  endocarditis  the  pulse  is  frequent,  strong,  full  and  often  irregular.  In 
myocarditis  increased  frequency  is  associated  with  gallop-rhythm  if  the 
affection  is  acute,  and  with  irregularity  if  it  is  chronic.  In  hypertrophy 
both  rate  and  volume  are  increased  unless  there  is  aortic  stenosis. 

The  rate  may  be  so  frequent  as  to  deserve  the  name  of  tachycardia. 
A  very  frequent  pulse  is  sometimes  present  in  children  taking  Tibbie's 
Cocoa  and  is  associated  with  nervous  irritability.  Bradycardia  or  Oligocardia 
is  usually  unimportant  unless  it  is  associated  with  irregularity.  It  may  be 
due  to  disorders  of  the  central  nervous,  digestive,  respiratory  or  genito- 
urinary system  ;  or  to  the  poisons  of  lead,  alcohol,  tobacco  or  digitalis. 
It  occurs  in  diphtheria,  cardiac  disease,  anaemia,  asthenia  and  certain  skin 
affections.  It  is  not  infrequent  in  convalescence  from  acute  fever  and  is 
common  at  the  onset  of  tuberculous  meningitis.  Sometimes  it  has  occurred 
paroxysmally. 

Functional  Heart  Murmurs. — Most  writers  state  that  functional  mur- 
murs are  rare  under  4  years  of  age.  This  is  certainly  not  true  of  the  systolic 
murmur  which  is  heard  over  the  pulmonary  area  and  is  quite  common. 
It  is  a  functional,  inorganic  or  haemic  murmur,  with  its  maximum  intensity 
over  the  second  left  interspace  close  to  the  sternum,  sometimes  more  to  the 
left  or  over  the  third  left  cartilage.  It  may  be  heard  only  in  the  second 
left  interspace  ;  over  an  area  from  the  second  to  the  fourth  spaces  ;  just 
above  and  within  the  apex  ;  or  over  the  sternum,  at  the  apex  and  even 
beyond  it.  Occasionally  it  is  heard  over  the  aortic  area  or  is  associated  with 
a  similar  murmur  in  this  situation,  due  to  the  same  cause,  or  with  a  venous 
bruit  in  the  neck  and  over  the  manubrium,  and  a  systolic  murmur  over 
the  carotids  and  subclavians.  The  typical  systolic  pulmonary  murmur 
is  superadded  to  the  first  sound,  which  is  distinctly  audible  ;  sometimes 
there  is  a  distinct  interval  between  them.  It  varies  in  duration  and 
character  from  soft  and  blowing  to  musical.  It  is  increased  in  loudness  in  the 
recumbent  posture  and  perhaps  only  heard  then.  It  is  increased  by 
exercise,  may  disappear  on  deep  inspiration,  and  is  best  heard  at  the  end 
of  forcible  expiration.  The  second  sound  is  usually  accentuated.  The 
cardiac  dulness  is  not  increased  and  the  position  of  the  apex  is  unaltered, 
unless  there  is  anaemia  and  cardiac  dilatation. 


The  Heart  and  Circulation.  451 

This  murmur  may  be  due  to  anaemia,  but  is  not  necessarily  so  caused. 
It  may  be  absent  in  severe  anaemia,  and  loud  although,  anaemia  is  slight  or 
absent.  It  is  probably  dependent  on  the  low  arterial  tension  in  the  pul- 
monary artery  and  a  dilatation  of  the  artery  causing  a  relative  stenosis 
at  the  orifice.  Arterial  tension  is  normally  lower  in  children  than  in  adults 
and  is  more  easily  reduced.  The  lumen  of  the  main  vessels  is  wide  and 
the  cardiac  cavities  are  small.  Both  the  pulmonary  artery  and  the  aorta 
are  more  easily  dilated  than  in  adults,  but  the  murmur  is  more  readily 
produced  at  the  pulmonary  orifice  because  of  the  thin  wall  of  that  artery. 
The  murmur  must  not  be  confused  with  that  due  to  anaemia  from  which  it 
•cannot  be  diagnosed  with  certainty,  except  by  a  blood  count  and  haemo- 
globin estimation.  It  has  also  to  be  diagnosed  from  the  organic  murmurs 
•of  pulmonary  stenosis  and  mitral  regurgitation,  the  pressure  of  enlarged 
bronchial  glands,  and  possibly  the  pressure  of  a  dilated  aorta  on  the 
pulmonary  artery. 

Diastolic  functional  murmurs  are  very  rare.  A  cardio-pulmonary  one 
is  less  common  than  in  adults.  It  is  a  short,  whiff-like  or  squeaking,  systolic 
murmur  due  to  the  impact  of  the  heart  on  the  lung  or  compression  of  the 
lung  by  the  heart.  It  is  heard  best  at  the  apex  and  along  the  left  border  of 
the  heart,  and  may  be  transmitted  a  little  to  the  left.  It  is  loudest  at 
the  end  of  inspiration  and  may  disappear  on  expiration,  especially  in 
recumbency. 

Functional  Disorders  of  the  Heart  are  rare  before  the  seventh  year  but 
are  not  infrequent  about  puberty.  The  most  common  causes  are  indigestion 
and  nervous  exhaustion.  Sometimes  there  is  a  definite  exciting  cause  such 
as  fright,  tea,  coffee,  cocoa  containing  kola  nut,  or  cigarette  smoking. 
Sometimes  it  occurs  during  or  after  acute  febrile  disease,  more  especially 
those  in  which  myocardial  degeneration  is  apt  to  develop.  At  puberty 
the  rapid  growth  of  the  body  may  exceed  the  development  of  the  heart  and 
is  a  frequent  cause  of  undue  rapidity  of  the  heart's  action,  particularly  if  it  is 
associated  with  anaemia,  overpressure  at  school  or  over-exertion. 

The  chief  symptoms  are  palpitations,  tachycardia  and  occasionally 
bradycardia.  A  slow  heart  has  already  been  referred  to  under  the  pulse. 
Paroxysmal  attacks  of  palpitation,  lasting  for  a  few  seconds  to  hours  at  a 
time,  produce  the  same  symptoms  as  in  adults. 

Tachycardia  is  the  most  interesting  of  these  affections.  The  attack 
comes  on  at  varying  intervals  and  is  of  variable  duration.  It  is  usually 
induced  by  exertion  or  fright,  and  comes  on  quite  suddenly.  The  symptoms 
include  pallor,  anxiety,  sweating,  exhaustion  and  palpitations.  The 
breathing  is  not  accelerated  and  the  urine  is  increased  in  quantity.  Some- 
times the  attacks  are  associated  with  repeated  vomiting,  though  they  persist 
after  the  vomiting  has  ceased,  or  with  constipation.  The  pulse  may  be 
uncountable  and  almost  imperceptible.  Tachycardia  is  probably  a  true 
neurosis  and  independent  of  any  heart  lesion.     It  has  been  ascribed  on 


452  Chapter   XL. 

insufficient  evidence  to  vagus  palsy,  compression  of  the  vagus  by  enlarged 
glands,  accelerator  stimulation  or  bulbar  mischief.  It  has  followed  pertussis 
and  measles. 

The  most  useful  treatment  is  by  bromides  and  valerianates,  and  careful 
regulation  of  the  digestion,  bowels  and  mode  of  life.  Stimulating  foods  and 
drinks  must  be  avoided.  During  the  attack  a  cold  compress,  ice  bag,  spray 
of  ether  or  ethyl  chloride,  or  mustard  leaf  may  prove  beneficial. 

Syncope. — Many  diseases  end  in  syncope,  sudden  and  permanent 
cessation  of  the  heart's  action.  "  Fainting  "  or  "  Swooning  "  is  a  mild 
form  of  syncope,  more  gradual  in  development  and  of  temporary  duration. 
The  loss  of  consciousness  is  due  to  the  failure  of  cerebral  circulation,  or 
alteration  in  intracranial  pressure.  An  actual  fall  in  blood  pressure  is  the 
chief  determining  factor.  This  is  brought  about  by  inhibition  of  the 
heart  and  vasomotor  centre,  and  vaso-dilatation.  Sudden  death  in  aortic 
regurgitation  seems  due  to  sudden  diminution  of  intracranial  pressure. 
In  other  cases  the  cardio-vascular  derangement,  diminishing  the  cerebral 
blood  supply,  is  due  to  stimulation  of  the  cardio-inhibitory  centres  in 
the  medulla,  e.g.,  by  sudden  intense  pain,  infantile  colic,  various  sights  and 
odours,  and  emotion.  Syncopal  attacks  can  be  induced  by  sudden  intense- 
cerebral  congestion,  as  in  the  paroxysms  of  pertussis. 

Fainting  is  apt  to  occur  in  school-children  during  morning  chapel. 
The  erect  posture,  empty  stomach,  lack  of  cerebral  stimulation  and  the 
ill-ventilated  building  are  all  exciting  causes.  These  children  often  exhibit 
albuminuria,  a  sign  of  vasomotor  instability,  and  in  some  no  doubt  the 
fainting  attack  is  dependent  on  masturbation  before  rising.  Fainting  is 
most  common  in  girls  about  puberty  and  is  then  a  sign  of  hysteria.  The 
chief  causes  are  the  sudden  assumption  or  prolonged  maintenance  of  the 
erect  posture  ;  rapid  loss  of  fluid  as  in  haemorrhage,  profuse  purging,  or  the 
evacuation  of  ascitic  fluid  ;  the  vaso-dilatation  induced  by  heat  after  the 
superficial  vessels  have  been  constricted  by  exposure  to  cold  ;  and  the 
purely  nervous  causes  already  mentioned.  Fainting  is  ushered  in  by  pallor,, 
a  sense  of  increasing  feebleness,  dimness  or  loss  of  sight  because  of  lack  of 
blood  supply  to  the  retina,  sighing  respiration,  and  frequently  undue 
consciousness  of  the  heart's  action  and  a  sense  of  nausea.  A  sinking  feeling 
in  the  epigastrium  is  due  to  splanchnic  vaso-dilatation.  Consciousness 
is  lost,  more  or  less  completely,  for  a  variable  time  but  not  so  suddenly  as 
in  epilepsy.  The  child  sinks  down  or  can  lie  down,  and  rarely  falls  so 
suddenly  as  to  cause  injury.  The  heart  beat  may  be  very  feeble  and  the 
radial  pulse  almost  imperceptible.  Consciousness  and  colour  return 
gradually,  without  any  mental  confusion  or  special  tendency  to  sleep. 

A  severe  faint  may  be  attended  with  muscular  spasm.  In  minor 
epilepsy  it  may  be  absent.  It  is  common  for  petit  mal  to  be  diagnosed  as 
fainting.  In  minor  epilepsy  there  is  no  initial  facial  pallor,  loss  of  con- 
sciousness is  sudden  and  recovery  as  sudden,  and  there  is  frequently  some 


The   Heart  and  Circulation.  453 

mental  confusion,  hysteroid  symptoms  or  sound  sleep  immediately  after. 
Both  are  due  to  the  failure  of  the  cerebral  circulation,  but  differ  in  the 
conditions  of  their  production  and  tendency  to  recurrence.  A  family 
history  of  epilepsy  may  be  present  or  an  exciting  cause  of  the  fainting 
attack.  Even  babies  have  fainting  attacks  which  are  extremely  difficult 
to  diagnose.  Swooning  is  treated  by  fresh  air,  recumbency,  lowering  the 
head,  loosening  the  clothes,  a  cold  douche,  stimulants  and  smelling  salts. 

Functional  Circulatory  Disorders  might  strictly  be  included  in  the 
section  on  nervous  diseases.  The  two  chief  ones  are  Chilblains  and 
Raynaud's  Disease. 

A  Chilblain  (erythema  'pernio)  or  Frost-bite  is  a  local  vascular  lesion 
dependent  on  altered  conditions  of  the  blood  or  circulation.  Primary 
vaso-constriction  is  followed  by  vaso-dilatation  and  in  this  respect  it  is 
analogous  to  Raynaud's  disease.  The  first  effect  is  local  anaemia,  and  it  is 
quickly  followed  by  hyperaemia  due  to  venous  engorgement  and  transuda- 
tion, and  then  by  thrombosis  and  even  gangrene.  Observations  on  the 
blood  have  shown,  in  one  class  of  case,  a  deficient  coagulability  and  conse- 
quent liability  to  serous  exudation  or  "  serous  haemorrhage,"  like  that  of 
urticaria.  The  predisposing  factors  are  heredity,  lowered  vitality,  feeble 
blood  supply  to  the  extremities,  insufficient  exercise  and  a  deficient  supply 
of  fatty  foods.  Children,  shop  girls,  old  people  and  the  feeble-minded  are 
very  liable  ;  so,  too,  the  anaemic,  those  with  a  tuberculous  tendency  or 
morbus  cordis,  and  those  who  live  a  sedentary  life.  The  main  exciting  cause 
is  rapid  change  in  external  temperature. 

In  the  early  stage  there  is  an  erythema  and  secondary  inflammation. 
The  heel, toes,  fingers,  nose  and  ears  are  the  common  sites.  The  part  affected 
is  swollen,  exhibits  a  superficial,  dusky  or  bluish  redness,  with  tenderness, 
itching  and  stiffness  of  the  skin.  The  itching  is  worst  when  warm.  In  mild 
cases  the  skin  desquamates  and  the  chilblain  gets  well.  If  neglected,  severe 
or  irritated,  vesicles  form  and  it  becomes  "  broken  "  or  ulcerated.  Cracks 
develop,  are  infected,  and  may  lead  to  deep  ulcers  or  more  serious  mischief. 
In  still  worse  cases  the  damaged  part  becomes  gangrenous,  a  line  of  demar- 
cation forms,  and  it  gradually  separates  and  drops  off.  The  diagnosis  is 
quite  simple.  Mild  Raynaud's  disease  may  be  overlooked.  Recurrence  is 
common. 

To  prevent  chilblains  attend  to  the  general  health.  Give  cod-liver  oil 
for  malnutrition  ;  iron  for  anaemia  ;  and  drugs  such  as  arsenic,  strychnia, 
ergotin,  belladonna  and  digitalis.  Calcium  salts  are  often  usefid,  by  increas- 
ing the  coagulability  of  the  blood,  if  given  for  only  1-3  days  at  a  time. 
Ichthyol  pills,  after  food,  can  be  tried.  Maintain  vascular  tone  by  alternate 
hot  and  cold  douching  of  the  limbs  for  15  minutes  nightly.  Guard  against 
cold,  damp  feet  and  hands,  and  order  plenty  of  exercise.  Rub  the  ex- 
tremities with  sp.  camph.  every  morning,  camphorated  vaseline,  gr.  75  ad 
oz.  1,  or  camphorated  soap.    In  the  erythematous  itching  stage  apply  Bier's 


454  Chapter   XL. 

method  of  artificial  hyperemia  ;  commercial  formalin,  half  strength,  once 
or  twice  daily,  and  then  vaseline  or  boroglyceride  ;  tr.  iodi,  iodine  2  per  cent, 
in  collodion,  silver  nitrate  solution  or  sp.  camph. ;  rubbing  with  methylated 
spirit  or  whisky  and  water  ;  liniments  of  aconite,  belladonna,  chloroform 
and  soap  ;  bals.  Peru,  ichthyol  or  thigenol,  10  per  cent,  in  oil  or  lanolin  ; 
or  with  tannin  gr.  \  ad  oz.  1  glycerine  and  rose  water,  p. a.  Bceck  of  Chris- 
tiania  recommends  ichthyol,  resorcin,  tannin  aa  gm.  1,  aqua  5  c.c,  painted 
on  nightly,  it  forms  a  varnish  in  a  few  minutes  and  causes  the  cedematous 
swelling  to  disappear,  the  part  looking  black  for  1-2  weeks.  If  there  is  much 
inflammation  apply  ung.  plumbi  oz.  1,  vaseline  oz.  1,  ol.  olivee  oz.  \,  ac. 
carbol.  gr.  10-20,  ol.  lavandulae  m.  20,  freely  on  lint  at  night. 

Open  blisters  and  dress  them  with  ac.  carbol.  2  per  cent,  in  Carron  oil, 
or  with  borated  vaseline.  Broken  chilblains  can  be  dressed  with  walnut 
leaves  soaked  in  hot  water,  or  lint  steeped  in  hydrag.  perchlor.  1  in  2000  ; 
painted  with  tr.  benzoin,  co.  ;  powdered  with  bismuth,  salicyl.  1,  amyli 
9  parts  ;  H202  (10  vol.  strength),  mixed  with  an  equal  amount  of  hot  water 
and  applied  for  15  minutes  twice  a  day  ;  weak  ointments  of  Friar's  balsam, 
liq.  carbonis  detergens  or  ol.  rusci ;  ung.  zinci ;  hydrarg.  ammon.  gr.  5, 
ichthyol  gr.  10,  zn.  oxid.  dr.  2,  amyli  dr.  2,  vaseline  oz.  \.  Lewis  Jones 
recommends  an  electric  footbath  for  10-15  minutes  nightly.  The  main 
principle  in  the  treatment  of  broken  chilblains  is  that  of  all  open  sores. 
Protect  them  from  infection,  keep  them  clean,  and  apply  soothing  or 
stimulating  ointments  according  to  the  stage  of  the  ulceration.  If  the 
ulcers  do  not  heal  touch  them  with  solid  nitrate  of  silver. 

Raynaud's  Disease  is  a  neurosis,  a  vasomotor  disturbance,  a  disorder  of 
function  and  not  of  structure.  It  affects  the  ringers,  toes,  ears  and  nose  ; 
less  often  the  hands,  feet,  face,  tongue  and  trunk.  Children  suffer  less 
severely  than  adults.  There  is  less  functional  impairment,  with  slight 
ulceration  and  destruction  of  tissue  and  practically  no  general  symptoms. 
Comby  (1905)  reported  3  cases,  aged  9  and  10  years,  with  local  asphyxia 
and  dry  gangrene  of  the  ears  and  ends  of  the  extremities. 

The  first  stage  is  that  of  "  Local  Syncope  "  or  dead  fingers,  due  to 
excessive  vaso-constriction.  Pain  may  be  considerable  or  absent.  This 
condition  may  arise  simply  from  cold  and  is  not  necessarily  due  to  Ray- 
naud's disease.  The  second  stage,  "  Local  Asphyxia,"  is  usually  but  not 
always  preceded  by  local  syncope.  It  is  produced  by  extreme  vaso-dilata- 
tion  and  great  venosity  of  the  stagnant  blood,  giving  rise  to  a  purplish  or 
black  discoloration.  It  is  very  painful,  especially  when  passing  off.  In 
the  third  stage  there  is  dry  "  Gangrene  "  of  the  extremity  or  a  local 
necrosis  with  the  formation  of  sores,  as  in  broken  down  chilblains  and  frost- 
bite. These  necrotic  areas  heal  readily  in  warm  weather,  leaving  scars. 
Thus  all  the  effects  are  such  as  can  be  produced  by  cold,  and  the  main 
characteristic  of  the  disease  is  that  the  subject  is  one  who  is  unusually 
susceptible  to  cold.     Hemoglobinuria  may  occur  at  the  onset  and  not 


The   Heart  and  Circulation.  455 

subsequently,  during  many  attacks,  or  even  independently.  Purpura  is 
less  common  and  may  be  recurrent.  Sclerodermia  and  melanodermia 
of  the  face,  trunk  and  joints  have  been  reported.  Cerebral  symptoms  are 
such  as  can  be  explained  by  vaso-constriction,  viz.,  transient  vacancy  or 
loss  of  consciousness  as  in  petit  mal,  temporary  aphasia  or  disorder  of 
speech,  hemiplegia,  delirium  and  mania ;  mental  torpor ;  convulsive 
attacks  of  an  epileptiform  or  hysterical  nature.  Impaired  vision  is  due  to 
constriction  of  the  central  retinal  arteries.  An  ultimate  cure  may  be 
effected.     The  disease  is  not  fatal. 

Treatment. — Avoid  cold,  fatigue  and  excitement.  Wash  in  warm 
water,  wear  warm  clothing,  protect  the  hands,  live  in  warm  rooms  and  a 
warm  climate.  Treat  local  syncope  in  the  same  way  as  frost-bite  with 
warm  cotton  wool,  immersion  in  tepid  water,  and  gentle  active  and  passive 
movements.  Vaso-dilators  are  useless.  Gangrene  is  treated  on  ordinary 
surgical  lines.  Between  the  attacks  attend  to  the  alimentary  system. 
Naphthol,  sulphocarbolates  and  other  intestinal  disinfectants  may  do 
good.  Electricity  should  be  applied  in  the  form  of  faradism  to  the  spine 
over  the  site  of  origin  of  the  affected  vasomotor  nerves  ;  and  to  the  affected 
limbs  by  immersion  in  a  salt  water  bath  through  which  a  constant  current, 
which  can  be  frequently  interrupted,  is  passed.  A  floating  kidney  may  be 
fixed.  Cushing  recommends  the  temporary  constriction  of  the  affected 
limb  for  some  minutes.  On  relaxation,  the  blood  flow  may  overcome  the 
spasm. 

Gangrene  is  occasionally  seen  in  the  newborn  as  the  result  of  pressure, 
asphyxia  or  of  uncertain  origin.  It  may  follow  infective  fevers  and  is 
then  generally  due  to  thrombosis,  secondary  to  endarteritis.  At  any  age  it 
can  occur  from  microbial  infection.  Sometimes  it  follows  the  application  of 
carbolic  acid  dressings,  independently  of  tight  bandaging,  waterproof 
dressing  or  the  nature  of  the  primary  injury.  This  is  probably  the  effect 
of  idiosyncrasy  and  is  independent  of  age,  sex,  and  the  state  of  the  health. 
Harrington  (1900)  collected  132  cases,  some  in  children.  It  is  a  dry  gangrene. 
The  skin  becomes  dry,  wrinkled  and  greyish  white  ;  then  darker  and  more 
shrivelled,  and  a  line  of  demarcation  forms.    Amputation  is  often  needed. 

Diseases  of  Blood  Vessels. — Arteritis  occurs  in  acute  infections  such  as 
scarlet  fever,  typhoid  fever,  diphtheria,  pneumonia  and  sepsis,  and  in 
congenital  syphilis  and  rheumatism.  Henning  (1890)  reported  endocarditis 
and  aortitis  of  a  few  weeks  duration  in  an  8-months  child  who  died  shortly 
after  birth.  One  valve  of  the  aorta  was  contracted.  The  mother  had 
rheumatism  during  pregnancy.  According  to  Barrie  (1905)  acute  rheumatic 
arteritis  usually  causes  aortitis  and  may  affect  the  coronary,  peripheral  and 
visceral  arteries.  It  comes  on  at  the  end  of  rheumatic  fever.  Pain  and 
tenderness  are  present  in  the  course  of  the  artery,  the  limb  is  swollen  and 
cold,  and  there  is  no  fever.  It  may  clear  up  in  1-2  weeks,  become  chronic 
and  cause  arterio-sclerosis,  or  obliterate  the  artery.    No  case  of  secondary 


456  Chapter  XL. 

gangrene  is  on  record.    If  it  affects  the  coronary  artery  it  may  cause  myo- 
cardial changes,  dilatation  and  sudden  death. 

AVeisel  (1906)  found  arteritis  in  80  young  subjects,  many  infants, 
secondary  to  diphtheria  in  20,  scarlet  fever  20,  and  other  infections  40. 
Similar  changes  were  present  in  all.  In  6-10  days  minute  yellowish  patches 
appear  in  the  aorta,  carotids  and  coronary  arteries  ;  with  secondary  minute 
calcareous  deposits  in  a  few.  It  usually  ends  in  regeneration,  but  occasion- 
ally in  atheroma  and  arterio-sclerosis  with  their  sequels. 

Congenital  syphilis  is  apt  to  produce  aortitis  and  aortic  atheroma, 
which  may  be  associated  with  valvular  lesions  or  with  generalised  arterio- 
sclerosis. Its  signs  are  increased  aortic  dulness,  murmur  and  thrill.  Arterio- 
sclerosis often  includes  many  varieties  of  endarteritis  and  arteritis  ;  some 
congenital,  others  due  to  the  various  causes  above  mentioned.  The  term 
should  be  restricted  to  the  type  seen  in  chronic  interstitial  nephritis.  Cal- 
careous degeneration  is  a  sequel  of  one  or  other  of  these  affections.  Calcifi- 
cation of  all  the  peripheral  arteries,  the  iliacs  like  pipe-stems  and  the 
aorta  hardly  affected,  has  been  reported  at  the  age  of  6  months  (Hale  White) ; 
calcareous  degeneration  of  the  media  of  the  aorta  and  pulmonary  artery 
at  6  days  (Durant)  ;  calcification  round  the  mitral  orifice  at  2  months 
(Goodhart) ;  calcification  of  the  aorta  and  valves  at  2  years  (Moutard), 
and  of  the  temporal  arteries  at  15  months  (Hodgson)  ;  and  a  few  cases  in 
older  children,  all  apparently  non-syphilitic.  Endarteritis  and  coronary 
sclerosis  have  both  been  found  in  infants  aged  5  months.  All  these  affections 
are  rarely  recognised  in  the  young  but  it  is  by  no  means  improbable  that 
arteritis  is  fairly  frequent  in  infective  disorders  and  accounts  for  some  of 
the  rare  cases  of  aneurysm,  thrombosis  and  gangrene. 

Aneurysm  is  a  rare  affection  in  children.  One  child  showed  aneurys- 
mal dilatation  of  the  pulmonary  artery  as  the  result  of  congenital  heart 
disease.  In  a  girl,  aged  16,  cerebral  hsemorrhage  was  due  to  the  rupture 
of  an  aneurysm  of  the  left  posterior  cerebral  artery,  the  result  of  infective 
endocarditis.  In  a  boy,  aged  18,  aneurysm  of  the  posterior  tibial  artery  was 
caused  by  embolism  from  valvular  heart  disease.  It  was  cured  by  ligature  of 
the  popliteal  artery.  Phanomenow  (1881)  found  endarteritis  and  aneurysm 
of  the  abdominal  aorta  in  a  7-months  foetus  ;  and  Martin  reported  one  of  the 
ductus  arteriosus  at  the  age  of  1  month.  Including  my  two  cases  and 
excluding  Phanomenow's  and  those  of  congenital  origin,  I  have  collected 
38  under  20  years  of  age  ;  25  of  them  under  13  years  old.  The  ratio  of  boys 
to  girls  is  2-1.  In  31  the  site  was: — thoracic  aorta  6,  abdominal  aorta  3, 
iliac  1,  femoral  5,  popliteal  2,  tibial  4,  carotid  3,  axillary  2,  and  innominate, 
coronary,  ulnar,  dorsalis  pedis  and  cerebral  1  each.  No  doubt  many  more 
cerebral  cases  are  on  record  and  are  described  under  the  head  of  the  primary 
disease.  The  main  cause  is  embolism,  from  simple  or  infective  endocarditis  ; 
and  others  have  been  due  to  endarteritis,  atheroma,  and  possibly  injury. 
Several  have  been  cured  by  ligature.    Other  cases  have  ended  fatally  from 


The   Heart  and  Circulation.  457 

the  primary  disease,  cerebral  haemorrhage  or  embolism,  rupture  into  the 
pericardium  and  into  the  trachea.  The  symptoms  and  treatment  are  the 
same  as  in  adults. 

Diseases  of  Veins.—  Dilatation  of  the  jugular  veins  and  of  the  super- 
ficial veins  on  the  chest  is  caused  by  pressure  on  the  superior  vena  cava 
by  enlarged  glands,  the  fibroid  contraction  in  mediastinitis  or  by  tumours. 
Occasionally  it  is  unilateral.  Dilatation  of  the  subcutaneous  veins  in  the 
legs  and  elsewhere  is  uncommon.  Haemorrhoids  are  sometimes  seen. 
Venous  dystrophy  of  the  cranial  veins  is  a  condition  in  which  the  veins  of 
the  scalp  in  infants  are  dilated  and  unusually  visible  through  a  thin  scalp. 
It  has  been  regarded  by  Fournier  as  a  sign  of  congenital  syphilis,  but  may 
be  due  to  malnutrition  and  venous  congestion  from  any  cause,  and  is 
quite  unimportant. 

Thrombosis  is  a  sequel  of  phlebitis,  or  dependent  on  altered  conditions 
of  the  blood  and  circulation.  It  is  found  in  the  sinuses  of  the  skull,  the 
cerebral  vessels,  internal  jugular  (generally  septic  and  secondary  to  ear 
disease),  the  superior  and  inferior  vena  cava,  iliac  and  other  veins.  Throm- 
bosis of  the  inferior  cava  is  not  very  rare  as  the  result  of  intra-abdominal 
tumours,  but  is  quite  exceptional  from  other  causes.  A  striking  case  was 
under  Dr.  Gould  May.  A  fat  anaemic  boy,  10  months  old,  had  an  attack 
of  diarrhoea  and  vomiting  for  2  days,  after  which  he  seemed  unduly 
prostrate.  Two  days  later  he  was  feverish  and  in  48  hours  the  legs  began  to 
swell.  When  seen  on  the  eleventh  day  of  the  illness  he  was  found  fat, 
anaemic  and  not  rachitic.  The  legs  were  greatly  swollen  and  the  abdominal 
veins  prominent,  forming  a  Caput  Medusa  above  the  umbilicus.  Two 
days  later  the  temperature  went  up  to  105°  F.  and  there  was  a  little  twitching 
for  which  no  cause  could  be  found.  The  left  leg  was  much  larger  than  the 
right,  and  the  veins  on  that  side  much  dilated.  Apparently  there  was 
thrombosis  of  the  left  iliac  and  only  partial  thrombosis  of  the  right  vein. 
Five  weeks  later  the  legs  were  quite  normal.  Thrombosis  is  apt  to  occur 
during  the  course  of,  or  in  convalescence  from,  infective  diseases,  more 
especially  typhoid  fever  and  diphtheria. 

(Edema  is  a  symptom.  Common  causes  are  backward  pressure  from 
cardiac  failure  or  obstruction,  renal  mischief,  general  malnutrition  and 
toxaemia.  Occasionally  it  follows  over-feeding  after  a  period  of  starvation. 
In  renal  disease  the  nutrition  of  the  vascular  epithelium  is  impaired,  the 
blood  is  hydraemic,  and  there  is  a  deficient  elimination  of  water  and  sodium 
■chloride.  This  salt  is  almost  entirely  eliminated  by  the  kidneys.  The 
pathology  is  practically  the  same  as  that  of  ascites  (p.  348).  Transudation 
into  the  subcutaneous  tissues  must  be  regarded  as  mainly  dependent  on 
impaired  nutrition  and  altered  blood  states.  Thus  it  is  quite  common  to 
see  a  moderate  amount  of  oedema  in  all  wasting  diseases,  notably  marasmus, 
towards  the  end.    But  there  are  other  cedematous  conditions  which  are  of 


458  Chapter   XL. 

different  causation  and,  though  not  strictly  of  purely  circulatory  origin,  may 
be  here  described. 

Angioneurotic  (Edema. — Syn.:  Acute  Circumscribed  (Edema  —  Acute 
Idiopathic  (Edema — Non-inflammatory  (Edema — Giant  Swelling — Periodic 
Swelling —  Urticaria  Tuberosa. — This  affection  is  characterised  by  extensive, 
circumscribed,  non-inflammatory  swellings  of  the  skin  and  subcutaneous 
tissues,  the  mucosa  and  the  submucosa.  It  affects  the  eyelids,  part  or  the 
whole  of  the  head,  face  or  one  limb,  lips,  tongue,  pharynx  and  larynx,  joints, 
external  genitals,  viscera  and,  indeed,  any  part  of  the  body.  It  appears 
and  disappears  with  remarkable  rapidity,  and  is  commonly  associated  with 
intestinal  symptoms  and  low  coagulability  of  the  blood.  It  is  most  common 
in  young  adults.  Cases  have  been  recorded  in  the  third  and  fourth  months 
of  life  and  at  one  year,  and  in  children  between  5  and  8  years.  It  may 
occur  at  any  age.  even  in  the  first  week.  Males  are  twice  as  liable  as  females- 
except  in  adult  life.  It  has  been  ascribed  to  exposure,  injury,  dietetic  and 
psychical  causes.  Undoubtedly  there  is  a  marked  hereditary  factor  in  many 
cases.  Quincke  referred  to  this  connection  and  Dinkelacher,  a  pupil  of  his,. 
in  the  same  year  (1882)  recorded  its  occurrence  in  a  matchmaker  and  his 
infant  son,  and  Valentin  (1885)  reported  that  a  second  son  had  been  affected 
since  the  first  week  of  life.  In  another  family  22  out  of  39  members  in 
5  generations  were  affected  (Osier,  1888)  ;  5  members  of  a  family  in  2  genera- 
tions (Apert  and  Delille,  1901). 

The  attacks  are  dependent  on  a  neurotic  individuality,  and  are  often 
induced  by  acid  fruits  and  wines,  special  articles  of  diet  and  other  causes. 
Many  cases  are  allied  to  urticaria  and  are  merely  an  exaggerated  form  of  it,, 
being  due  to  toxaemia.  In  others  the  hereditary  tendency  is  the  main 
feature.  The  two  factors  may  be  associated.  Perhaps  it  is  a  pure  vasomotor 
neurosis.  There  is  an  actual  exudation  of  serum,  and  sometimes  extra- 
vasation of  blood.  In  this  respect  it  is  comparable  to  Henoch's  purpura. 
In  a  woman,  aged  29,  in  whom  laparotomy  was  done  for  a  severe  abdominal 
attack,  the  intestines  were  found  much  congested,  with  a  cylindrical  enlarge- 
ment of  the  ileum,  2  ins.  long,  near  the  ileo-csecal  valve,  elastic  and  not 
pitting  (Harrington,  1905). 

The  onset  is  sudden,  perhaps  preceded  by  indefinite  malaise.  The 
swelling  appears  in  a  few  minutes  to  a  few  hours  and  disappears  equally 
rapidly.  It  gives  rise  to  no  discomfort  or  merely  such  as  would  be  due  to  the 
unusual  distension  ;  sometimes  sensory  disturbances,  e.g.,  fidness,  throb- 
bing, burning,  pricking,  numbness.  It  is  whitish  in  colour  and  does  not 
itch  or  pit  on  pressure.  Occasionally  it  is  reddish  and  followed  by  dis- 
coloration like  purpura,  for  which  it  may  be  mistaken.  It  affects  any  part,, 
may  even  cause  exophthalmos,  and  is  rare  on  the  scalp.  Fever,  if  present. 
is  moderate.  The  gastro-intestinal  symptoms  are  epigastric  pain,  colic,, 
nausea,  profuse  vomiting  and  diarrhoea,  perhaps  preceded  by  constipation. 
Suppression  of  urine,  albuminuria  and  heemoglobinuria  have  been  noted. 
Glottic  oedema  produces  severe  asphyxia. 


The   Heart  and  Circulation.  459 

Cases  have  to  be  diagnosed  from  the  urticarial  swelling  due  to  stings 
and  bites,  cellulitis  and  purpura.  Severe  intestinal  symptoms  suggest 
peritonitis,  appendicitis,  Henoch's  purpura,  and  even  intussusception  in 
infancy. 

The  prognosis  must  be  guarded  because  of  the  liability  to  death  from 
oedema  of  the  larynx  or  acute  pulmonary  oedema.  Recurrence  becomes  more 
frequent  with  advancing  age.  The  intervals  between  the  attacks  vary 
greatly  in  different  individuals.  Slight  scaling  of  the  epidermis  may  follow 
the  attack  and  the  skin  be  left  a  little  thickened. 

Treat  the  neurotic  state  and  the  alimentary  tract.  (Edema  of  the 
larynx  is  treated  by  ice,  adrenalin,  scarification,  and  tracheotomy  if  it  does 
not  yield  to  the  simpler  measures.  General  measures  are  rest  in  bed,  cold 
douching,  ice  or  fomentations,  cooling  lotions,  atropine,  strychnia,  calcium 
salts,  bromides  and  tonics. 

Trophoedema. — Syn. ;  Hereditary  (Edema  of  the  Lower  Limbs — Chronic 
Congenital  Elephantiasis. — Milroy  of  Omaha  (1892)  described  a  solid  oedema 
of  one  or  both  legs,  congenital,  except  in  one  child  in  whom  it  began  at 
12  years,  in  22  members  out  of  97  of  one  family  in  6  generations.  Its 
occurrence  has  been  recorded  in  other  families  : — 8  out  of  36  (Nonne), 
8  in  4  generations  (Meige),  4  in  3  generations  (Tobeison),  5  males  and 
8  females  in  5  generations  (Hope  and  French).  This  last  family  was  peculiar 
in  that  some  of  its  members  had  acute  attacks  with  violent  pain.  Instances 
in  brothers  or  in  sisters,  and  isolated  cases  have  also  been  recorded.  Rolles- 
ton  reported  cases  in  a  boy  aged  13,  and  his  sister  aged  16  years,  with  a 
peculiar  oedema  of  the  legs,  more  marked  after  exercise  and  warm  baths, 
but  disappearing  after  rest  in  bed  for  some  days.  The  mother  had  been 
affected  since  10  years  of  age  and  5  other  children  had  escaped. 

The  oedema  is  generally  congenital  but  may  not  develop  for  several 
years.  It  is  unilateral  or  bilateral,  affects  the  lower  limbs  wholly  or 
partially,  and  is  limited  by  the  larger  joints.  It  increases  gradually  when 
the  patients  are  up  and  decreases  on  lying  down.  The  skin  is  pale  and  cold, 
natural  in  colour  if  the  limb  is  warm,  blue  and  liable  to  chilblains  in  cold 
weather.  Usually  there  is  a  history  of  lividity  at  birth.  Pitting  is  induced 
by  pressure  and  leaves  a  pallid  area  for  some  time  on  account  of  the  weak 
circulation.  Lividity  is  increased  by  gravity.  Mental  condition,  develop- 
ment, sensation  and  reflexes  are  normal.  Blood  examinations  are  negative. 
No  obstructive  disease  of  the  heart  or  circulation  has  been  found.  There 
is  no  evidence  of  deficiency  of  valves  in  the  veins,  nor  of  lymphatic  obstruc- 
tion. The  absence  of  skin  changes  is  against  lymph  stasis.  Possibly  it  is 
the  result  of  excessive  transudation,  due  to  some  inherent  defect  in  the 
blood  vessels  or  blood.  If  so,  it  presents  analogies  with  haemophilia.  The 
condition  seen  in  children,  especially  about  puberty,  in  which  the  hands  and 
feet  are  swollen,  cold,  and  more  or  less  livid  (acro-cyanosis),  often  associated 
with  orthotic  albuminuria,  is  unlikely  to  be  mistaken  for  this  affection, 


460  Chapter  XL. 

though  it  suggests  a  similar  vascular  pathology.  Angioneurotic  oedema  is 
of  much  more  sudden  and  temporary  character. 

Occasionally  one  sees  infants  with  a  fairly  solid  oedema  of  the  feet, 
dorsal  and  plantar,  involving  the  toes  and  perhaps  extending  above  the 
ankles.  If  the  weather  is  cold,  the  feet  are  cold  and  livid.  It  may  have  been 
present  from  birth  or  vary  from  time  to  time,  sometimes  in  accordance  with 
the  amount  of  urine  passed.  Probably  some  of  these  cases  depend  on  renal 
inadequacy  or  actual  disease,  and  this  diagnosis  may  be  supported  by 
morning  oedema  of  the  eyelids  or  conjunctiva.  Sometimes  urinalysis  only 
shows  a  few  hyaline  casts  and  renal  cells.  The  ultimate  result  and  the 
pathological  anatomy  of  these  cases  require  investigation.  In  the  future  it 
may  be  found  that  all  these  different  varieties  of  oedema  are  more  or  less 
identical  in  their  pathology,  differing  in  acuteness  and  chronicity,  depending 
on  a  vasomotor  neurosis,  a  circulatory  or  haemic  defect,  a  lymphatic 
peculiarity,  or  combinations  of  two  or  more  of  these  several  factors. 

Hereditary  oedema  is  of  importance  from  a  prognostic  point  of  view. 
It  is  harmless  and  persistent;  but  troublesome  by  reason  of  the  clumsiness 
and  weight  of  the  limb,  and  because  of  the  coldness  and  liability  to  chil- 
blains. 

Bandages  afford  some  support  but  the  oedema  appears  above  them. 
Best  and  elevation  are  temporary  measures  of  relief.  Vascular  tone  is 
improved  by  ergot,  digitalis  and  galvanism.  The  limbs  must  be  kept  warm 
and  massaged  daily  in  an  upward  direction. 


Chapter  XLI. 

CONGENITAL    HEART    DISEASE. 

Cardiac    Development —  Foetal    Circulation — Pathogenesis — Malpositions— 
Defects  in  the  Septa —  Arterial  Defects —  Valvular  Lesions. 

Development  of  the  Heart. — In  its  earliest  stage  the  heart  is  formed 
by  the  coalescence  of  two  symmetrical  ventral  tubes  into  a  single  cavity. 
This  becomes  bent  on  itself  and  divided  into  an  auricle  and  ventricle 
conjoined  by  a  short  narrow  segment  called  the  auricular  canal.  Opening 
into  the  auricle  is  the  sinus  venosus,  formed  by  the  coalescence  of  the 
allantoic,  hypoblastic  and  lateral  somato-pleural  veins  which  convey  to  the 
heart  all  the  blood  in  the  body.  From  the  ventricle  the  blood  passes  to  the 
bulbus  arteriosus  through  a  much  constricted  part,  the  fretum  Halleri, 
thence  to  the  aorta. 

In  the  next  stage  the  auricular  canal  is  divided  by  the  ultimate  fusion 
of  two  small  tubercles  which  grow  from  the  anterior  and  posterior  surfaces 
until  they  meet.  The  auriculo-ventricular  valves  develop  within  this  canal. 
The  ventricular  septum  begins  in  the  fourth  or  fifth  week  and  is  completed 
about  the  eighth  week.  It  grows  upward  from  the  apex  and  its  plane 
alters  in  course  of  development.  Were  it  not  for  this  alteration  in  the  plane, 
the  central  part  of  the  septum  would  join  the  left  and  posterior  side  of  the 
bulb  and  shut  off  the  left  ventricle  from  all  arterial  connection.  The  aorta 
and  pulmonary  artery  would  then  arise  from  the  right  ventricle.  In  the  base 
of  the  septum  is  the  "  Membranous  Space."  This  is  somewhat  lozenge- 
shaped,  situated  beneath  the  anterior  and  right  posterior  aortic  cusps, 
and  eventually  closed  by  a  thin  membrane.  Its  origin  is  uncertain  but 
probably  it  develops  from  the  posterior  wall  of  the  bulbus,  not  from  the 
septum,  for  it  has  been  found  present  in  the  absence  of  the  septum.  By 
completion  of  the  ventricular  septum  the  Cor  Triloculare,  consisting  of  one 
auricle  and  two  ventricles,  is  formed. 

Failure  in  the  development  of  the  membrane  closing  the  membranous 
space  leaves  a  patent  interventricular  septum,  or  an  interventricular  foramen. 
In  the  human  embryo  the  foramen  is  closed  during  the  second  month  by  the 
development  of  the  muscular  band  characteristic  of  the  mammalian  right 
ventricle.  It  develops  from  the  inner  layer  of  the  ventricular  muscle,  bends 
inward  to  reach  the  base  of  the  aorta  and  fuses  at  its  origin  with  the  flat 
band  on  the  infundibular  septum.    In  systole  the  margin  of  the  band  falls 


462  Chapter  XLI. 

across  the  foramen  and  closes  it.  The  band  may  be  absent  or  fail  to  join 
the  septal  band,  especially  in  cases  of  pulmonary  stenosis. 

The  septum  of  the  bulb  is  completed  a  few  days  before  that  of  the 
ventricle.  It  begins  as  two  small  tubercles  on  the  anterior  and  posterior 
walls  of  the  bulb  between  the  fourth  and  fifth  branchial  arches.  The 
course  of  development  is  from  above  downwards  and  antero-posteriorly. 
The  plane  gradually  alters  by  rotation  towards  the  left  until  it  is  placed 
transversely,  the  left  vessel  or  pulmonary  artery  being  in  front  of  the 
right  or  aorta. 

The  auricular  septum  is  not  fully  formed  until  the  fifth  month.  It 
develops  by  the  formation  of  two  separate  septa  which  coalesce.  The  pri- 
mary septum,  "  septum  primum  of  Born,"  starts  from  the  superior  surface 
of  the  cavity,  a  little  to  the  left  of  the  median  line,  and  grows  downward 
to  unite  with  the  anterior  and  posterior  tubercles  of  the  auricular  canal. 
At  first  the  septum  is  sickle-shaped  and  a  large  aperture  is  left,  next  a 
complete  septum  is  formed  between  the  two  auricles,  and  then  the  central 
portion  becomes  perforated  by  a  number  of  minute  holes.  One  of  these 
enlarges  and  persists,  while  the  others  close  up.  A  secondary  septum 
develops  close  to  the  primary  one.  It  arises  from  the  median  line  and 
grows  down  from  the  superior  surface  of  the  cavity.  It  is  incomplete  but 
the  aperture  does  not  coincide  with  that  in  the  primary  septum.  The  two 
septa  fuse  together  and  leave  an  oblique  opening,  the  foramen  ovale.  The 
valve  of  this  orifice  is  derived  from  the  primary  septum. 

The  right  auricle  consists  of  the  auricular  canal,  or  primitive  part  of  the 
cardiac  tube,  and  the  auricle  proper.  The  latter  is  developed  as  a  diver- 
ticulum from  the  auricular  canal.  It  consists  of  all  that  part  of  the  auricle 
in  which  the  muscle  is  arranged  as  musculi  pectinati,  and  includes  the 
appendix.  The  effects  of  its  systole  must  be  taken  into  account  for  it  is 
not  merely  a  passive  open  chamber.  At  first  sight  it  is  not  obvious  why  the 
auricle  drives  the  blood  into  the  ventricle  and  not  backward  through  the 
orifices  of  the  great  veins,  unprotected  by  valves,  nor  why  the  blood  from 
the  inferior  vena  cava  should  pass  through  the  foramen  ovale. 

Venous  pulsation  may  be  visible  in  the  internal  jugular  vein  during 
health  and  is  much  more  visible  in  cases  of  backward  pressure.  Two  waves 
of  pulsation  may  then  be  seen  in  the  veins.  The  first  is  auricular  systolic 
in  time  and  due  to  the  blood  stream  being  dammed  by  the  systole  of  the 
auricle.  The  second  wave  is  visible  towards  the  end  of  ventricular  systole 
and  merges,  in  the  later  stages  of  backward  pressure,  into  and  absorbs  the 
auricular  wave.  In  backward  pressure  there  is  actual  regurgitation.  The 
auricular  wave  would  be  due  to  regurgitation  were  it  not  for  the  presence 
of  certain  structures  which  close  the  orifices  of  the  great  veins.  In  fishes, 
amphibians  and  reptiles  all  the  veins  unite  to  form  the  sinus  venosus,  which 
is  guarded  at  its  orifice  into  the  auricle  by  two  strong  valves  to  prevent 
regurgitation.    The  sinus  and  valves  are  present  in  the  mammalian  embryo 


Congenital   Heart    Disease.  463 

in  the  early  months  of  foetal  life.  During  the  third  to  the  fifth  month  the 
left  valve  almost  entirely  disappears.  The  upper  part  of  the  right  valve 
disappears  and  the  lower  part  forms  the  Eustachian  and  Thebesian  valves, 
which  help  to  guard  the  opening  of  the  inferior  vena  cava  and  coronary 
sinus.  The  sinus  venosus  is  absorbed  into  the  right  auricle  and  its  original 
orifice  becomes  divided  into  three  parts  ior  the  vena  cava  superior,  vena 
cava  inferior,  and  the  coronary  sinus.  In  the  basal  portion  of  the  right 
valve  a  large  bundle  of  muscle  develops  and  forms  the  right  taenia  ter- 
minalis.  This  muscle  is  the  main  factor  in  closing  the  orifices  of  the  cava? 
during  auricular  systole.  The  opening  of  the  vena  cava  superior  is  more 
strongly  guarded  than  that  of  the  vena  cava  inferior.  Clinically  we  find 
venous  pulsation  in  the  tributaries  of  the  former  vein  before  it  is  seen  in 
those  of  the  latter.  The  closure  of  the  cava!  orifices  is  not  due  to  any 
sphincter  muscle  action,  for  no  annular  fibres  surround  the  termination  of 
the  vena  cava  inferior,  and  those  round  the  vena  cava  superior  are  few  and 
weak.  The  disappearance  of  these  valves  and  the  modifications  in  their 
structure  in  mammals  are  distinctly  advantageous.  Instead  of  a  rigid 
mechanism  we  have  one  which  will  allow  regurgitation  during  engorgement 
of  the  auricle.  In  reptiles  and  amphibians  there  is  an  interventricular 
foramen,  and  the  right  ventricle  can  relieve  itself  by  driving  blood  through 
the  foramen  into  the  left  ventricle. 

Myogenic  Theory. — The  heart  muscle  originates  and  maintains  con- 
traction independently  of  nerve  stimulation.  A  small  node  of  tissue,  the 
"  sino-auricular  node,"  has  been  found  by  Keith  and  Flack  at  the  mouth  of 
the  vena  cava  inferior.  It  is  supposed  to  represent  a  portion  of  the  sinus 
venosus  from  which  the  heart  contraction  starts.  Further  remains  have  been 
found  in  the  "  auriculo-ventricular  node"  (Knoten  of  T award),  in  the 
right  auricular  wall  near  the  mouth  of  the  coronary  sinus.  From  this 
the  auriculo-ventricular  bundle  (Bundle  of  His),  arises  and  passes  over  the 
auriculo-ventricular  septum,  dividing  into  branches  to  the  right  and  left 
ventricle.  "  Nodal  rhythm  "  is  a  simultaneous  contraction  of  auricles  and 
ventricles  starting  at  the  auriculo-ventricular  node.  It  occurs  in  most  cases 
of  severe  heart  failure. 

The  foramen  ovale  is  surrounded  incompletely  by  the  annulus  ovalis, 
composed  of  two  limbic  muscular  bands  united  at  one  end  and  having  a 
shape  and  arrangement  somewhat  like  that  of  the  merry-thought  of  a  duck. 
In  foetal  life  about  one-third  of  the  blood  passes  through  the  lungs  and  the 
remainder  through  the  foramen  ovale.  As  the  limbic  muscle  bands  contract 
during  auricular  systole,  they  pull  forward  the  vena  cava  inferior  and 
direct  the  blood  flow  through  the  foramen.  At  birth  the  diaphragm  descends 
and  drags  down  the  orifice  of  the  vein.  Hence  the  plane,  in  which  the  limbic 
bands  act,  becomes  more  vertical  in  direction.  The  course  of  the  blood 
stream  is  altered  and  the  contraction  of  the  bands  assists  in  closing  the 
foramen.    Closure  is  aided  by  the  rise  of  pressure  in  the  left  auricle,  due  to 


464  Chapter    XLI. 

establishment  of  the  pulmonary  circulation,  and  the  fall  of  pressure  in  the 
right  auricle.  The  two  septa  are  more  closely  opposed  and  become  united 
by  adhesion.  Closure  takes  place  a  few  weeks  or  months  after  birth,  but 
is  often  incomplete  and  leaves  a  valvular  orifice.  This  orifice  is  of  no 
importance  for  it  is  kept  closed  during  life  by  the  higher  pressure  in  the 
left  auricle.  Patency  of  the  foramen  is  due  to  mal-development  of  the 
primary  or  secondary  septum  of  the  auricle. 

The  left  auricle  is  a  modified  development  of  the  auricular  canal.  The 
pulmonary  veins  unite  and  enter  the  auricular  canal  by  a  common  trunk. 
As  the  lungs  grow  forward  over  the  heart  and  the  heart  sinks  into  the  chest, 
the  orifices  of  the  pulmonary  vein  become  separated  into  right  and  left 
veins  and  later  on  into  upper  and  lower  divisions  on  each  side.  As  the 
orifices  separate,  the  muscle  of  the  auricular  canal  grows  over  and  fills 
up  the  intervals,  thus  producing  the  structure  known  as  the  vestibule. 
Ultimately  the  vestibule  forms  the  largest  part  of  the  auricle.  The  muscle 
fibres  of  the  vestibule  and  of  the  left  taenia  terminalis  close  the  orifices  of  the 
pulmonary  veins  and  prevent  regurgitation.  In  mitral  stenosis  the  taenia 
becomes  greatly  hypertrophied. 

The  right  ventricle  consists  of  a  sinus  and  an  infundibulum.  The 
latter  is  called  the  "  conus  arteriosus  or  pulmonalis  "  and  communicates- 
with  the  pulmonary  artery.  In  the  turtle's  heart  there  are  three  ventricles. 
The  right  gives  rise  to  the  right  aortic  arch,  the  left  to  the  left  aortic  arch,, 
and  the  central  one  to  the  pulmonary  artery.  In  the  mammalian  heart 
the  development  of  the  septum  shuts  off  the  part  corresponding  to  the 
central  ventricle  of  the  turtle.  An  abnormal  septum  is  rarely  present  in 
the  right  ventricle  ;    still  more  rarely  in  other  cavities. 

Branchial  vascular  arches. — The  five  pairs  of  primitive  arches  do  not 
all  co-exist  at  the  same  time.  The  permanent  vessels  are  developed  by  the 
persistence  of  certain  parts  and  obliteration  of  others.  The  primitive  aortic 
bulb  is  divided  into  2  vessels,  the  aorta  and  pulmonary  artery.  The  fourth 
and  fifth  pairs  of  arches  arise  from  this  primitive  stem,  and  the  other 
pairs  are  branches  of  a  secondary  stem  from  the  fourth  arch  on  either  side. 
The  fifth  arch  on  the  left  side  persists  as  the  ductus  arteriosus  and  gives  off 
the  pulmonary  artery  as  a  branch.  The  fourth  left  arch  persists  as  the 
aorta  into  the  descending  part  of  which,  just  below  the  common  origin  of  the 
subclavian  and  vertebral  arteries,  the  ductus  arteriosus  enters.  Thus  the 
pulmonary  artery  is  a  branch  of  the  fifth  arch  and  any  interference  with  its 
development,  causing  stenosis  or  atresia,  will  maintain  patency  of  the 
ductus.  The  three  remaining  arches  on  the  left  side  unite  and  form  the 
carotids,  coming  off  by  a  common  root,  the  common  carotid.  On  the  right 
side  the  fifth  arch  is  obliterated.  The  fourth  persists  as  the  subclavian  and 
comes  off  by  a  common  root  from  the  aorta  forming  the  innominate  artery. 
The  carotids  arise  in  the  same  way  as  on  the  left  side,  but  their  common  root 
unites  with  that  of  the  subclavian  to  form  the  innominate. 


Congenital   Heart    Disease.  465 

Both  fourth  arches  may  develop  and  form  a  double  tube  round  the 
trachea,  uniting  to  form  a  common  aorta.  The  subclavian  and  vertebral 
arteries  then  arise  from  the  fourth  arch  in  a  similar  manner  to  that  on  the 
left  side.    The  coronary  arteries  are  occasionally  imperfect  in  development. 

Abnormalities  in  veins. — Both  the  superior  and  inferior  vena  cava 
may  be  duplicated.  Both  veins  have  been  found  entering  the  left  auricle  ; 
the  pulmonary  vein  opening  into  the  right  auricle  ;  the  right  and  left  inno- 
minate veins  opening  separately  into  the  right  auricle  ;  and  the  left 
vena  azygos  entering  the  coronary  sinus. 

The  Foetal  Circulation. — Blood  is  carried  from  the  foetus  to  the  placenta 
by  the  hypogastric  or  umbilical  arteries,  branches  of  the  iliac  arteries. 
It  returns  from  the  placenta  by  the  omphalo-mesenteric  or  vitelline  veins. 
These  unite  to  form  the  umbilical  vein  which  enters  the  abdomen  and 
communicates  by  one  branch  with  the  portal  vein  and  liver  and  by  another, 
the  "  ductus  venosus  Arantii,"  is  continued  into  the  hepatic  vein,  vena 
cava  inferior  and  right  auricle.  The  inferior  vena  cava  conveys  blood  from 
the  umbilical  vein,  portal  vein  and  lower  half  of  the  body.  Most  of  this 
blood  is  directed  by  the  Eustachian  valve  through  the  foramen  ovale  to  the 
left  auricle.  It  then  passes  through  the  left  ventricle  and  aorta,  and  part  of 
it  is  distributed  by  the  common  carotid  and  subclavian  arteries  to  the 
head  and  upper  limbs.  The  remainder  passes  onward  and,  mixed  with 
venous  blood  which  reaches  the  aorta  through  the  ductus  arteriosus,  is 
distributed  to  the  rest  of  the  body.  Thus  the  head  and  upper  limbs  receive 
a  purer  supply  of  blood  than  the  trunk  and  lower  limbs.  The  blood  from 
the  head  and  upper  limbs  is  more  venous  than  that  in  the  inferior  vena  cava. 
It  is  conveyed  by  the  superior  vena  cava  to  the  right  auricle  and  ventricle 
and  thence  through  the  ductus  arteriosus  into  the  descending  aorta.  Some 
of  it  passes  through  the  pulmonary  artery  to  the  lungs  and  left  auricle. 
From  the  aorta  it  passes  to  the  placenta  by  the  umbilical  arteries  and  is  there 
oxygenated. 

At  birth  the  placental  circulation  is  abolished,  the  lungs  are  inflated 
with  air,  the  diaphragm  descends  and  the  pulmonary  artery  rapidly  dilates. 
The  blood  passes  from  the  right  auricle  through  the  pulmonary  artery 
instead  of  the  ductus  arteriosus.  The  umbilical  arteries  from  the  hypogas- 
tric trunk  to  the  umbilicus  are  obliterated,  usually  in  2-4  days.  The 
umbilical  vein  is  obliterated  from  the  umbilicus  to  the  portal  vein,  as  well 
as  the  branch  forming  the  ductus  venosus.    The  foramen  ovale  is  closed. 

Pathogenesis  of  Congenital  Heart  Disease. — Many  of  the  deformities 
are  due  to  developmental  error  in  the  first  two  months  of  foetal  life.  The 
defect  is  generally  an  arrest  of  the  formative  processes  by  which  the  various 
septa  are  formed,  or  possibly  in  the  development  of  the  valves  and  branchial 
arches.  All  the  great  ante-natal  developmental  processes  are  completed 
before  the  end  of  the  second  month  and  the  heart  is  then  almost  as  well 
formed  as  it  is  a  few  days  before  birth.    In  the  intervening  period  it  grows 

2  H 


466  Chapter   XLL 

in  size  and  weight.  Hence  is  it  improbable  that  endocarditis  can  produce 
any  great  structural  defect.  If  it  is  responsible,  it  must  occur  very  early 
in  foetal  life  and  during  a  very  limited  period  of  time.  Other  malformations 
are  often  found  in  the  body  and  mental  defects  such  as  mongolism,  idiocy 
and  deaf-mutism.  More  than  one  child  in  a  family  may  be  affected,  e.g., 
6  cases  of  patent  ductus  arteriosus  in  one  family  (de  la  Camp).  The  second 
great  cause  is  endocarditis,  due  to  rheumatism,  sepsis  or  specific  fevers 
affecting  the  mother  during  pregnancy.  The  endocarditis  is  usually  an 
inflammation  of  the  sclerotic  variety  but  vegetations  may  occur.  It  is  rare 
before  the  fourth  month.  Both  endocarditis  and  valvular  developmental 
errors  are  more  common  on  the  right  than  on  the  left  side  because  of  the 
higher  pressure  there  during  foetal  life. 

If  endocarditis  causes  pulmonary  stenosis,  it  would  have  to  occur 
before  the  end  of  the  second  month  to  produce  any  effect  on  the  ventricular 
septum.  At  this  early  age  an  inflammatory  affection  of  the  pulmonary 
artery  would  almost  certainly  involve  the  aorta.  But  the  combination  of 
aortic  and  pulmonary  stenosis  is  very  rare.  Stenosis  is  always  a  process  of 
slow  and  gradual  development  and  unlikely  to  have  any  effect  on  the 
development  of  the  septum.  Furthermore  there  is  no  microscopical  evidence 
of  inflammatory  action  in  these  stenosed  orifices.  Yet  the  association  of 
pulmonary  stenosis  and  patent  ventricular  septum  is  extremely  common. 

Maldeveloped  hearts  are  more  susceptible  than  normal  ones  to  foetal 
■endocarditis.  Endocarditis  affects  the  tricuspid  valves  most  often,  less 
frequently  the  mitral,  and  rarely  the  pulmonary  or  aortic.  It  may  produce 
changes  in  the  circulation  which  affect  the  closure  of  the  foramen  ovale  or 
ductus  arteriosus. 

Errors  of  development  have  been  ascribed  to  syphilis,  tuberculosis, 
alcoholism,  mental  disturbance  and  injury  during  pregnancy  (p.  21). 
Moncorvo  (1900)  found  more  or  less  distinct  signs  of  congenital  syphilis 
in  2  out  of  every  3  cases.  Hochsinger  only  found  7  cases  among  500 
congenitally  syphilitic  children.  In  my  experience  syphilis  is  an  occasional 
but  by  no  means  constant  factor. 

Malposition  of  the  Heart. — Ectopia  cordis  may  occur  alone  or  as  part  of 
eventration.  It  is  incompatible  with  life.  The  heart  lies  outside  the  body, 
with  or  without  a  pericardial  covering.  The  sternum  is  more  or  less  absent 
and  the  skin  normal  or  lacking.  In  mesocardia  the  heart  is  in  a  mesial  position, 
the  apex  in  the  epigastrium,  and  the  cardiac  sounds  are  best  heard  behind 
the  sternum.  In  dextro-  or  dexio-cardia  the  heart  alone  is  developed  on 
the  opposite  side.  If  the  viscera  are  also  transposed,  it  is  spoken  of  Situs 
Inversus.  Of  this  the  first  case  was  recorded  in  1643  and  about  200  since. 
Probably  it  is  much  more  frequent  than  these  figures  suggest,  for  the 
condition  is  usually  only  discovered  accidentally  or  post  mortem.  Two 
girls  with  complete  transposition  and  a  boy  with  dextrocardia  have  come 
under  my  observation  during    two    years.      In    none  of    them  had  the 


Congenital   Heart   Disease.  467 

malformation  given  rise  to  any  disturbance  of  function.  It  may  be  associated 
with  congenital  heart  lesion  and  possibly  these  children  are  more  liable  to 
■endocarditis.  As  a  rule  it  in  no  way  interferes  with  prolonged  life.  It  is 
likely  to  be  mistaken  for  cardiac  displacement  due  to  pleural  effusion, 
contraction  of  the  lung  and  other  causes. 

Developmental  Errors. — The  bilocular  heart,  normal  in  fishes,  consists 
■of  one  auricle  and  one  ventricle,  and  a  main  vessel  arising  from  the  ventricle. 
The  trilocular  or  reptilian  heart  consists  of  two  auricles  and  one  ventricle. 
There  may  be  a  rudimentary  septum  in  the  ventricle.  Other  abnormalities 
are  often  present,  e.g.,  patent  foramen  ovale,  auricular  septum  almost 
entirely  absent,  transposition  of  pulmonary  artery  and  aorta,  both  vessels 
situated  to  the  left  of  the  ventricle.  The  left  auricle  may  communicate  with 
the  ventricle  only  by  the  blood  passing  through  a  patent  foramen  ovale. 
More  often  the  right  auricle  does  not  communicate  with  the  ventricle.  The 
pulmonary  valve  is  frequently  adherent,  sclerosed  or  even  calcified.  In  a 
boy,  aged  4  months,  who  died  from  general  bronchitis,  there  was  a  loud 
systolic  murmur  all  over  the  precordium  and  no  cyanosis,  a  trilocular  heart 
and  patent  foramen  ovale  were  the  only  lesions.  It  is  compatible  with 
several  years  of  life.    Thus  10  collected  cases  lived  from  11-39  years. 

Patent  Foramen  Ovale. — The  valvular  orifice  through  which  a  probe 
•can  be  passed  after  death  is  very  common.  It  is  unimportant  unless  the 
pressure  in  the  left  auricle  exceeds  that  in  the  right  and  causes  an  overflow 
of  blood  into  the  right  auricle  and  secondary  venous  stasis.  Sometimes  the 
valve  is  completely  absent  and  an  orifice  of  varying  size  is  left.  The  orifice 
may  be  single  or  cribriform.  There  may  be  patency  of  the  orifice  with 
smaller  holes  in  the  septum,  due  to  the  persistence  of  the  holes  in  the 
primary  septum.  In  other  instances  the  septum  is  membranous  and 
contains  numerous  orifices.  A  still  rarer  condition  is  the  presence  of  Chiari's 
net-work,  previously  described  by  Rokitansky.  It  is  a  fine  network  in  the 
right  auricle  extending  from  the  Eustachian  valve  to  the  region  between  the 
two  caval  orifices  and  is  not  incompatible  with  prolonged  life.  The  septum 
maybe  completely  absent,  or  its  inferior  part  may  be  absent,  and  cause  inter- 
communication between  the  four  cavities.  Perforations  are  occasionally 
found  in  the  lower  part  of  the  septum.  A  patent  foramen  ovale  may  give 
rise  to  no  symptoms.  A  murmur,  if  present,  ought  to  be  presystolic  or 
diastolic  and  heard  over  the  centre  of  the  sternum.  Sometimes  there  is 
moderate  cyanosis  and  a  systolic  murmur,  as  in  the  case  of  trilocular  heart, 
and  probably  dependent  on  other  cardiac  defects.  It  is  exceedingly  difficult 
to  time  these  murmurs.  The  diagnosis  is  rarely  possible,  though  patency  can 
be  suspected,  if  slight  respiratory  or  cardiac  affections  cause  cyanosis. 

Patent  Septum  Ventriculorum. — Of  this  there  are  all  degrees,  from  a 
pin-point  orifice  to  complete  absence  of  the  septum.  It  may  give  rise  to  no 
•symptoms  or  physical  signs.  The  septum  is  rarely  perforated  from  disease 
in  later  life.    Perforation  is  usually  in  the  anterior  portion,  in  front  of  the 


468  Chapter   XLI. 

infundibulum  and  between  the  arterial  orifices,  that  is,  in  the  part  known 
as  the  undefended  or  membranous  space.  It  is  uncommon  as  an  isolated 
lesion,  being  usually  associated  with  pulmonary  stenosis  and  hypertrophy 
of  the  right  ventricle,  less  often  with  other  defects.  A  small  perforation 
may  be  closed  by  contraction  of  the  septum  during  systole.  Seeing  that 
the  pressure  is  greater  in  the  left  than  the  right  ventricle,  the  right  ventricle 
may  become  overloaded  and  hypertrophied,  and  the  pulmonary  second 
sound  accentuated.  A  difference  in  pressure  in  the  two  ventricles  will  give 
rise  to  a  murmur  during  systole,  though  such  murmur  is  often  absent.. 
The  characteristic  murmur  is  harsh,  systolic,  with  its  maximum  intensity 
in  the  third  and  fourth  left  interspaces  near  the  sternum  or  in  the  fourth 
left  space  ^  in.  above  the  nipple.  Its  character  and  site  of  maximum 
intensity  are  by  no  means  constant.  Generally  it  is  heard  all  over  the  front 
of  the  chest,  and  over  the  back  when  the  aorta  rises  partly  from  the  right 
ventricle.  Sometimes  there  is  a  marked  systolic  thrill.  The  murmur  and 
accentuated  pulmonic  second  sound  are  the  main  diagnostic  points.  If  it 
is  associated  with  pulmonary  stenosis,  the  pulse  is  practically  normal  but  the 
pulmonary  second  sound  is  not  accentuated.  In  uncomplicated  pulmonary 
stenosis  the  pulse  is  weak.  Patency  of  the  septum  is  compatible  with  pro- 
longed life,  but  death  may  result  from  valvular  insufficiency. 

Defects  in  the  Septum  of  the  Bulb  may  cause  the  pulmonary  artery  to- 
rise  from  the  left  ventricle.  Transposition  of  the  two  main  vessels  is  due  to 
lack  of  rotation  of  the  septum  between  them.  The  aorta  rises  anteriorly  from 
the  right  and  the  pulmonary  artery  posteriorly  from  the  left  ventricle.  It  is 
associated  with  patency  of  the  foramen  ovale  and  ductus,  and  enlargement 
of  the  right  auricle  and  ventricle.  It  is  usually  fatal  under  1  year  of  age 
(in  20  out  of  25  collected  cases,  Eauchfuss),  though  patients  have  lived  as- 
long  as  40  years.  One  child,  cyanosed  from  birth,  died  at  the  age  of  7  weeks. 
Another,  with  moderate  cyanosis  and  clubbing  and  a  systolic  pulmonary  and 
apical  murmur,  lived  to  11  months  of  age  : — the  right  ventricle  gave  off 
a  normal  aorta  from  which  the  great  vessels  arose  by  a  common  origin  ; 
the  pulmonary  artery  was  somewhat  stenosed  because  of  the  fusion  of  2  of 
its  valves  and  arose  from  the  left  ventricle  ;  the  ductus  arteriosus  was. 
normal,  the  foramen  ovale  patent,  and  a  small  orifice  was  present  in  the 
interventricular  septum.  It  is  difficult  to  account  for  the  maintenance  of 
the  circulation  in  this  case.  In  an  almost  similar  one,  a  boy  lived  to  the 
age  of  11  years  (Kauffmann,  1906).  Pure  transposition  gives  rise  to  much 
cyanosis,  hypertrophy  of  the  right  ventricle,  an  abnormally  loud  second 
sound  but  no  murmur.  In  other  cases  the  cyanosis  varies  in  type.  Older 
children  may  have  convulsions  and  attacks  of  suffocation. 

The  septum  may  be  completely  absent  or  there  may  be  a  direct  com- 
munication, aortico-pulmonary,  of  variable  size  between  the  two  vessels 
with  no  other  abnormalities.  In  one  such  case  was  a  double  murmur  ; 
in  another,  a  systolic  murmur  and  accentuated  second  sound.     The  right 


Congenital   Heart    Disease.  469 

ventricle  is  generally  hypertrophied.  Cyanosis  is  sometimes  present  ; 
occasionally  patency  of  the  ductus  and  foramen  ovale,  patency  of  ventri- 
cular septum,  or  partial  obliteration  of  the  aortic  arch  between  the  origin 
of  the  innominate  and  carotid  arteries. 

Patent  Ductus  Arteriosus. — Premature  closure  during  fcetal  life  causes 
death  of  the  foetus.  Closure  after  birth  is  brought  about  in  the  following 
manner.  Before  birth  the  duct  enters  the  aorta  obliquely  and  forms  a 
crescentic  projection,  in  consequence  of  the  higher  pressure  in  the  pul- 
monary artery.  At  birth  the  pressure  rises  in  the  aorta  and  falls  in  the 
pulmonary  artery.  The  wall  of  the  aorta  then  projects  into  and  partially 
blocks  the  opening  of  the  ductus.  The  descent  of  the  diaphragm  pulls  down 
the  heart  and  consequently  the  ductus  is  no  longer  approximately  on  the 
same  level  as  the  aorta  but  ascends  obliquely  to  open  into  it.  The  flow  of 
blood  is  obstructed  in  much  the  same  way  as  it  would  be  in  a  stretched  rubber 
tube.  Actual  closure  is  due  to  contraction  and  thickening  of  the  coats. 
The  duct  is  functionally  impervious  after  respiration  has  continued  for  a 
few  minutes  ;  no  longer  patent  in  7-10  days  ;  and  completely  closed  in 
3  weeks,  occasionally  not  for  6  weeks.  In  premature  infants  it  is  often  late 
in  closing.  It  may  be  partially  patent,  though  blocked  in  some  part  of  its 
course.  Occasionally  it  is  absent  or  irregular  in  its  origin,  e.g.,  arising  from 
the  left  branch  of  the  pulmonary  artery.    There  may  be  two  ducts. 

Persistent  patency  may,  or  may  not,  be  associated  with  other  defects. 
As  an  isolated  lesion  it  is  rare.  It  is  due  to  failure  in  the  normal  process  of 
closure,  some  defect  in  the  relative  blood  pressures,  atelectasis,  pulmonary 
stenosis,  disease  of  other  orifices  and  transposition  of  the  main  vessels.  The 
blood  pressure  may  be  abnormally  high  in  the  pulmonary  artery  in  some  of 
these  conditions.  In  aortic  stenosis  and  atresia  the  pressure  in  the  aorta 
is  unduly  low.  A  patent  duct  varies  greatly  in  size  and  is  very  susceptible 
to  atheroma.    Aneurysm  and  rupture  have  occurred. 

There  may  be  no  symptoms,  no  indication  of  circulatory  disturbance, 
and  no  murmur.  Cyanosis  is  almost  always  absent,  for  even  more  blood 
goes  to  the  lungs.  Weak  and  premature  infants  have  attacks  of  apnoea  and 
cyanosis,  which  are  often  fatal.  Symptoms  are  apt  not  to  develop  until 
the  end  of  the  first  year  or  later.  The  chief  ones  are  palpitations,  dyspnoea, 
inability  for  severe  exertion,  and  occasionally  anginal  attacks.  Cyanosis, 
cardiac  incompetence  and  oedema  develop  in  some  cases  and  towards  the 
•end. 

The  physical  signs  include  cardiac  hypertrophy,  a  murmur  and  a 
thrill.  The  right  ventricle  is  enlarged  slightly  unless  the  septum  is  incom- 
plete ;  for  the  obstruction  to  complete  systole  by  an  inflow  of  blood  from 
the  aorta  into  the  pulmonary  artery,  which  becomes  dilated,  gives  it  more 
work  to  do.  Dulness  in  the  second  right  interspace  is  not  uncommon. 
Gerhardt  has  described  a  narrow  band  of  dulness  for  ^-1  in.  to  the  left 
of  the  sternum,  from  the  first  or  second  space  to  the  third  space.    It  is  due 


470  Chapter   XLI. 

to  dilatation  of  the  ductus.  Gibson  describes  the  murmur  as  accompanying 
the  latter  part  of  the  first  sound,  filling  the  short  pause,  accompanying  the 
second  sound  which  may  be  accentuated  in  the  pulmonary  area  and  is- 
often  doubled,  and  dying  away  during  the  long  pause.  In  a  child,  aged 
15  months,  who  died  from  ileo-colitis  there  was  no  cyanosis  or  clubbing. 
A  systolic  murmur,  loudest  in  the  pulmonary  area,  was  heard  all  over 
the  precordium  and  behind.  The  patent  ductus  was  the  only  cardiac  defect. 
Much  importance  is  attached  by  some  writers  to  the  conduction  of  the 
murmur  into  the  upper  part  of  the  left  interscapular  space.  As  a  rule  the 
murmur  is  loudest  over  the  second,  or  second  and  third,  left  intercostal 
spaces  near  the  sternum  and  is  transmitted  into  the  vessels  of  the  neck, 
being  louder  on  the  left  side.  It  is  prolonged  into  the  beginning  of  diastole. 
The  murmur  in  children  is  rarely  of  the  type  described  by  Gibson.  It  may 
not  develop  for  a  few  months,  not  until  the  duct  dilates.  The  thrill  is  most 
palpable,  when  present,  in  the  same  situation  as  that  of  maximum  intensity 
of  the  murmur.  The  pulmonary  second  sound  is  accentuated  unless  the 
pressure  is  so  great  as  to  limit  the  opening  of  the  valves.  The  aortic  second 
sound  may  be  much  exaggerated  and  the  closure  of  the  valves  cause  a. 
palpable  diastolic  shock  in  the  second  left  space.  Combined  systolic  and 
diastolic  murmuis,  and  a  single  diastolic  one  have  also  been  described. 

The  prognosis  depends  on  the  degree  of  patency  and  the  presence  of 
other  abnormalities.  Of  41  uncomplicated  cases  (Wells,  1908)  12  died 
under  1  year,  5  more  under  10,  4  under  20,  and  3  lived  over  50  years. 
Death  is  due  to  intercurrent  disease  or  cardiac  failure.  No  doubt  the 
defect  is  more  common  than  these  figures  suggest.  Cases  of  recovery  have 
been  reported,  the  duct  closing  and  the  murmur  disappearing. 

Congenital  Closure  of  Orifices. — If  the  foramen  ovale  is  so  constricted 
as  to  affect  the  heart,  the  right  auricle  and  ventricle,  pulmonary  artery 
and  ductus  are  abnormally  large,  while  the  left  side  of  the  heart  and  the 
aorta  are  unduly  small.  The  ventricular  septum  may  be  patent  and  the 
aorta  arise  from  both  ventricles.  If  the  ductus  closes  before  the  septumr 
the  pulmonary  artery  will  be  atrophied.  All  the  orifices  of  the  heart  and 
main  vessels  may  be  stenosed  or  obliterated. 

Valvular  Lesions. — The  auriculo-ventricular  valves  are  rarely  abnor- 
mal in  number,  but  there  may  be  redundant  segments.  At  times  the  valves 
are  adherent  and  the  orifice  stenosed.  A  double  mitral  valve  has  been 
recorded.  Mitral  stenosis  is  uncommon  before  6  years  of  age.  A  few 
cases,  probably  congenital,  have  been  reported  in  younger  children.  In 
two  of  them  the  ductus  was  also  patent.  It  may  be  associated  with 
tricuspid  stenosis,  a  defective  septum  or  other  defects.  Possibly  some  late 
cases  of  mitral  stenosis  take  their  origin  in  a  mild  congenital  affection. 
Mitral  incompetence  is  still  more  rare.  In  one  case  I  regarded  the  disease  as 
of  foetal  origin.  This  was  a  girl,  aged  22  months  at  death,  who  had  pre- 
sented all  the  ordinary  signs  of  advanced  mitral  regurgitation  during  life. 


Congenital  Heart    Disease.  471 

The  mitral  orifice  was  very  large  and  the  cusps  were  represented  by  a  thick, 
shrunken,  fibrous  mass  of  horse-shoe  shape.  Some  of  the  chordse  tendinese 
were  attached  to  the  wall  of  the  ventricle,  not  to  the  valves.  There  was 
partial  adhesion  of  the  aortic  valves  and  one  of  the  tricuspids  was  a  little 
thickened  at  the  edge.  The  foramen  ovale  was  closed.  Apparently  the 
child  suffered  from  endocarditis  during  the  later  months  of  foetal  life.  The 
mother  had  mitral  regurgitation  and  had  rheumatic  pains  during  pregnancy. 

Tricuspid  stenosis  is  more  frequent  than  mitral  stenosis.  The  foramen 
ovale  is  patent.  Regurgitation  may  be  due  to  faulty  development  of  the 
valves,  which  is  associated  with  an  unduly  large  pars  membranacea  of 
the  septum. 

The  semilunar  valves  may  be  absent  or  represented  by  a  mere  fleshy 
ring.  There  may  be  only  2,  equal  or  unequal  in  size,  and  occasionally  a 
third  rudimentary  one.  Sometimes  they  are  redundant,  three  or  four  of 
equal  size  and  one  or  two  smaller  ones,  or  show  other  variations.  The  pulmon- 
ary are  very  much  more  frequently  affected  than  the  aortic  valves,  in  the 
proportion  of  109-29  collected  cases.  No  matter  the  number,  they  may  be 
adherent,  united  into  a  cone  and  narrowing  the  orifice  to  a  pin-point,  an 
elongated  slit  or  a  small  triangle.  Sometimes  they  present  cribriform 
perforations  ;  often  they  are  opaque,  thickened,  puckered,  even  calcareous. 
Subsequent  rheumatic  and  calcareous  changes  affect  the  valves  more  often 
when  they  are  deficient  in  number  than  when  they  are  in  excess. 

The  Pulmonary  Artery  and  Orifice  are  affected  in  about  half  the  cases 
of  congenital  heart  disease.  Out  of  181  cases  Peacock  found  the  pulmonary 
orifice  more  or  less  contracted  in  90,  and  the  orifice  or  trunk  obliterated  in  29. 
Slight  stenosis  may  be  unassociated  with  other  defects.  Usually  there  are 
found  patency  of  the  septum  of  the  auricle  and  ventricle,  one  or  both. 
There  are  three  varieties  of  pulmonary  stenosis.  The  trunk  of  the  vessel 
may  be  constricted  or  show  complete  atresia,  but  the  latter  is  very  rare. 
More  frequently  there  is  constriction  of  the  infundibular  part  of  the  right 
ventricle,  known  as  intra-cardiac  conus  stenosis  or  atresia  of  the  conus 
pulmonalis.  Still  more  often  there  is  adhesion  or  malformation  of  the 
valves  or  stenosis  of  the  ostium.  Stenosis  of  the  orifice  or  conus,  of  varying 
degree  up  to  complete  atresia,  is  due  to  contraction  of  the  zone  at  the  outlet 
of  the  ventricle,  the  infundibulum,  from  thickening  of  the  endocardium  or 
localised  muscular  hypertrophy.  It  is  more  probably  developmental  than 
inflammatory  in  origin.  Stenosis,  due  to  adhesion  of  the  valves,  is  associated 
with  patency  of  the  foramen  ovale  and  ductus,  and  either  enlargement  of 
the  infundibulum  and  right  ventricle  or  narrowing  of  the  infundibulum  and 
patency  of  the  ventricular  septum.  In  stenosis  the  ductus  arteriosus  is 
generally  closed,  while  in  atresia  it  is  almost  always  patent. 

The  effects  of  the  above  conditions  on  the  heart  vary  with  their  degree 
and  period  of  development.  In  slight  stenosis,  with  perfect  septum,  the 
only  result  is  moderate  hypertrophy  of  the  right  ventricle.     This  is  more 


472  Chapter   XLI. 

marked  if  the  foramen  ovale  is  patent,  and  still  more  if  both  septa  are 
patent.  If  the  ventricular  septum  is  patent,  hypertrophy  is  greater,  the 
more  the  aorta  arises  from  the  right  ventricle.  Sometimes  the  septum  is 
pushed  so  much  to  the  left  that  the  aorta  rises  entirely  from  the  right 
ventricle.  In  atresia,  developing  while  the  ventricular  septum  is  being 
formed,  the  right  side  of  the  heart  is  enlarged  and  the  left  is  diminished. 
If  it  develops  subsequent  to  the  formation  of  the  septum,  the  right  ventricle, 
tricuspid  valve  and  orifice  are  atrophied,  the  foramen  ovale  remains  patent 
and  the  left  side  of  the  heart  is  hypertrophied.  The  blood  is  carried  to  the 
lungs  by  a  backward  stream  through  the  patent  ductus,  possibly  by  the 
bronchial  arteries,  or  by  special  branches  from  the  large  vessels  of  the 
aortic  arch.    There  may  be  a  direct  aortico-pulmonary  communication. 

The  physical  signs  are  those  of  hypertrophy  of  the  right  ventricle, 
with  a  systolic  pulmonary  murmur  and  a  weak  pulmonary  second  sound. 
The  murmur  may  be  absent  in  high-grade  stenosis,  because  of  the  slight 
blood  current  and  overflow  through  the  septum  into  the  left  ventricle. 
Or  it  may  be  transmitted,  via  a  defective  septum,  into  the  aorta  and 
carotids.  The  characteristic  murmur  is  localised  over  the  second  left 
interspace  close  to  the  sternum,  and  is  not  conducted  into  the  vessels  in  the 
neck.  A  louder  one  is  most  intense  between  the  second  left  cartilage 
and  the  xiphoid,  and  an  inch  or  so  on  either  side.  Sometimes  its  point  of 
maximum  intensity  is  over  the  pulmonary  orifice,  occasionally  midway 
between  the  nipple  and  sternum  at  the  level  of  the  nipple.  It  is  not 
conducted  much  beyond  the  cardiac  area,  possibly  rather  more  towards 
the  left  clavicle  than  the  right,  and  sometimes  all  over  the  back,  being 
louder  on  the  left  side  and  heard  in  the  left  axilla.  Carpenter  has  pointed 
out  that  if  there  is  a  patent  ventricular  septum,  the  murmur  will  probably 
be  heard  in  the  carotids.  In  a  girl  who  was  born  blue,  presented  moderate 
cyanosis  and  clubbing  and  died  at  5  months  of  age,  there  was  no  murmur 
during  life.  The  pulmonary  valves  were  adherent  and  left  only  a  pin- 
point orifice.  No  other  cardiac  defect  was  present.  In  a  boy  of  12  months 
with  extreme  stenosis  of  the  conus  pulmonalis,  the  orifice  admitting  only 
a  No.  1  catheter,  a  soft  systolic  murmur  was  heard  in  the  pulmonary 
region  and  to  the  left  of  the  sternum.  It  was  not  conducted  into  the 
neck  nor  heard  behind.  The  ventricular  septum  was  patent  and  the 
aorta  arose  from  both  ventricles.  The  right  ventricle  was  much  thicker 
than  the  left. 

A  systolic  thrill  may  be  also  present  and  most  marked  in  the  region  of 
maximum  intensity  of  the  murmur.  It  is  by  no  means  constant  and  is 
likely  to  be  wanting  if  the  stenosis  is  extreme.  In  pure  pulmonary  stenosis, 
and  possibly  if  the  foramen  ovale  is  also  patent,  the  pulmonary  second 
sound  is  weak.  It  is  clear  and  distinct  if  there  is  associated  patency  of  the 
ventricular  septum,  and  accentuated  if  the  ductus  is  patent.  The  charac- 
ter of  the  second  sound  is  only  of  diagnostic  value  in  early  childhood.    Later, 


Congenital   Heart    Disease.  473 

hypertrophy  of  the  right  ventricle  may  cause  so  much  blood  to  flow  through 
the  narrowed  orifice  that  the  pulmonary  tension  is  increased  and  the 
second  sound  is  accentuated.  The  sound  depends  greatly  on  the  size  of  the 
orifice  and  the  mobility  of  the  valves.  Hypertrophy  of  the  right  ventricle 
displaces  the  cardiac  apex  to  the  left.  The  pulse  is  larger  in  volume  if  the 
septum  is  patent  than  in  pure  pulmonary  stenosis.  If  the  tricuspid  orifice 
becomes  incompetent,  a  regurgitant  pulse  is  visible  in  the  jugulars  and 
the  liver  is  enlarged  and  pulsates. 

The  symptoms  vary  with  the  degree  of  obstruction.  In  the  mildest 
form  they  may  be  absent.  In  others  there  are  cyanosis,  clubbing  and 
other  evidence  of  venous  stasis.  Cyanosis  may  be  present  at  birth.  It  is 
often  of  high  grade  and  increased  by  exertion  and  crying.  Paroxysmal 
cough,  dyspnoea,  suffocative  attacks,  fainting,  vertigo  and  fits  may  be 
present.  These  children  are  easily  chilled,  stand  mental  and  physical 
exertion  badly,  and  are  very  susceptible  to  infection.  Many  die  from 
tuberculosis  or  exanthemata  ;  some  from  cardiac  failure  during  an  attack 
of  dyspnoea  or  the  result  of  asthenia,  a  few  from  cardiac  failure  and  dropsy  ; 
and  others  from  infective  endocarditis.  About  one-fifth  of  the  cases  of 
stenosis  die  in  the  first  year  of  life  and  only  about  one-fourth  live  over 
10  years.  Two-thirds  of  the  cases  of  atresia  die  in  the  first  year  and  about 
15  per  cent,  live  over  5  years.  It  is  surprising  how  minute  a  pulmonary 
orifice  is  compatible  with  life,  even  though  the  ductus  is  closed.  The  patient 
may  live  50  years  or  more.  A  child  with  complete  absence  of  the  pulmonary 
artery  lived  for  6  years  (Gutkind). 

Pulmonary  stenosis  may  be  followed  by  infective  endocarditis,  des- 
truction of  the  valves  and  regurgitation;  or  the  valves  may  contract 
sufficiently  to  permit  regurgitation.  Newton  Pitt  in  Allbutt's  "  System 
•of  Medicine  "  refers  to  99  cases  of  regurgitation,  verified  post  mortem, 
■of  which  more  than  half  were  due  to  infective  endocarditis.  Only  2  were 
under  10  years  of  age.  A  girl,  aged  15  years,  died  after  having  been  under 
my  care  for  3  years.  Heart  disease  had  been  diagnosed  in  the  second  year 
of  life.  When  first  seen  she  presented  a  thrill  and  murmur  and  other 
signs  of  pulmonary  stenosis.  Several  months  before  death  the  systolic 
murmur  and  thrill  were  replaced  by  diastolic  ones.  The  diastolic  murmur 
was  loudest  in  the  pulmonary  region  on  expiration  and  in  the  upright 
posture,  and  conducted  down  the  left  edge  of  the  sternum.  She  died  after 
a  period  of  irregular  fever  and  several  attacks  of  hsemoptysis,  the  last  one 
proving  fatal,  and  infective  endocarditis  was  found  post  mortem  and 
infarcts  in  the  lungs.  The  pulmonary  valves  were  alone  involved,  thick- 
ened, puckered  and  showing  warty  vegetations. 

In  another  girl,  10  weeks  old,  blue  at  birth  and  always  a  bad  colour, 
death  resulted  from  bronchitis.  A  loud  systolic  murmur  was  heard  all  over 
the  precordium  and  back.  There  was  no  thrill.  The  pulmonary  artery 
arose  from  the  aorta,  the  ventricular  septum  was  patent,  the  foramen  ovale 


474  Chapter   XLI. 

fenestrated,  and  the  inferior  vena  cava  opened  into  the  left  ventricle.  Such 
a  case  is  impossible  of  diagnosis. 

The  Aorta  and  Aortic  Orifice. — The  aorta  may  show  stenosis  or  atresia 
of  the  conus  arteriosus,  ostium  or  valves,  complete  obliteration  of  the 
initial  part  of  the  artery  or  hypoplasia.  The  signs  of  Stenosis  of  the  Ostium 
are  the  same  as  in  the  acquired  disease.  It  is  rarely  present.  T.  Fisher 
reported  a  case  in  a  girl,  aged  4  months,  the  valves  being  thickened  and 
adherent.  A  7-year  old  boy  under  my  care  presented  all  the  signs  of  aortic 
stenosis,  and  heart  disease  had  been  diagnosed  at  2  years  of  age,  so  it  was 
probably  congenital.  In  another  boy,  aged  14  years,  undergrown  and  free 
from  cardiac  symptoms,  the  physical  signs  were  those  of  pure  aortic  stenosis. 
He  died  suddenly  a  week  later  and  the  valves  were  found  puckered  and 
adherent,  the  orifice  very  small.  There  was  nothing  in  the  previous  history 
to  suggest  an  attack  of  endocarditis.  Both  boys  had  a  loud  systolic  murmur 
and  marked  thrill  over  the  aortic  area,  and  a  small  slow  pulse.  Friedmann 
has  recorded  a  similar  case  in  a  boy,  aged  21  months,  the  murmur  being- 
recognised  at  4  months  of  age. 

Hypoplasia,  sometimes  called  "  congenital  stenosis  of  the  arterial 
system,"  is  rarely  limited  to  the  aorta.  About  20  cases  are  on  record,. 
15  verified  after  death.  It  is  a  uniform  and  general  narrowing  of  all  the 
vessels  usually  associated  with  infantilism,  sexual  abnormalities  and 
rickets.  Its  etiology  is  doubtful  and  symptoms  may  be  latent  until  puberty, 
when  compensation  begins  to  fail.  The  patients  are  small,  weakly  and 
anaemic,  easily  fatigued  mentally  and  physically,  and  suffer  with  palpita- 
tions and  dyspnoea,  sometimes  subnormal  temperature  and  oedema.  The 
vessel  walls  are  thin,  the  pulse  weak  or  absent,  and  the  left  ventricle  small 
at  first.  Later  on  it  hypertrophies  and  generally  ends  in  dilatation  before- 
the  age  of  30  years.    Tuberculosis  is  common. 

Isthmus  Stenosis  or  Co-arctation  of  the  Aorta,  complete  and  incomplete,, 
is  also  rare.  About  100  cases  are  on  record,  only  15  per  cent,  complete. 
The  sex-incidence  is  7  males  to  2  females.  The  isthmus  of  the  aorta  is  that 
portion  which  corresponds  with  the  left  posterior  aortic  root  between  the 
fourth  and  fifth  branchial  arches,  that  is,  between  the  origin  of  the  left 
subclavian  artery  and  the  entrance  of  the  ductus.  It  is  thin  and  narrow 
during  foetal  life  and  develops  rapidly  after  birth.  This  portion  of  the- 
aorta  may  be  absent,  and  the  separation  between  the  transverse  and 
descending  aorta  complete.  It  may  be  reduced  to  a  fibrous  cord  for  about 
a  centimetre  in  length  ;  present  a  double  constriction  with  a  dilated  inter- 
vening portion  ;  or  have  an  unduly  narrow  lumen  (incomplete  co- 
arctation). The  narrowing  may  take  place  at  the  point  of  entry  of  the 
ductus.  The  constriction  is  sudden  or  gradual.  Usually  the  vessel  is 
dilated  or  funnel-shaped  on  the  proximal  side,  and  thin  and  small  on  the. 
distal  side. 

The  ductus  may  supply  or  give  rise  to  the  descending  aorta,  and  in 


Congenital   Heart    Disease.  475 

still  rarer  cases  is  entirely  absent.  Isthmus  stenosis  is  associated  in  one- 
third  of  the  cases  with  valvular  and  arterial  anomalies  and  other  congenital 
malformations.  The  supply  of  blood  to  head  and  upper  limbs  is  quite 
normal.  If  the  ductus  is  not  patent,  the  collateral  circulation  is  carried  on 
by  anastomoses  between  the  upper  intercostal  arteries  from  the  second  part 
of  the  subclavian  with  the  first  aortic  intercostals  ;  and  by  the  posterior 
scapular  arteries  from  the  second  part  of  the  subclavian,  the  subscapular 
branches  and  the  internal  mammary  arteries,  anastomosing  with  the  super- 
ficial epigastric  and  posterior  intercostals.  Cases  of  mild  grade  develop  no 
collateral  circulation,  but  the  left  ventricle  is  hypertrophied  and  the 
aortic  second  sound  accentuated.  In  the  more  serious  cases  the  ventricle 
fails  to  stand  the  strain  of  the  anastomotic  circulation  and  death  results 
from  cardiac  failure.  If  slight,  the  condition  cannot  be  diagnosed  in  early 
life  for  the  signs  develop  gradually.  Eventually  there  are  present  many 
thick,  tortuous  arteries  under  the  skin;  excessive  pulsation  in  the  arteries 
of  the  head,  neck  and  upper  extremities  ;  hypertrophy  and  dilatation  of  the 
heart,  bulging  forward  of  the  aorta  in  the  neck  ;  a  loud  murmur  over  the 
preeordium,  especially  over  the  manubrium,  and  murmurs  in  the  arteries 
of  the  head  and  upper  extremities.  If  incomplete,  a  systolic  murmur 
may  be  heard  over  the  descending  aorta  between  the  scapula  and  the  spine. 
The  pulse  is  exaggerated  in  the  radial  artery,  and  feeble  or  absent  in  the 
abdominal  aorta  and  the  femorals,  etc. 

Clinical  symptoms  may  be  absent  or  limited  to  dyspnoea,  and  later 
on  those  of  cardiac  failure.  In  a  case  of  incomplete  isthmus  stenosis  in  a 
girl,  aged  5  weeks,  there  were  no  symptoms  except  slight  lividity  on  crying, 
and  no  murmur.  Death  was  due  to  bronchitis.  The  ductus  was  widely 
patent.  The  aorta  gave  off  normal  vessels  and  then  suddenly  narrowed 
at  the  isthmus,  and  the  ventricular  septum  was  patent.  This  condition  was 
quite  compatible  with  life  had  it  not  been  for  the  bronchitis.  In  an  adult 
navvy,  seen  many  years  ago,  the  arterial  dilatation  and  tortuosity  of  the 
vessels  were  very  marked,  but  there  were  no  symptoms  whatever.  The 
prognosis  varies  inversely  as  the  degree  of  stenosis  and  directly  as  the 
completeness  of  the  collateral  circulation.  If  there  is  incomplete  stenosis 
of  moderate  degree,  life  may  be  prolonged.  The  average  duration  of  life 
is  about  30  years.  A  case  of  Reynaud's  lived  92  years.  Rupture  of  the 
auricle,  ventricle  or  aorta  has  occurred,  and  secondary  saccular  or  dissecting 
aneurism.    The  aortic  valves  are  often  defective  or  diseased. 

General  Symptoms. — Cyanosis  and  clubbing  of  the  extremities  are  the 
two  symptoms  which  require  most  consideration.  Less  frequently  there 
are  noted  one  or  more  of  the  following  : — dyspnoea,  constant,  on  exertion 
only,  or  in  paroxysmal  attacks  during  which  cyanosis  becomes  so  intense 
that  the  extremities  may  turn  black  ;  attacks  of  suffocation  with  loss  of 
consciousness,  thready  pulse  and  lividity,  lasting  up  to  15  minutes  and 
perhaps  fatal ;    syncopal  attacks ;    paroxysmal  or  constant  cardiac  pain ; 


476  Chapter    XL  I. 


a 


variable,  intermittent  or  irregular  pulse;  tachycardia;  headaches, 
somnolence,  extreme  irritability,  convulsions  and  coma;  subnormal  tem- 
perature,  cold  extremities  ;  delayed  physical  and  mental  development, 
delicate  bones,  tendency  to  kyphosis,  late  sexual  development  (infan- 
tilism). These  children  feel  the  cold  much,  and  are  liable  to  "  catch  cold  " 
and  develop  tuberculosis,  especially  in  pulmonary  stenosis.  Symptoms  as 
a  whole  are  most  frequent  in  pulmonary  stenosis  for  it  is  more  compatible 
with  prolonged  life.  Haemorrhages  may  occur.  True  angina  is  extremely 
rare  ;    two  cases  have  been  recorded  in  infants  under  6  months  of  age. 

Cyanosis  or  Morbus  Cceruleus  is  by  no  means  always  present  and  may 
be  entirely  absent,  the  face  being  normal  in  colour,  unduly  bright- 
complexioned  or  presenting  an  unusual  pallor.  Sometimes  capillary 
stigmata  are  seen  on  the  cheeks.  If  cyanosis  is  present,  it  is  not  necessarily 
of  cardiac  origin.  When  it  is,  it  varies  greatly  in  severity  and  distribution, 
may  be  limited  to  the  extremities  or  involve  the  whole  body  and  the 
mucous  membranes.  It  is  always  increased  by  effort,  crying  and  emotional 
disturbance,  and  may  only  be  present  under  these  conditions.  Paroxysmal 
attacks  of  greatly  increased  severity  are  not  uncommon.  The  blueness 
may  not  develop  for  some  months  or  years  after  birth,  and  is  then  the 
result  of  some  illness,  such  as  bronchitis  or  a  specific  fever,  or  because  the 
heart  does  not  grow  sufficiently  for  the  growth  of  the  child.  When  it  is 
present  it  is  almost  invariably  persistent,  though  variable  in  intensity. 
It  is  most  noticeable  in  the  cheeks,  lips,  ears  and  extremities.  Some  of  these 
infants  are  plum  coloured  at  first,  and  the  colour  may  fade  or  disappear 
as  the  child  grows.  The  greater  the  cyanosis  at  birth,  the  worse  is  the 
prognosis.  Other  causes  of  congenital  cyanosis  are  atelectasis,  pulmonary 
apoplexy,  diaphragmatic  hernia,  cerebral  haemorrhage  and  sepsis.  Two 
cases  in  which  there  was  hyperglobulia  without  heart  lesion  have  been 
reported  by  Weil.  One  of  them  showed  changes  in  the  bone  marrow  and 
thymus,  and  an  enlarged  spleen.  Cyanosis  is  always  due  to  deficient 
aeration  of  the  blood  and  is  perhaps  aided  by  the  imperfect  development 
of  the  special  affinity  of  haemoglobin  for  oxygen.  The  blood  contains  a  large 
increase  in  the  number  of  red  cells  and  percentage  of  hremogiobin  ;  up  to 
red  cells  10  million,  haemoglobin  percentage  160,  specific  gravity  1070. 
The  increased  number  of  red  cells  is  compensatory  to  the  increased  per- 
centage of  C02  in  the  blood.  Other  factors  sometimes  present  are  venous 
congestion,  and  the  mixing  of  venous  and  arterial  blood  in  consequence  of 
the  cardiac  defects. 

Not  much  importance  can  be  attached  to  the  mixing  of  blood,  for 
cyanosis  can  exist  without  admixture  and  complete  mixing  may  occur 
without  cyanosis. 

Pulmonary  stenosis  causes  deficient  aeration  when  the  stenosis  is 
sufficient  to  prevent  the  proper  amount  of  blood  being  driven  through  the 
lungs.     Otherwise  there  is  no  lividity  until  compensation  fails.     General 


Congenital   Heart    Disease.  477 

cyanosis  is  most  marked  when  the  aorta  arises  from  the  right  ventricle. 
It  is  increased  by  dilatation  of  the  right  ventricle  and  venous  stasis,  for  the 
blood  in  the  systemic  veins  becomes  still  more  de-oxygenated.  Venous  stasis 
is  followed  bv  venous  dilatation.  There  is  much  liabilitv  to  haemorrhage. 
The  retinal  vessels  are  tortuous  and  distended,  causing  cyanosis  retinas  and 
perhaps  neuro-retinitis.  A  patent  foramen  ovale  will  only  give  rise  to 
cyanosis  when,  for  any  reason,  such  as  pulmonary  affections  or  cardiac 
defects,  there  is  a  rise  of  pressure  in  the  right  auricle  sufficiently  great  to 
drive  the  blood  into  the  left  auricle.  Under  such  conditions  the  cyanosis 
develops  quite  unexpectedly.  Out  of  77  cases  of  cyanosis  in  congenital 
heart  disease  the  pulmonary  artery  or  orifice  was  obstructed  in  53  (Stille). 
In  a  series  of  50  cases,  cyanosis  was  present  in  23.  Of  these,  7  out  of  13 
fatal  ones  were  cyanotic,  2  only  on  crying,  and  the  defects  were  pulmonary 
in  6,  viz.,  transposition  of  the  aorta  and  pulmonary  artery  in  2,  pulmonary 
stenosis  and  regurgitation,  atresia  of  the  conus  pulmonalis,  the  pulmonary 
artery  rising  from  the  aorta  and  the  inferior  vena  cava  opening  into  the 
left  ventricle,  pure  pulmonary  stenosis,  and  in  the  seventh  isthmus 
stenosis  with  patent  ductus  and  septum.  The  last  case  only  became  blue  on 
crying.  In  18  out  of  37  cases,  not  verified  post  mortem,  a  pulmonary 
lesion  was  diagnosed  or  suspected  and  16  showed  more  or  less  cyanosis. 
Cretins  are  sometimes  very  blue. 

Clubbing  is  most  obvious  in  the  terminal  phalanges  of  the  fingers  and 
toes,  but  it  is  not  peculiar  to  congenital  heart  disease.  It  is  seen  in  chronic 
phthisis,  bronchiectasis,  prolonged  empyema  and  pressure  on  the  axillary 
vein.  In  morbus  cordis  it  is  due  to  the  same  causes  as  the  cyanosis,  does 
not  occur  independently  thereof,  and  varies  in  degree  with  the  severity 
and  duration  of  the  lividity.  It  is  due  to  congestion,  engorgement  of  the 
veins  and  thickening  of  the  vessel  walls.  There  is  no  increase  in  the  con- 
nective tissue.  After  many  years  in  severe  cases  a  hypertrophic  osteo- 
arthropathy, an  ossifying  periostitis,  of  the  knees  and  elbows  may  develop. 

Complications  and  sequels  are  numerous.  In  order  of  frequency 
may  be  mentioned  bronchitis  and  broncho-pneumonia,  gastro-intestinal 
troubles,  epistaxis,  haemoptysis  independently  of  phthisis,  tuberculosis, 
albuminuria,  jaundice  and  rarely  dropsy  ;  sometimes  endocarditis,  simple 
or  malignant,  occasionally  sores  about  the  genitals,  anus  and  extremities, 
gangrene,  rheumatism,  chorea,  amenorrhcea  and  metrorrhagia.  Sudden 
death,  secondary  cardiac  failure  and  cerebral  thrombosis  may  ensue. 
Out  of  449  collected  cases  of  pulmonary  stenosis  160  developed  tuberculosis, 
of  the  lungs  (Norris,  1904).  It  may  also  occur  in  other  forms  of  congenital 
morbus  cordis. 

Diagnosis. — Cyanosis  without  murmur  may  be  due  to  a  mono- 
ventricular  heart,  stenosis  of  the  isthmus  aortas  and  patent  ductus,  atresia 
of  the  conus  pulmonalis  or  irregular  origin  of  vessels.  If  it  is  associated 
with  a  basic  murmur  it  is  due  to  pulmonary  stenosis  in  75  per  cent.,  with 


478  Chapter   XLI. 

or  without  other  lesions,  or  to  multiple  abnormalities.  In  conjunction  with 
an  apical  murmur  I  have  found  it  due  to  transposition  of  the  main  vessels 
or  multiple  defects.  A  murmur  without  cyanosis  may  be  due  to  a  patent 
interventricular  septum  and  lesions  such  as  are  found  in  acquired  heart 
disease.  A  diastolic  murmur  is  generally  due  to  pulmonary  regurgitation. 
Considerable  displacement  of  the  apex  to  the  left  is  a  sign  of  grave  defects. 

Abnormally  loud  murmurs  are  almost  pathognomonic  but  congenital 
morbus  cordis  can  exist  without  murmurs.  In  comparison  with  the 
acquired  forms  stress  must  be  laid  on  a  loud,  harsh  or  musical  murmur, 
with  little  or  no  increase  in  dulness,  and  a  weak  apex  beat ;  increased 
dulness  to  the  right  ;  no  apical  murmur  ;  a  weak  pulmonary  second 
sound  in  pulmonary  stenosis  ;  and  the  evidence  afforded  by  X-ray  examina- 
tion. Functional  pulmonary  murmurs  are  common  during  life.  A  diagnosis 
of  pulmonary  stenosis  and  phthisis  must  be  accepted  with  caution  unless 
verified  after  death. 

Prognosis  depends  on  the  symptoms  rather  than  the  physical 
signs  ;  on  the  nature  of  the  defect,  whether  developmental  or  inflammatory 
in  origin  ;  upon  its  effects  on  the  heart  and  circulation  ;  the  maintenance 
and  duration  of  compensation  ;  and  the  effect  on  the  growth  of  the  child. 
A  loud  murmur  is  quite  compatible  with  normal  life,  while  a  fatal  issue 
may  ensue  very  early,  although  there  may  be  no  murmur  and  indeed  no 
evidence  of  cardiac  defect.  Patients  become  more  or  less  used  to  cyanosis, 
but  as  a  general  rule  the  prognosis  is  worse  in  proportion  to  the  degree  of 
lividity.  Cyanosis  may  prove  fatal  from  syncope,  fits,  coma  or  secondary 
lung  trouble.  Indications  of  a  guarded  prognosis  as  regards  duration  of 
life  are  the  evidence  of  cardiac  dilatation  and  hypertrophy,  especially  of 
the  left  ventricle,  unduly  frequent  pulse,  shortness  of  breath  or  attacks 
of  dyspnoea,  with  or  without  exertion,  and  delayed  physical  and  mental 
•development.  Convulsions,  paroxysmal  dyspnoea,  persistent  low  tempera- 
ture and  haemorrhages  are  bad  signs. 

Periods  of  stress  are  likely  to  arise  from  pulmonary  affections,  whooping 
cough,  gastro-intestinal  troubles  and  other  ailments.  Murmurs  may  dis- 
appear entirely,  or  disappear  and  return  during  respiratory  distress.  At 
puberty  undue  stress  is  thrown  upon  the  heart  by  reason  of  the  cardiac 
and  vascular  changes.  Nevertheless  I  have  seen  no  special  ill-effect  in  these 
-cases  at  this  time  of  life. 

Peacock's  statistics  show  that  out  of  181  cases  119  presented  defects 
of  the  pulmonary  artery,  orifice  or  conus  ;  and  that  86  per  cent,  of  the 
cases  of  cyanosis  which  survived  the  twelfth  year  had  pulmonary  stenosis. 
Out  of  64  with  pulmonary  stenosis  and  patent  septum  14  lived  over  15  years. 
Of  20  in  which  the  stenosis  was  associated  with  a  patent  foramen  ovale, 
11  lived  over  15  years,  1  to  57  years.  The  average  duration  of  life  of  28 
with  an  impervious  pulmonary  artery  was  3  months  ;  3  lived  to  9  or  10, 
and  1  to  12  vears. 


Congenital   Heart    Disease.  479 

In  bilocular  heart  death  ensues  in  a  few  days.  A  trilocular  one  is 
compatible  with  adult  life.  Simple  patency  of  the  ventricular  septum  may 
be  quite  unimportant  for  the  orifice  may  be  closed  during  systole.  Some 
patients  live  a  remarkably  long  time  though  the  defect  is  serious.  As  a 
whole  it  is  rare  for  the  subjects  of  congenital  heart  disease  to  live  long. 
About  one-quarter  die  in  the  first  year,  half  in  the  first  5  years,  three- 
quarters  in  the  first  15  years,  and  only  10  per  cent,  live  over  30  years. 

The  social  and  hygienic  surroundings  of  the  child  must  be  taken  into 
consideration  because  of  the  liability  to  rheumatism  and  phthisis.  Muscular 
exertion  and  privation  are  often  injurious  and  lead  to  failure  of  compensa- 
tion. The  susceptibility  to  secondary  infective  endocarditis  must  always 
be  remembered. 

Treatment.— Little  can  be  done  beyond  bringing  the  child  up  under  the 
best  conditions  of  life  available,  and  treating  cardiac  failure  and  compli- 
cations as  they  arise.  The  child  must  be  warmly  clad  and  well  cared  for 
generally.  It  is  a  mistake  to  bring  these  children  up  as  chronic  invalids. 
Let  them  live  the  ordinary  life  of  childhood,  as  far  as  is  compatible  with  the 
nature  of  the  mischief  and  the  effect  on  the  general  health.  Provided  the 
child  grows  at  the  normal  rate  and  there  is  no  circulatory  disturbance, 
no  evidence  of  mischief  beyond  the  murmur,  little  attention  need  be  paid  to 
the  local  trouble.  If  there  is  much  hypertrophy,  over-exertion  must  be 
guarded  against.  Protect  them  from  chills  and  exposure  to  infection, 
from  excitement  and  outbursts  of  passion,  and  from  errors  of  diet. 


Chapter  XLII 

ACQUIRED    HEART    DISEASE. 

The  Myocardium — Cardiac  dilatation — Endocarditis —  Valvular  defects — 
Pericarditis  and  effusion — Mediastino-pericarditis —  Adherent  Peri- 
cardium. 

The  muscular  walls  of  the  heart  are  affected  by  hypertrophy,  dilatation, 
and  various  forms  of  inflammation  and  degeneration.  The  common  causes 
of  hypertrophy  of  the  left  ventricle,  in  order  of  frequency,  are  mitral 
regurgitation,  adherent  pericardium,  aortic  stenosis  and  regurgitation,  and 
chronic  interstitial  nephritis.  Hypertrophy  of  the  right  ventricle  is  present 
in  many  forms  of  congenital  heart  disease  and  various  causes  of  increased 
pulmonary  tension,  e.g.,  pertussis,  chronic  bronchitis  and  other  lung 
affections,  mitral  stenosis  and  mitral  regurgitation.  Undue  exposure  of 
the  surface  of  the  heart  from  retraction  of  the  lungs,  rickets  or  other  causes 
must  not  be  mistaken  for  hypertrophy. 

Overstrain  due  to  Exercise. — The  ceaseless  activity  of  children, 
notably  boys,  causes  moderate  hypertrophy.  Both  sexes  have  a  special 
aptitude  for  short  spells  of  active  exercise  and  are  unfitted  for  prolonged 
fatigue.  Long  distance  bicycling,  walking,  paper-chases  and  similar 
exercises  may  produce  serious  or  even  fatal  illness.  The  paper-chase  must 
not  be  entirely  condemned,  for  the  boy  is  not  compelled  to  run  the  whole 
time  or  the  whole  distance.  After  such  a  strain  he  may  be  merely  tired  ; 
or  may  faint  or  vomit  by  the  way  and  be  obliged  to  lie  down  and  rest ; 
or  may  vomit  all  the  evening  after  ;  or  become  insensible  while  running 
and  remain  so  for  hours  ;  or  die  while  running  (Dukes).  Two  factors  are  in 
action,  viz.,  fatigue  and  auto-intoxication  by  the  products  of  active 
metabolism.  They  may  produce  dilatation  of  the  heart,  acute  or  gradual 
in  onset ;  or  simple  hypertrophy  and  dilatation.  This  is  most  apt  to  occur 
when  the  heart  muscle  is  already  weakened  by  some  toxin,  such  as  that  of 
influenza,  measles  or  an  infectious  cold. 

Vomiting  is  the  most  important  sign.  The  symptoms  of  overstrain 
are  anaemia,  languor,  shortness  of  breath  on  exertion  and  perhaps  a  sharp 
pain  at  the  heart.  Examination  shows  dilatation,  increased  frequency 
and  irregularity  of  the  heart  and  pulse,  and  perhaps  a  murmur.  The 
ordinary  signs  of  over- exertion  are  inability  to  eat  a  proper  meal,  disturbed 
sleep,  and  shortness  of  breath  on  exertion. 


Acquired  Heart    Disease.  481 

Fatalities  from  overstrain  are  rare.  The  boy  recovers  with  complete 
rest  for  a  few  weeks  and  careful  supervision  for  some  months  after.  The 
younger  the  child,  the  better  is  the  prognosis,  but  there  remains  a  liability 
to  recurrent  dilatation.  After  puberty  irritability  of  the  heart,  cardiac 
pain,  palpitations  and  dyspnoea  may  persist  for  months  or  years.  Gentle 
exercise  must  be  resumed  after  a  time.    Smoking  and  alcohol  are  injurious. 

Exercises  for  children  should  be  interesting  rather  than  formal,  bearing 
in  mind  that  it  is  the  pace  that  kills.  Children  should  be  allowed  to  walk, 
not  made  to  walk,  and  the  distance  must  be  limited.  Streets  are  unsuitable. 
Croquet,  bowls,  easy  tennis,  bicycling  on  level  ground,  golf  and  other  mild 
games  are  the  most  suitable,  if  for  any  reason  the  amount  of  exercise  has 
to  be  limited.  The  child  must  rest  for  half  an  hour  before  meals,  especially 
before  dinner. 

Dilatation  of  the  Heart  occurs  with  exceptional  ease  in  children  and  is 
most  serious  when  it  is  on  the  right  side.  It  is  the  result  of  diminution  or 
loss  of  muscular  tone,  and  work  beyond  the  power  of  the  impaired  muscle. 
The  output  of  blood  from  the  ventricle  is  remarkably  constant  but  the 
peripheral  resistance  varies.  The  muscle  has  much  power  of  accommoda- 
tion. The  ventricle  does  not  empty  itself  completely  at  each  systole  and 
the  amount  of  residual  blood  varies  with  the  degree  of  diastolic  distension, 
and  this  depends  on  the  tonus  of  the  muscle  and  increases  pari  passu  with 
diminution  of  tone.  Tone  is  greatly  dependent  on  the  nervous  system. 
If  it  is  insufficient  to  cope  with  the  distensile  stress  of  intra-ventricidar 
pressure,  dilatation  results.  The  dilatation  often  comes  on  suddenly  and 
subsides  almost  as  suddenly.  It  is  irregular  in  its  development,  rather 
than  steady  and  continuous,  showing  that  it  is  not  due  to  impaired 
contractile  power.  In  cloudy  swelling  and  myocarditis  both  contractile 
power  and  tone  are  defective. 

Acute  dilatation  is  apt  to  occur  during  influenza  and  prove  rapidly 
fatal.  Within  24  hours,  it  is  due  to  the  action  of  the  toxin  on  the  bulb. 
The  pulse  is  very  frequent  and  often  intermittent ;  respirations  reach 
60-70  per  minute  ;  and  there  is  an  increase  in  the  area  of  cardiac  dulness. 
Cyanosis  and  coldness  of  the  extremities  may  be  present.  In  about  12-72 
hours  the  symptoms  subside  and  the  temperature  falls  to  normal.  I  have 
known  cases  in  babies  in  which  tachycardia  has  been  the  only  sign. 

A  more  common  and  more  dangerous  type  of  dilatation,  acute  or 
chronic,  is  seen  at  a  later  stage  of  influenza,  diphtheria,  rheumatic  fever, 
scarlatina,  nephritis,  pneumonia  and  pertussis,  or  other  infective  disorders. 
It  is  due  to  the  direct  action  of  a  toxin  on  the  cardiac  muscle,  producing 
cloudy  swelling  or  myocarditis.  The  pulse  is  weak,  slow,  irregular  and 
often  intermittent.  Precordial  or  angina-like  pains  are  not  uncommon  ; 
and  there  are  marked  symptoms  of  cardiac  collapse,  with  attacks  of  faint- 
ness  or  syncope  which  may  prove  fatal.  Such  a  condition  may  follow  the 
ordinary  infectious  cold.     Dilatation  also  occurs  in  malnutrition,  local  or 

2  i 


482  Chapter   XLII. 

general,  when  an  extra  strain  is  thrown  on  the  heart  by  increased  muscular 
•exertion,  raised  blood  pressure,  and  cough.  It  is  due  also  to  valvular  disease 
and  pericardial  adhesions.  In  some  of  these  affections  the  dilatation 
affects  all  the  cavities  of  the  heart,  while  in  others  it  is  limited  to  the  right 
or  left  ventricle  chiefly,  if  not  entirely.  More  than  one  of  the  different 
factors,  viz.,  malnutrition,  toxaemia  and  mechanical  strains,  are  active  in 
some  of  the  cases.    For  instance,  in  pertussis  all  are  involved. 

In  acute  dilatation  we  find  marked  increase  in  cardiac  dulness,  a  feeble 
and  diffused  apex  beat,  faint  first  sound  at  the  apex,  accentuation  of  the 
aortic  and  pulmonary  second  sounds,  niurnmrs,  dyspnoea,  weak  pulse, 
precordial  pain,  and  tendency  to  collapse.  Mild  cases  show  merely  irregu- 
larity of  the  heart  and  shortness  of  breath.  In  more  severe  ones  there  are 
dyspncea,  distress  and  sleeplessness.  Bronchial  breathing  over  the  base  of 
the  left  lung  is  not  infrequent.  Anorexia,  gastralgia,  nausea  and  vomiting, 
and  diarrhoea  or  constipation,  are  more  common  than  purely  cardiac 
symptoms.  In  cardiac  insufficiency  dilatation  of  the  right  ventricle,  tri- 
cuspid regurgitation  and  anasarca  are  less  common  than  in  adults.  The 
liver  is  early  and  much  affected,  and  breathing  more  than  the  pulse. 
Pulmonary  catarrh  and  deficient  urine  are  earlier  signs  than  anasarca. 

Myocarditis  is  a  common  complication,  perhaps  the  only  sign,  of  rheu- 
matic fever  and  liable  to  occur  in  diphtheria,  specific  fevers  and  infective 
disorders.  It  is  present  to  a  slight  extent  in  endocarditis  and  still  more  in 
pericarditis.  In  the  absence  of  these  affections  it  is  often  overlooked  or 
mistaken  for  simple  dilatation. 

Myocardial  disease  is  primary,  due  to  the  action  of  toxins,  or  secondary 
to  cloudy  swelling  or  inflammation.  The  physical  signs,  symptoms  and 
prognosis  are  much  the  same  in  each  case,  and  it  is  not  always  possible  to 
make  an  exact  clinical  diagnosis  of  the  state  of  the  cardiac  muscle.  Cloudy 
swelling  is  not  strictly  inflammatory.  It  occurs  in  infective  disease  with 
high  fever,  notably  acute  rheumatism,  typhoid  fever  and  diphtheria,  and  is 
due  to  the  action  of  toxins.  The  muscle  may  be  soft  and  friable  as  early  as 
the  fourth  day.  The  heart,  especially  the  left  ventricle,  is  dilated.  The 
granules  in  the  muscle  fibres  are  soluble  in  acetic  acid  and  in  caustic  potash. 
They  are  not  fatty,  but  on  their  way  to  become  fat.  Acute  segmentary 
degeneration  is  sometimes  a  further  stage.  Myomalacia,  cordis  is  rare  in 
childhood  and  depends  on  coronary  obstruction  and  disease.  Fatty 
degeneration  is  very  apt  to  occur  in  diphtheria,  scarlet  fever,  typhoid  and 
pertussis.  It  has  been  produced  in  animals  by  the  injection  of  diphtheritic 
albumoses  (Sidney  Martin).  Waxy  degeneration  and  Zencker's  type  are 
very  rare. 

Myocarditis  is  acute  or  chronic,  interstitial  or  parenchymatous,  diffuse 
or  circumscribed.  The  acute  interstitial  type  is  due  to  osteomyelitis,  septic 
scarlatina  and  other  infections.  It  is  almost  invariably  focal,  when  due  to 
pyaemia,  and  may  terminate  in  an  abscess  which  bursts  into  the  pericardial 


Acquired  Heart    Disease.  483 

cavity  or  through  the  endocardium.  The  focal  lesions  may  consist  of  organ- 
isms and  round  cells,  and  are  not  necessarily  abscesses.  The  chronic  form 
is  of  syphilitic  origin,  or  secondary  to  valvular  disease  or  adherent  peri- 
cardium. It  produces  fibroid  or  sclerotic  patches,  "  scar  of  the  heart," 
in  the  myocardium.  The  diffuse  form  is  generally  syphilitic.  The  term, 
Chronic  Myocarditis,  is  sometimes  used  to  include  all  chronic  myocardial 
degenerative  affections,  whether  fatty,  fibroid  or  due  to  coronary  obstruc- 
tion. These  are  more  strictly  results.  Pericarditis  does  not  extend  to  the 
myocardium  as  an  acute  interstitial  inflammation,  but  causes  some  cloudy 
•swelling  and  segmentary  degeneration  of  the  underlying  muscle.  A 
true  interstitial  myocarditis,  with  or  without  pericarditis,  is  rare  in 
rheumatism. 

The  parenchymatous  type  is  almost  always  a  cloudy  swelling,  with 
little  or  no  interstitial  inflammation,  and  secondary  fatty  degeneration. 
It  is  the  most  important  form  of  cardiac  inflammation  in  the  young,  chiefly 
.seen  in  acute  rheumatism  (q.v.).  Irregularity  of  the  pulse  is  the  first  sign. 
It  is  extraordinary  how  slight  and  indefinite  the  symptoms  may  be. 
Perhaps  there  is  only  a  little  restlessness  at  night,  impaired  appetite, 
•disinclination  for  exertion  and  an  evening  rise  of  temperature.  The  child 
may  look  quite  well,  a  little  pallid  or  slightly  livid.  Occasionally  there  is 
•cough  and  definite  shortness  of  breath,  increased  by  exertion.  Dyspnoea 
may  be  severe,  and  associated  with  coldness  and  lividity  of  the  extremities. 
Tiapid  emaciation  may  be  the  chief  symptom. 

On  examination  the  heart  is  found  dilated,  the  degree  of  dilatation 
•varying  with  the  severity  of  the  case.  The  apex  beat  is  displaced  outward, 
perhaps  not  palpable  ;  the  impulse  diffused  and  weak  ;  dulness  extends 
•one  or  more  finger-breadths  beyond  the  apex  and  to  the  right  of  the  sternum, 
and  even  up  to  the  third  rib  ;  the  first  sound  at  the  apex  is  short  and 
weak  and  may  be  replaced  by  a  murmur,  and  the  second  sound  is  some- 
times inaudible,  or  the  sounds  are  foetal  in  character.  A  murmur  is  by 
no  means  constant,  even  in  great  dilatation.  It  is  usually  systolic,  rarely 
presystolic.  The  absence  of  a  murmur  may  lead  to  neglect  of  complete 
-examination  of  the  heart,  the  non-recognition  of  the  dilatation,  and  a 
failure  in  diagnosis.  The  dilatation  affects  all  the  cavities  or  may  be  limited 
to  the  left  ventricle.  The  pulse  is  increased  in  frequency,  soft  and  irregular, 
sometimes  very  feeble  and  very  frequent. 

Post  mortem  the  cavities  and  orifices  of  the  heart  are  found  dilated, 
the  lung  displaced  and  the  left  lower  lobe  compressed.  The  amount  of 
fatty  change  is  variable.  Naked  eye  appearances  show  little  or  no  change. 
In  the  rheumatic  type  Aschoff  has  found  submiliary  nodules  in  the 
sub-endothelial  and  sub-pericardial  tissues  in  the  neighbourhood  of  the 
•arterioles.  Chronic  myocarditis  is  indicated  by  arrhythmia,  bradycardia, 
irregular  breathing,  and  greatly  increased  frequency  of  pulse  and  respira- 
tions on  slight  bodily  or  mental  excitement. 


484  Chapter   XLII. 

Diagnosis  is  difficult  for  it  may  be  impossible  to  differentiate  the 
inflammatory  affection  and  its  resulting  dilatation  from  the  dilatation  due 
to  loss  of  muscular  tone  and  degenerative  changes.  If,  however,  dilatation 
is  found  in  the  course  of  rheumatic  fever,  or  in  the  absence  of  any  exciting 
cause  in  a  child,  it  must  be  regarded  as  probably  due  to  rheumatic  myo- 
carditis and  treated  accordingly.  Much  dilatation  can  occur  in  miid 
diphtheria  and  occasionally  in  septic  throat  affections.  Limitation  of  the 
mischief  to  the  left  ventricle  is  in  favour  of  diphtheria  as  the  cause. 

The  prognosis  depends  on  the  cause,  degree  of  dilatation  and  the- 
treatment.  It  is  better  in  rheumatism  than  in  diphtheria  or  influenza.. 
Provided  the  affection  is  rheumatic,  that  the  child  is  seen  early  before  the 
dilatation  is  extreme,  and  that  complete  rest  in  bed  for  6  weeks  or  more  is 
insisted  on,  the  patient  will  recover.  In  the  degenerative  cases,  such  as 
diphtheria,  the  more  the  dilatation  extends  beyond  the  nipple  line,  the 
greater  is  the  danger.  Sudden  death  may  occur  at  any  time,  even  in 
moderate  dilatation.  It  is  more  common  in  diphtheria  than  rheumatism.. 
Sudden  death  in  the  course  of  myocarditis  must  be  distinguished  from  death 
due  to  paralysis  of  the  vasomotor  centre  in  the  bulb  and  profound  fall  in 
blood  pressure,  with  extreme  dilatation  of  the  vessels  in  the  splanchnic- 
area.  This  is  characterised  by  rapid  fall  in  blood  pressure,  weak  and 
empty  pulse,  pallor  and  collapse,  in  the  course  of  an  infective  disease.  It 
may  come  on  with  appalling  suddenness,  the  child  sitting  up  in  bed  and 
falling  back  dead.  Sometimes  death  is  preceded  by  a  period  of  profound 
collapse,  dilated  pupils  and  feeble  cardiac  action,  the  respiration  being 
little  or  not  at  all  affected.  No  change  is  found  in  the  cardiac  muscle  after 
death.  Bulbar  palsy,  in  the  course  of  diphtheria,  etc.,  is  closely  allied. 
It  causes  cardio-pulmonary  paralysis,  dyspnoea  and  rapid  death.  In  a 
milder  type  it  produces  dyspnceic  attacks,  named  by  Guthrie  "  Bulbar 
Crises."  Endocarditis,  and  pericarditis  still  more  so,  increases  the  gravity 
of  the  case.  Vomiting,  coldness  and  collapse  are  bad  signs.  The  pulse- 
rate  is  a  reliable  guide. 

Treatment. — Complete  rest  is  of  vital  importance,  with  careful  feeding, 
the  avoidance  of  all  foods  liable  to  cause  indigestion,  and  freedom  from 
excitement  and  worry.  Rely  on  digitalis  in  all  cases  of  insufficiency  of 
cardiac  muscle  but  remember  that  it  is  cumulative  and  must  not  be  given 
for  long  periods  at  a  time.  There  is  no  contra-indication  in  the  shape  of  high 
blood  pressure.  Stimulants  are  necessary,  and  occasionally  oxygen 
inhalations  and  possibly  venesection.  An  ice  bag  over  the  precordium  is 
sometimes  useful.  Camphor  is  given  for  fainting  and  collapse  ;  and  spar- 
teine sulphate,  strychnia  and  other  such  drugs. 

Endocarditis  is  a  more  insidious  disease  in  children  than  in  adults  and 
almost  the  sole  cause  of  valvular  mischief  after  birth.  Often  it  produces  no 
symptoms  until  well  advanced.  It  may  be  present  in  the  newborn.  Apart 
from  congenital  cases  it  is  rare  under  2  years  of  age,  and  uncommon  before 


Acquired   Heart    Disease.  485 

the  fifth  year.  It  attacks  mainly  the  valves  exposed  to  the  highest  tension 
and  therefore  liable  to  injury.  Hence  it  is  most  frequent  on  the  right  side 
before  birth  and  the  left  after  birth  ;  and  in  children  most  often  affects  the 
mitral  valves,  the  aortic  being  less  liable  to  injury  by  reason  of  the  low 
blood  pressure  in  childhood.  From  60-80  per  cent,  of  the  attacks  are  due 
to  the  poison  of  acute  rheumatism  ;  and  the  remainder  to  chorea,  tubercu- 
losis, scarlatina,  measles,  diphtheria,  pneumonia  and,  rarely,  other  infections. 
Not  infrequently  it  is  impossible  to  find  a  history  of  any  antecedent  disease 
as  a  probable  cause.  In  such  cases  a  family  history  of  rheumatic  fever  or 
morbus  cordis  is  suggestive  of  a  rheumatic  infection.  In  specific  fevers  the 
endocarditis  may  occur  with  or  without  articular  symptoms.  It  may  follow 
scarlet  fever  long  after  the  fever  has  passed  away  and  without  any  pyrexia. 
Post-scarlatinal  rheumatism  is  closely  allied  to  true  rheumatic  fever. 

The  valves  and  tendinous  cords  are  swollen  and  infiltrated.  On  the 
endocardium  may  be  a  deposit  of  lymph  which  is  subsequently  organised 
into  fibrous  tissue.  As  it  contracts  it  causes  adhesion,  stiffness,  thickening 
and  puckering  of  the  valves  :  thickening,  shortening  and  sometimes  rupture 
of  the  cords.  Three  types  are  found  post  mortem : — (1)  Verrucose,  in  which 
there  are  vegetations  of  various  sizes.  The  small  nodules  often  found  on  the 
valves  of  the  newborn  must  not  be  mistaken  for  vegetations.  In  chorea., 
and  sometimes  in  rheumatic  fever,  the  valves  are  slightly  affected  ;  a  row  of 
minute  granulations  being  found  on  one  or  more  valves.  (2)  Sclerotic,  in 
which  there  is  contraction  of  the  valves  and  orifices.  (3)  Ulcerative, 
affecting  both  the  valves  and  walls  of  the  cavities.  Endocarditis  can  be 
subdivided  into  two  groups.  In  the  first,  or  rheumatic  group,  a  secondary 
infection  may  lead  to  the  development  of  the  second  or  septic  form,  liable 
to  become  ulcerative.  The  septic  variety  may  be  primary,  in  that  it  is  not 
preceded  by  a  rheumatic  infection  or  a  damaged  valve,  but  it  is  secondary 
to  some  local  source  of  infection  in  the  throat,  lungs,  bones,  etc.  The 
common  organisms  are  the  streptococcus,  staphylococcus,  pneumococcus 
and,  less  often,  the  gonococcus,  influenza  bacillus,  B.  coli,  etc. 

Infective  Endocarditis  is  uncommon  in  the  young  and  rims  the  same 
course  as  in  adults.  There  is  no  sharp  line  of  distinction  from  acute  endo- 
carditis. The  name  is  generally  limited  to  cases  due  to  pyogenic  organisms, 
and  ulceration  is  not  invariable.  Nor  is  it  always  fatal.  In  most  instances 
it  is  secondary  to  rheumatic  endocarditis  or  congenital  heart  disease.  Cases 
arc  septic,  typhoidal,  cerebral  or  cardiac  in  type,  according  to  the  pre- 
dominance of  the  particular  symptoms. 

Symptoms. — There  may  be  no  signs  of  the  endocarditis  at  the  onset ; 
or  perhaps  a  little  irregularity  of  the  pulse  and  slight  rise  of  temperature, 
occasionally  precordial  pain  and  some  breathlessness  on  excitement  or 
exertion.  There  is  little  or  no  increase  in  dulness  for  blood  pressure  is  low 
and  the  cardiac  muscle  resistant.  Slight  dilatation  of  the  left  auricle  is 
difficult  to  recognise.    The  cardiac  first  sound  at  the  apex,  in  mitral  disease, 


4S6  Chapter   XLII. 

is  weakened  or  impure.  Presently  a  murmur  develops,  localised  for  a  time 
and  then  extending.  It  is  more  readily  conducted  than  in  adults  and 
of  higher  pitch,  accentuated  by  crying,  unaffected  by  breathing,  and 
constant.  It  may  become  musical  quite  early.  Rapid  breathing  and  rales- 
interfere  with  its  recognition.  The  most  common  site  is  over  the  left 
ventricle,  perhaps  it  is  best  heard  in  the  third  left  interspace  near  the 
sternum.  It  must  be  differentiated  from  venous  bruits,  haeniic  murmurs 
and  cardio-pulmonary  ones. 

In  the  infective  type  we  find  anaemia,  greater  fever,  more  frequent 
pulse  and  respiration  rates,  irregularity  and  intermittence  of  the  pulse,, 
sweating,  emaciation,  vomiting,  purpuric  eruptions,  embolic  infarction,, 
diarrhoea,  melsena,  haematemesis,  albuminuria  and  hsematuria,  cardiac  pain 
and  syncopal  attacks.  The  fever  is  septic  or  typhoidal  in  type,  rarely  run- 
ning the  low  irregular  course  often  seen  in  adults.  The  heart  is  enlarged  ; 
and  the  murmurs  vary  from  day  to  day,  are  more  or  less  constant,  or  may 
be  absent.  Foetal  heart  sounds  and  gallop-rhythm  may  be  noted,  if  there  is- 
no  murmur.  The  blood  shows  leucocytosis.  The  liver  and  spleen  are 
enlarged.  Pulmonary  catarrh,  pleurisy,  infarction  and  haemoptysis  may 
occur  :  and  other  signs,  varying  with  the  distribution  and  infectivity  of  the 
emboli. 

The  autopsy  may  show  recent  endocarditis,  adherent  pericardium,, 
endocarditis  and  ulceration  of  the  valves,  exuberant  granulations  on  the 
valves  and  endocardium  (in  one  child  they  were  limited  to  the  surface  of  the 
auricle)  up  to  the  size  of  a  small  marble,  perisplenitis,  enormous  spleen 
(e.g.,  15  oz.  in  a  boy,  aged  13  years),  and  infarcts  in  various  organs,  some 
of  which  may  be  red,  others  firm  and  white  or  softening  and  breaking  down. 
In  a  girl,  aged  13,  a  secondary  abscess  was  found  in  the  right  corpus  stria- 
tum, although  infarcts  in  the  spleen  showed  no  sign  of  necrosis.  Another 
girl,  aged  15,  died  from  pulmonary  haemorrhage,  due  to  infarction.  The 
diagnosis  of  the  infective  character  of  endocarditis  is  based  on  the  course  of 
the  case  and  the  presence  of  some  of  the  above  symptoms  in  combination, 
especially  a  pyaemic  type  of  fever  associated  with  morbus  cordis  and  indi- 
cations of  infarction.  The  prognosis  is  not  absolutely  hopeless.  Judson 
(1905)  reported  a  case  of  recovery  from  the  pneumococcal  form,  in  a  boy 
aged  10.  In  1891 1  recorded  the  recovery  of  a  boy,  21  years  old,  with  tricuspid 
regurgitation,  anaemia,  large  spleen,  profuse  sweating,  and  a  hectic  tem- 
perature for  2-3  months.  The  outlook  depends  on  the  virulence  of  the 
infective  organisms.  Treatment  is  symptomatic,  An  attempt  should  be 
made  to  isolate  and  cultivate  the  organism,  and  prepare  and  give  a  vaccine. 

Pneumococcal  Endocarditis. — The  endocarditis  present  in  1  per  cent. 
of  all  pneumonias  and  4-5  per  cent,  of  fatal  cases  is  not  always  due  to  the 
pneumococcus.  This  organism  is  responsible  for  J-i  of  the  cases  of  infective 
endocarditis.  The  disease  is  twice  as  common  in  females  as  in  males  ;  rare 
under  30  years  of  age  ;   and  generallv  affects  the  aortic  or  mitral  valves,  or 


Acquired   Heart    Disease.  487 

both,  being  much,  more  frequent  on  the  left  side.  The  vegetations  are 
usually  massive.  It  may  occur  before,  during  or  after  the  lung  mischief. 
Netter  found  it  associated  with  pneumonia  and  meningitis  in  45  out  of  63 
cases.  The  pulse  is  rapid,  leucocytosis  often  absent,  and  the  organism  can 
be  grown  from  the  blood.  It  lasts  from  a  few  days  to  months,  and  is 
generally  severe  or  malignant. 

Tuberculous  Endocarditis. — Minute  vegetations  are  sometimes  found 
on  the  valves,  chiefly  the  aortic  and  mitral,  of  children  dying  from  miliary 
tuberculosis.  A  true  tuberculous  endocarditis  is  a  very  rare  condition.  The 
bacillus  is  often  present  in  the  blood  stream,  but  the  endocardium  and  the 
lining  of  the  blood  vessels  are  insusceptible  to  infection.  Tuberculous 
arteritis  starts  in  the  adventitia,  and  it  is  probable  that  the  rare  tuberculous 
infection  of  valves  is  through  their  blood  or  lymph  supply.  Anatomically 
it  is  like  other  forms  of  infective  endocarditis  ;  and  is  vegetative,  verrucose, 
fungating  and  ulcerative.  The  bacillus  is  present  but  no  giant  cells.  The 
mere  recovery  of  the  organism  from  a  vegetation  is  no  certain  proof  that  it  is 
the  causative  agent.    It  may  be  merely  superimposed. 

Tuberculosis  of  the  Myocardium  was  mentioned  by  Laennec  in  1826 
and  recorded  by  Townsend  in  1832.  It  has  been  described  as  a  primary 
disease,  though  its  existence  in  this  form  is  not  generally  accepted.  Nearly 
half  the  patients  are  under  15  years  of  age.  Both  sexes  are  equally  liable. 
Usually  the  primary  source  is  a  tuberculous  bronchial  or  mediastinal  gland, 
and  many  owe  their  origin  to  extension  from  the  pericardium,  while  the 
rest  are  a  part  of  a  general  tuberculous  blood  infection.  Miliary  tubercles 
are  found  underlying  the  endocardium,  most  frequently  in  the  ventricles. 
Large  tubercles  may  be  formed  in  the  auricle,  ventricle  or  inter- ventricular 
septum.  They  vary  in  size  from  that  of  a  millet  seed  to  a  hen's  egg,  are 
yellowish  in  colour,  may  have  a  caseous  centre,  and  closely  simulate  gurn- 
mata.  Sometimes  this  variety  is  associated  with  interstitial  myocarditis. 
This  may  occur  alone,  due  to  diffuse  infiltration  with  round  cells  and  con- 
nective tissue,  giant  cells,  caseous  areas,  and  no  tubercle  bacilli.  Such  a 
case  was  reported  in  a  boy,  aged  3  years  (W.  M.  Smith,  1902).  It  is  com- 
parable with  tuberculous  cirrhosis  of  the  liver.  A  diffuse  tuberculous 
infiltration,  caseous  in  character,  is  a  rare  sequence  of  tuberculous  peri- 
carditis. The  chief  symptoms  are  dyspnoea,  gallop-rhythm,  tachycardia 
or  bradycardia,  arrhythmia,  palpitation  and  cyanosis.  They  may  be  entirely 
lost  in  those  of  the  general  disease.  A  gumma  is  more  grey  in  colour  and 
more  sharply  circumscribed.  No  inflammatory  nodule  in  the  heart  should 
be  diagnosed  as  a  gumma,  unless  there  are  other  signs  of  syphilis  and  no 
evidence  of  tuberculous  disease. 

Tuberculosis  of  the  Pericardium  is  due  to  extension  from  a  caseous 
gland,  especially  the  pretracheal  gland ;  occasionally  from  the  lungs, 
pleura,  myocardium  or  bones  ;  rarely  part  of  a  general  tuberculosis  or  a 
tuberculous  polyserositis.     In  general  miliary  tuberculosis  miliary  tubercles 


488  Chapter  XL1I. 

are  scattered  about  the  surface,  chiefly  at  the  base.  In  the  other  varieties 
there  is  an  infiltration  and  great  thickening  of  the  pericardial  layers,  with 
obliteration  of  the  sac.  The  heart  may  seem  to  be  ensheathed  in  a  sort  of 
cuirass  which  to  the  naked  eye  does  not  suggest  tuberculosis.  Sometimes 
it  sets  up  a  serous,  sero-fibrinous,  purulent  or  hemorrhagic  pericarditis. 
In  rare  instances  it  is  primary  and  acute  in  onset.  Usually  there  is  an 
interstitial  myocarditis  as  well.  The  chief  sequels  are  adherent  pericardium, 
ascites,  nutmeg  liver,  cyanosis,  polyserositis,  and  sometimes  mediastinitis, 
The  disease  is  chronic,  slowly  progressive,  and  ends  fatally  in  4-8  months. 

Valvular  Disease  is  the  sequel  of  endocarditis,  omitting  those  cases 
which  are  of  developmental  origin.  It  is  impossible  to  give  accurate 
statistics  of  the  frequency  with  which  the  different  valves  are  affected,  and 
of  the  relative  frequency  of  valvular  affections  to  other  cardiac  inflam- 
mations for  constantly  two  or  more  varieties  are  combined.  Taking  cardiac 
diseases  as  a  whole,  the  order  of  frequency  of  the  different  affections  is 
simple  dilatation,  myocarditis,  endocarditis  and  valvular  lesions,  peri- 
carditis, pericardial  effusion  and  adherent  pericardium.  The  mitral  valve 
is  involved  in  4  out  of  every  5  cases,  and  in  three-quarters  of  these  there  is 
simple  regurgitation. 

Mitral  regurgitation  produces  practically  the  same  signs  as  in  adults, 
except  that  there  is  less  tendency  to  anasarca,  oedema  of  the  lungs,  nutmeg 
liver  and  ascites,  though  all  these  develop  in  late  stages.  In  other  words 
there  is  greater  compensatory  power  in  the  heart  muscle.  The  pulse  is 
generally  regular,  and  arrhythmia  is  rare  under  12  years  of  age.  The  left 
Ventricle  hypertrophies  readily  and  leads  to  the  production  of  the  cm 
hovimtm.  The  area  of  dulness  and  pulsation  is  large,  the  apex  displaced 
outward  and  downward,  the  impulse  heaving,  and  the  right  ventricle  rests 
on  the  diaphragm  and  causes  epigastric  pulsation.  Usually  the  child  is 
pale  and  wasted,and  the  chief  symptoms  are  referable  to  the  digestive  organs. 
The  character  and  mode  of  conduction  of  the  murmur  are  valuable  aids  to 
diagnosis  and  prognosis.  When  the  left  auricle  and  ventricle  are  of  normal 
size,  the  cardiac  sounds  are  not  heard  behind,  for  lung  tissue  is  between 
them  and  the  posterior  thoracic  wall.  If  these  cavities  are  dilated,  the 
lung  is  partly  compressed  or  pushed  aside,  and  the  heart  comes  more 
or  less  into  contact  with  the  posterior  thoracic  wall  and  the  bodies  of  the 
vertebrae.  Under  such  conditions  the  murmur  of  mitral  regurgitation  is 
conducted  down  the  left  side  of  the  spine,  and  the  degree  of  conduction 
and  loudness  of  the  murmur  are  a  fair  measure  of  the  dilatation  and  the 
amount  of  regurgitation.  Simple  loudness  of  the  murmur  in  the  inter- 
scapular region,  without  conduction  downward,  suggests  a  dilated  and 
failing  left  auricle.  A  loud  murmur  may  reach  the  head,  sacrum  and 
extremities.  The  character  of  the  pulmonary  second  sound  is  of  very  great 
assistance.  If  it  is  loud  and  ringing,  it  indicates  high  pulmonary  tension 
and  considerable  regurgitation.     And  the  first  sign  of  cardiac  failure  is 


Acquired  Heart    Disease.  489 

some  weakening  in  the  loudness  of  this  sound.  Dilatation  of  the  right 
ventricle  is  a  sequel  of  the  hypertrophy  developed  to  overcome  the  increased 
pulmonary  tension. 

Mitral  stenosis  is  raiely  congenital,  seldom  detected  under  6  years  of 
age,  and  not  very  uncommon  in  youth.  A  marked  case  in  a  3-year-old  boy, 
due  to  rheumatism,  ended  fatally  from  chorea.  It  is  more  frequent  in 
girls  than  boys.  The  button-hole  orifice  is  rare.  Generally  it  is  funnel 
shaped,  from  adhesion  of  the  edges  of  the  valves.  It  is  often  conjoined  with 
mitral  regurgitation,  or  a  sequel  of  it,  and  may  be  present  without  a  murmur, 
€ven  in  the  worst  cases.  The  murmur  is  auricular  systolic  in  time,  generally 
presystolic,  sometimes  mid-diastolic.  An  early  diastolic  murmur  is  due 
to  the  suction  action  of  the  diastole  of  the  ventricle.  Increased  dulness  in 
the  third  left  space  shows  enlargement  of  the  left  auricle.  The  second  sound 
at  the  base  is  often  reduplicated  and  the  pulmonary  second  sound  always 
accentuated.  At  the  apex  the  first  sound  is  loud,  clear,  abrupt,  banging  or 
thumping,  perhaps  a  regular  thud  ;  sometimes  reduplicated.  The  heart's 
action  is  cantering.  The  pulse  is  very  variable.  If  the  right  ventricle 
remains  sound  and  the  degree  of  stenosis  is  small,  the  pulse  is  about  normal. 
If  the  orifice  is  very  small,  it  becomes  very  small,  weak  and  irregular, 
because  the  left  ventricle  receives  a  scanty  supply  of  blood.  The  more 
frequent  the  pulse  rate,  the  greater  is  the  failure  of  the  right  ventricle. 
The  failure  of  development  of  the  left  ventricle  produces  general  wasting 
and  maldevelopment  of  the  body.  So  much  is  this  the  case  that  delayed 
growth  in  morbus  cordis  is  strong  evidence  of  mitral  stenosis.  The  facial 
aspect  is  a  curious  dusky  pallor.  The  backward  pressure  in  the  lungs  leads 
to  pulmonary  catarrh,  haemoptysis,  congestion  and  collapse  of  the  lobules, 
cell  proliferation  and  diapedesis,  and  brown  induration  of  the  lung.  Later 
on  the  ordinary  signs  of  backward  pressure  develop  but  it  is  not  accom- 
panied by  ascites  or  anasarca,  unless  there  is  also  mitral  regurgitation  and 
tricuspid  regurgitation.  The  chief  symptoms  are  dyspnoea,  digestive 
troubles,  sometimes  epistaxis  or  haemoptysis  ;  and  the  effects  of  emboli, 
carried  to  the  lungs  from  small  fibrinous  clots  forming  in  the  right  auricle 
or  ventricle,  or  from  the  left  auricle  to  the  brain,  spleen,  kidneys  and, 
rarely,  the  liver. 

Tricuspid  stenosis  is  rarely  congenital.  It  is  most  common  in  girls, 
whereas  congenital  morbus  cordis  affects  both  sexes  equally.  It  is  almost 
always  associated  with  mitral  stenosis,  and  often  with  aortic  stenosis  as 
well.  Its  etiology  is  the  same  as  that  of  endocarditis  of  the  mitral  valve. 
Dyspnoea  on  exertion  is  the  most  constant  symptom.  Finally  dyspnoea 
occurs  when  the  child  is  at  rest,  and  orthopncea,  paroxysms  of  urgent 
dyspnoea  and  cyanosis,  Cheyne-Stokes  breathing  and  precordial  pain. 
Cyanosis,  sometimes  clubbing  of  the  fingers,  and  dropsy  may  be  present. 
In  pure  tricuspid  stenosis  the  child  is  anaemic.  If  there  is  mitral  stenosis  as 
well,  we  find  catarrh  of  the  lungs,  haemoptysis  and  the  dusky  facial  aspect. 


490  Ckapter  XL1I. 

Subjective  symptoms  are  constantly  absent  or  due  to  cardiac  failure.  The 
veins  in  the  neck  are  much  dilated  and  show  auricular  pulsation.  In  pure 
stenosis  the  ventricular  pulse  in  the  veins  should  be  absent.  The  cardiac 
defects  vary  in  accordance  with  the  degree  of  stenosis,  the  purity  of  the 
lesion,  or  the  presence  of  stenosis  of  other  orifices.  The  right  ventricle  and 
auricle  are  dilated  and  sometimes  hypertrophied,  but  not  so  markedly  as 
is  the  left  auricle  from  mitral  stenosis,  for  there  is  less  resistance  to  back- 
ward pressure  in  the  great  veins.  The  amount  of  dilatation  and  hyper- 
trophy of  the  right  ventricle  depends  on  the  presence  and  extent  of  mitral 
stenosis.  The  disease  is  often  overlooked  because  the  signs  are  masked 
by  those  of  mitral  stenosis.  The  physical  signs  are  a  presystolic  thrill  and 
murmur,  with  evidence  of  dilatation  of  the  right  auricle,  pulsation  in  the 
jugular  veins,  absence  of  ventricular  pulse  in  the  jugulars,  and  pulsation 
of  the  liver.  Pericarditis,  adherent  pericardium  and  infective  endocarditis 
are  apt  to  ensue.  The  congenital  cases  live  from  a  few  weeks  to  a  few  years. 
The  acquired  disease  is  most  frequently  fatal  in  the  third  or  fourth  decade 
of  life,  at  an  average  age  of  35  years. 

Tricuspid  Regurgitation  is  the  sequel  of  failure  of  the  right  ventricle 
from  any  cause,  chiefly  mitral  and  pulmonary  valvular  affections  or  lung 
diseases,  including  asthma.  It  gives  rise  to  the  usual  signs  of  backward 
pressure,  viz.,  dilated  veins  in  the  neck  with  auricular  and  ventricular 
pulsation  therein,  nutmeg  liver,  pulsation  of  the  liver,  enlarged  spleen,, 
ascites,  anasarca  and  cardiac  kidneys.  The  murmur  is  systolic,  loudest  at 
the  junction  of  the  fifth  right  cartilage  with  the  sternum,  conducted  upward 
along  the  left  edge  of  the  sternum,  outward  to  the  right  and  toward  the 
apex,  being  gradually  lost  as  it  nears  the  apex  and  accentuated  again  by  the 
mitral  regurgitant  murmur,  if  there  is  mitral  incompetence.  In  the  few 
cases  in  which  it  is  heard  behind,  it  is  conducted  to  the  right  of  the  spine. 

Aortic  Stenosis  is  rarely  found  in  a  pure  form.  It  is  occasionally  con- 
genital. In  the  acquired  type  it  is  generally  associated  with  aortic  regur- 
gitation. Mitral  regurgitation  is  a  common  sequel,  either  due  to  secondary 
dilatation  of  the  ventricle  or  an  associated  endocarditis  of  the  mitral  valve. 
The  murmur  is  often  heard  over  the  back,  louder  over  the  upper  than  the 
lower  dorsal  vertebrae,  the  reverse  of  what  is  the  case  in  the  murmur  of 
mitral  regurgitation.  Aortic  regurgitation  is  exceptional  as  an  isolated 
lesion  in  early  life.  Seiffert  has  noted  it  at  the  age  of  18  months.  Two  cases 
have  been  under  my  care.  The  physical  signs  and  course  are  the  same  as  in 
later  life,  except  in  so  far  as  the  lesion  is  not  a  progressive  degenerative  one 
and  good  compensation  may  be  established  and  maintained. 

Prognosis  in  Heart  Disease. — Much  too  grave  a  view  has  been  taken 
in  the  past,  and  indeed  is  still  prevalent,  of  the  serious  outlook  in  all  forms- 
of  cardiac  disease.  Both  acute  endocarditis  and  pericarditis  are  more  likely 
to  end  fatally  in  children  than  in  adults,  because  of  the  myocarditis  which  is 
so  often  present  in  addition  and  the  consequent  tendency  to  dilatation  and 


Acquired   Heart    Disease.  191 

cardiac  failure.  The  cardiac  muscle  has  not  the  powers  of  resistance  to 
strain  which  it  attains  in  later  life.  Children  succumb  during  an  acute 
attack  from  rapid  dilatation.  Or  gradual  dilatation,  with  cardiac  failure 
and  dropsy,  may  ensue  within  a  few  months.  Similarly  the  prognosis  in 
rheumatic  fever  is  more  grave  on  account  of  the  liability  to  myocarditis  and 
endocarditis.  The  possibility  of  subsequent  attacks  makes  the  prospect 
worse,  for  each  illness  is  likely  to  accentuate  the  cardiac  mischief.  Endocar- 
ditis in  chorea  is  not  of  serious  import.  The  duration  and  severity  of  the 
chorea  do  not  appear  to  influence  the  severity  of  the  endocarditis. 

As  a  general  rule  the  prognosis  of  valvular  disease  is  less  serious  than  in 
adults.  Before  puberty  compensation  is  much  more  readily  established 
and  does  not  break  down.  High  arterial  tension  is  comparatively  very  rare 
in  early  life.  Even  children,  who  have  presented  serious  symptoms  and  had 
several  valves  involved,  may  recover  and  lead  a  long  and  active  life.  A  boy, 
aged  14,  developed  double  aortic  and  mitral  regurgitant  murmurs  during  an 
attack  of  rheumatic  fever.  He  subsequently  lived  an  active  life  at  the  bar, 
bicycled  freely,  and  in  spite  of  hard  drinking  bouts,  with  mania  a  potu, 
lived  to  48  years  of  age.  Compensation  in  childhood  is  not  likely  to  break 
down  from  severe  mental  strain  or  emotional  distress.  Physical  strain  is  less 
severe,  and  the  common  causes  of  cardiac  and  arterial  degeneration,  syphilis 
and  chronic  alcoholism,  are  wanting. 

If  hypertrophy  cannot  take  place  at  a  rate  equivalent  to  that  of  bodily 
growth,  the  prognosis  is  bad.  An  adherent  pericardium  is  of  very  grave 
import  and  must  be  regarded  as  the  most  serious  cardiac  affection  of  early 
life.  The  heart  cannot  hypertrophy  efficiently  and  breaks  down  at  the 
periods  of  rapid  growth,  notably  at  puberty.  This  is  a  critical  time  of  life 
in  most  cardiac  cases,  for  compensation  constantly  remains  good  until  then. 
All  lung  affections,  by  throwing  an  extra  strain  on  the  musculature  of  the 
heart,  aggravate  valvular  lesions  ;  so,  too,  anaemia  and  any  prolonged  illness 
by  their  effect  on  the  cardiac  muscle.  A  fatal  result  may  ensue  from  wasting 
and  increasing  weakness,  with  few  or  no  signs  of  backward  pressure.  Dropsy, 
albuminuria  and  cardiac  irregularity  may  all  be  absent. 

In  valvular  disease  the  prognosis  depends  on  the  cause,  the  valves 
and  number  of  valves  affected,  the  nature  of  the  lesion,  the  character  of  the 
murmur,  the  effects  on  the  heart  and  circulation,  and  the  effect  on  growth. 
Is  the  lesion  traumatic? — i.e.,  due  to  injury,  strain  or  an  acute  disease  which 
sooner  or  later  comes  to  an  end.  If  so,  the  primary  mischief  ceases  as  an 
active  process,  although  the  mischief  already  done  remains.  This  is  the 
usual  position  in  childhood.  Rheumatic  fever  is  the  common  cause  and 
ceases.  The  valves  or  orifices  are,  however,  liable  to  further  contraction,  or 
to  secondary  infection  and  infective  endocarditis.  In  congenital  disease  the 
mischief  is  not  progressive  and  the  whole  question  of  prognosis  comes  to 
depend  on  the  other  factors  mentioned. 

The    prognosis    of    stenosis    is    always    more    grave    than  that    of 


492  Chapter   XLIL 

incompetence,  especially  at  the  auriculo-ventricular  orifices.  Mitral  stenosis 
causes  less  distress  than  incompetence,  but  the  heart  is  more  liable  to 
break  down  under  extra  strain  and  there  is  greater  liability  to  embolism. 
The  tendency  of  stenosis  is  to  gradual  increasing  obstruction,  actual  or 
relative,  for  the  orifice  cannot  grow  with  the  heart.  In  dealing  with  mitral 
incompetence  we  have  to  decide  whether  it  is  structural,  due  to  partial 
destruction  or  contraction  of  valves,  or  dependent  upon  general  dilatation  of 
the  cavities  and  orifices.  A  structural  defect  is  more  serious  than  relative 
incompetence.  Sometimes  the  murmur  of  mitral  incompetence  is  replaced 
by  that  of  stenosis,  by  reason  of  gradual  contraction  of  the  orifice.  If  the 
regurgitant  murmur  is  not  heard  well  in  the  interscapular  region  and  is  not 
conducted  down  the  vertebrae  at  all,  the  prognosis  is  good,  no  matter  how 
loud  it  may  be  at  the  apex.  But  if  it  is  heard  all  down  the  spine  to  the 
lumbar  region,  the  damage  to  the  valves  is  considerable  and  the  outlook  is 
more  grave.  Simple  loudness  is  of  much  less  serious  import  than  con- 
duction. Aortic  disease  is  more  serious  than  mitral  and  may  prove  suddenly 
fatal.    Few  cases  live  beyond  puberty. 

Endocardial  murmurs  due  to  anaemia  or  dilatation  will  disappear.  That 
of  true  endocarditis  may  slowly  disappear,  and  possibly  remain  per- 
manently absent  or  reappear  under  strain  in  later  life.  Temporary  dis- 
appearance during  convalescence,  the  murmur  returning  when  the  child 
gets  up,  is  of  dubious  outlook  if  it  is  truly  valvular  in  origin  and  not 
functional. 

The  amount  of  hypertrophy,  with  or  without  dilatation,  is  the  best 
measure  of  the  magnitude  of  the  lesion,  provided  the  duration  is  taken 
into  consideration.  It  is  the  proof  that  compensation  has  been  more  or 
less  completely  attained.  If  the  hypertrophy  is  very  great,  it  is  not  very 
likely  to  be  lasting,  for  the  more  a  muscle  exceeds  its  normal  bulk,  the 
more  difficult  is  it  to  maintain  its  normal  nutrition  and  functional  activity. 
Dilatation,  if  it  has  existed  for  some  time  and  does  not  improve  at  once 
under  treatment,  is  a  proof  that  compensation  has  broken  down  and  may 
not  be  regained.  The  effect  on  the  circulation,  arterial  and  venous,  and  the 
consequent  changes  in  nutrition  of  distant  organs  and  the  body  generally, 
and  the  presence  of  dropsical  effusions,  must  also  be  considered.  General 
improvement  in  nutrition  and  gain  in  weight  are  good  signs.  Malnutrition 
is  a  fair  measure  of  the  incapacity  of  the  heart  for  its  proper  functions. 

Compensation  must  be  maintained  as  well  as  produced,  so  we  must 
further  consider  whether  the  personal  and  social  conditions  of  the  patient 
are  favourable  to  healthy  cardiac  nutrition.  Favourable  features  are  youth, 
a  family  tendency  to  longevity,  equable  temperament,  strong  will,  and  the 
absence  of  hereditary  tendency  to  disease.  The  occupation  and  mode  of 
life  shoidd  be  such  that  the  patient  can  regulate  at  will  the  amount  of  work 
and  rest,  changes  of  climate,  diet,  and  freedom  from  worry  and  excitement. 
Out-of-door  exercise  is  of  the  utmost  importance  as  long  as  it  does  not 


Acquired   Heart    Disease.  493 

cause    pain,    palpitation,    dyspnoea,    anorexia    and   sleeplessness.      These 
children  must  not  be  brought  up  as  chronic  invalids. 

The  prognosis  is  particularly  bad  if  a  temperature  persistently  hectic 
in  type  or  irregular  and  an  enlarged  spleen  indicate  infective  endocarditis  ; 
and  if  there  are  frequent  severe  attacks  of  cardiac  pain. 

Treatment. — The  subjective  symptoms  of  heart  disease  are  constantly 
absent.  When  present  they  are  commonly  due  to  cardiac  failure  and 
include  pallor,  headache,  dyspepsia,  high  colour,  blueness  of  the  extremities, 
dyspnoea,  palpitations,,  pulmonary  catarrh  and  so  on,  according  to  the 
nature  of  the  mischief.  The  child  is  often  indolent,  irritable  and  capricious. 
In  almost  all  cases  the  condition  of  the  myocardium  is  the  main  indication 
for  treatment,  because  of  its  great  liability  to  dilatation  during  acute  car- 
ditis and  for  a  considerable  time  afterwards.  Therefore,  prolonged  rest  is 
the  first  and  most  cardinal  measure  in  treatment.  It  should  be  continued  for 
1-3  months  after  acute  symptoms  have  subsided  and  compensation  has- 
been  established.  As  a  rule  children  are  allowed  up  much  too  soon.  Special 
care  is  needed  at  puberty  on  account  of  the  extra  strain  thrown  on  the  heart 
bv  growth  and  development.  The  chief  factors  to  estimate  in  the  applica- 
tion of  remedial  measures  are  the  nutrition  and  functional  power  of  the 
heart  muscle,  the  nature  of  the  mischief  and  the  valves  affected,  the 
idiosyncrasy  and  environment  of  the  child,  the  irresponsibility  of  childhood, 
and  the  difficulty  in  securing  the  co-operation  of  the  parents  as  soon  as  the 
troublesome  symptoms  have  subsided. 

Accurate  diagnosis  is  of  supreme  importance.  A  murmur  is  not  always- 
a  sign  of  valvular  disease  and  some  of  the  worst  forms  of  heart  disease  have 
no  murmur.  Nor  is  digitalis  always  required  when  a  murmur  is  present. 
Do  not  give  heart  stimulants,  if  recumbency  alone  is  sufficient  or  after- 
compensation  is  established.  Use  it  carefully  in  small  doses,  for  large  ones- 
may  exhaust  and  injure  a  dilated  feeble  heart.  Digitalis  and  strophanthus 
should  be  tried  alternately  to  find  out  which  suits  the  child  best.  Stro- 
phanthus is  often  the  more  efficacious  in  stenosis  and  bad  dilatation 
Strychnia  is  a  useful  adjuvant  but  cannot  be  relied  on  alone.  In  mitral 
stenosis  digitalis  is  often  beneficial,  if  given  for  a  few  days  at  a  time.  It 
should  not  be  given  in  aortic  regurgitation,  except  for  failure  of  compensa- 
tion and  then  the  child  must  be  kept  in  bed  under  strict  observation. 
Drugs  are  most  efficacious  if  engorgement  of  the  right  side  of  the  heart  is 
first  relieved  by  dry  cupping,  leeches  or  venesection.  As  soon  as  compen- 
sation is  fairly  well  established,  give  iron  tonics. 

Subsequently  rely  on  good  diet  and  hygiene  to  maintain  cardiac  and 
general  nutrition.  Regulate  the  amount  and  character  of  the  exercise.  In 
any  case  in  which  the  myocardium  has  been  affected  or  the  endocarditis 
well  marked,  only  allow  walking  exercise  on  level  ground  for  3-12  months  ; 
and  after  this,  minor  gymnastics,  hill  climbing  and  bicycling  on  the  level. 
Running,  swimming,  and  prolonged  athletic  or  competitive  games  must  be 


494  Chapter   XLII. 

forbidden.  Some  of  these  children  may  be  allowed  to  go  to  school,  but  such 
permission  must  only  be  given  after  the  most  careful  consideration  of  all 
the  factors  in  the  case.  Tea,  coffee,  alcohol  and  tobacco  are  contra- 
indicated.  Nervous  excitement  must  be  guarded  against.  If  good  com- 
pensation has  been  maintained  for  some  years,  the  child  can  live  pretty 
much  the  same  life  as  its  healthy  comrades,  especially  if  the  lesion  is  only  a 
mild  degree  of  mitral  regurgitation.  It  must  be  carefully  watched  for  signs 
of  cardiac  strain,  viz.,  anorexia,  impaired  nutrition,  aneemia,  dyspepsia, 
cough  and  shortness  of  breath. 

Cardiac  failure,  due  to  weakness  of  the  muscle,  requires  rest  and  tonic 
treatment.  If  it  is  associated  with  backward  pressure,  enlargement  of  the 
liver  and  congestion  of  the  lungs,  increase  the  power  of  the  heart  by 
strychnia,  mix  vomica,  digitalis,  squills,  strophanthus,  convallaria  or 
caffeine.  Mercury  is  most  beneficial  for  the  relief  of  congestion,  as  a  diuretic 
and  a  mild  purgative.  Strong  purgatives  and  diaphoretics  are  too  severe 
•remedies  and  only  of  temporary  benefit. 

Diuretin  grs.  2-10,  four  times  daily,  sometimes  succeeds  when  digitalis 
fails.  One  of  the  first  signs  of  the  benefit  of  digitalis  is  an  increase  in  the 
secretion  of  urine.  The  amount  should  be  measured  daily  and  a  marked 
increase  is  generally  found  in  3-4  days. 

Mercurials,  diuretics,  purgatives,  oxygen  inhalations  and,  possibly, 
bleeding  are  indicated  if  the  blood  is  de-oxygenated.  Subcutaneous  injec- 
tions of  strychnia  are  useful  in  cardiac  fatigue,  with  sleeplessness  and 
ilatulent  distension.  The  diet  must  consist  of  small  easily  digestible  feeds. 
Limit  the  amount  of  fluids.  Guard  against  over-feeding  and  setting  up 
■distension  of  the  stomach.  Alcohol,  in  small  frequent  doses,  is  needed  in 
acute  dilatation,  myocardial  affections  and  cardiac  failure.  Sal  volatile 
is  a  valuable  emergency  stimulant.  Morphia  or  codeia  are  perhaps  required 
for  severe  dyspnoea,  cough  and  insomnia. 

Pericarditis. — Simple,  plastic  or  "  dry  "  pericarditis,  localised  or 
affecting  the  whole  pericardium  ;  pericarditis  with  effusion  of  serum,  sero- 
pus,  pus,  fibrin  or  blood  ;  hydropericardium  and  adherent  pericardium 
■occur  in  children  in  the  same  forms  and  from  the  same  causes  as  in  adults. 
They  are  due  to  direct  extension  from  the  lungs  or  pleura,  thoracic  glands, 
myocardium,  thoracic  walls,  oesophagus,  thymus  or  inflammation  below 
the  diaphragm  ;  and  to  blood  states  or  microbial  infections,  e.g.,  rheumatic 
fever,  pyaemia,  osteomyelitis,  scarlet  fever,  nephritis,  septic  throat,  otitis 
media,  etc. 

Rheumatism  is  the  great  cause  and  for  this  reason  rheumatic  peri- 
carditis is  rare  before  the  seventh  year,  and  most  common  from  this  up  to  the 
tenth  year.  Pericarditis  in  the  newborn  is  due  to  puerperal  fever  or  other 
infective  disease  in  the  mother,  umbilical  infection  or  vaccination.  It  is 
■more  often  chronic  than  acute,  frequently  associated  with  pleurisy,  and 


Acquired  Heart    Disease.  495 

usually  fatal.  Purulent  pericarditis  is  set  up  by  streptococci,  staphylococci, 
the  pneumococcus  or  the  bacillus  coli.  The  tuberculous  form  has  been 
described  above  (p.  487).  Pericardial  effusion  associated  with  pneumonia 
or  empyema  is  nearly  always  purulent.  A  primary  pneumococcal  form 
may  occur.  Poynton  (1908)  analysed  100  fatal  cases  from  various  sources. 
Of  these  83  were  under  4  years  of  age  ;  two-thirds  from  1-3  years  old.  One 
possibly  was  primary.  Empyema  accounted  for  60  per  cent.,  either  by 
direct  extension,  or  a  secondary  or  simultaneous  blood  infection  ;  and 
40  per  cent,  were  associated  with  acute  pleurisy  or  pneumonia.  The 
frequency  of  pneumococcal  pericarditis  under  4  years  of  age  is  a  striking 
contrast  to  the  rarity  of  the  rheumatic  variety,  and  is  to  be  expected  on 
account  of  the  susceptibility  to  pneumococcal  infection  in  early  life. 

Anatomically  there  are  found  a  few  flakes  of  fibrino-pus  and  a  little 
turbid  fluid  ;  a  flbrino-plastic  exudation,  much  as  is  seen  in  the  rheumatic 
affection  ;  creamy  pus  ;  or  a  thickened  pericardium  and  inspissated  pus. 
In  a  girl,  aged  11  years,  the  pericardium  was  thick,  velvety,  and  con- 
tained half  a  pint  of  thin  streptococcal  pus.  Pleural  adhesions  were  present 
at  the  left  base  and  over  the  whole  right  lung.  There  was  no  endocarditis 
and  no  local  source  of  infection  discoverable.  Her  illness  lasted  14  days 
and  was  characterised  by  high  fever,  a  little  swelling  of  the  right  knee  and 
left  ankle,  sordes,  dilated  pupils,  dyspnoea,  delirium,  hallucinations  of 
vision  and  semi-consciousness.  A  more  typical  case  was  that  of  a  boy,  21 
months  old,  who  was  admitted  with  general  bronchitis,  cough  and  "  bad 
breathing  "  of  2  weeks  duration.  The  chief  symptoms  were  attacks  of 
collapse  and  lividity,  subnormal  temperature  towards  the  end,  very  bad 
colour,  frequent  vomiting  and  an  imperceptible  pulse.  The  pericardium 
was  covered  with  a  thick,  pile-like  deposit  of  lymph  and  contained  much 
sero-pus.  Two  small  collections  of  greenish  pus  were  present  in  the  pleural 
cavity  on  the  left  side. 

Physical  Signs. — The  signs  of  dry  pericarditis  are  often  limited  to 
friction,  which  may  be  felt.  It  is  called  "Latent"  when  only  found  by 
chance  on  examination,  rarely  so  in  children.  Friction  varies  in  degree, 
character  and  extent.  Its  maximum  intensity  is  at  the  base  of  the  heart 
in  the  third  and  fourth  interspaces,  sometimes  in  the  second,  on  the  left  side 
near  the  sternum.  Occasionally  it  is  limited  to  the  apex  and  may  simulate 
a  presystolic  murmur.  It  is  localised  over  the  place  of  production.  If  the 
inflammation  starts  behind,  friction  is  not  heard  until  it  has  spread 
anteriorly.  The  spread  is  often  very  rapid.  At  first  the  sound  may  be 
systolic.  More  generally  it  has  a  to-and-fro  character  like  a  double  aortic 
murmur.  It  is  increased  by  the  pressure  of  the  stethoscope,  altered  by 
change  of  posture,  louder  on  sitting  up,  sounds  much  nearer  the  ear  than  an 
aortic  murmur,  and  is  not  conducted  beyond  the  cardiac  area.  Sometimes 
there  is  a  single  or  double  thrill.  If  the  heart  muscle  is  involved,  signs  of 
cardiac  insufficiency  develop. 


496  Chapter  XLII. 

Fluid  is  often  present  as  well,  sometimes  localised.  Large  effusions  are 
uncommon  in  rheumatic  fever.  As  the  fluid  increases  in  quantity  the 
physical  signs  alter.  The  precordium  bulges.  The  apex  is  elevated  and 
perhaps  not  palpable.  It  may  alter  with  change  in  position  and  be  only 
palpable  in  the  genu-pectoral  posture.  The  impulse  is  diffused,  wavy  and 
indistinct.  Friction  may  disappear,  through  separation  of  the  two  layers 
of  the  pericardium  by  the  fluid  ;  or  it  may  be  increased  in  the  supine  posture, 
through  the  heart  being  floated  up  more  in  contact  with  the  chest  wall. 
The  left  side  of  the  chest  is  enlarged  and  its  respiratory  movements  deficient 
or  absent. 

In  small  effusions  there  may  be  no  change  in  the  area  of  cardiac  dulness. 
Dulness  in  the  fifth  right  interspace  is  often  the  first  sign,  for  in  early  stages 
the  fluid  collects  in  the  lower  part  of  the  sac,  especially  at  the  right  edge  of 
the  sternum.  The  cardio-hepatic  angle,  normally  a  right  angle,  becomes 
obtuse  through  displacement  of  the  lung.  In  large  effusions  the  shape 
of  the  dulness  is  that  of  a  trapezium  with  the  base  downwards.  It  extends 
to  the  second  rib  and  the  fourth  and  fifth  right  interspaces,  rendering  the 
cardio-hepatic  angle  still  more  obtuse  and  the  right  border  of  the  heart 
convex.  It  extends  below  and  to  the  left  of  the  apex  and  of  the  left  edge 
of  the  heart.  Difficulty  arises  in  apportioning  its  proper  share  in  the  dulness 
to  the  dilatation  of  the  heart  so  often  present.  There  is  an  abrupt  transition 
from  the  dull  area  to  the  resonant  lung.  Marked  resistance  is  noted  on 
percussion. 

The  heart  sounds  are  progressively  muffled,  weak  and  distant,  embryo- 
cardial  in  type,  pendulum-like ;  and  there  is  often  a  murmur  indicative 
of  endocarditis.  Compression  of  the  lower  lobe  of  the  left  lung  produces 
a  patch  of  dulness,  somewhat  quadrilateral  in  shape,  and  bronchial  breathing 
or  absent  breath  sounds  near  the  angle  of  the  left  scapula.  It  may  be  mis- 
taken for  consolidation.  Occasionally  Skodaic  resonance  is  present  over 
the  upper  part  of  the  lung. 

Symptoms. — The  onset  is  insidious,  especially  in  the  rheumatic 
affection.  Arrhythmia,  undue  frequency  of  the  pulse,  slight  fever,  rather 
an  increased  rate  of  breathing,  precordial  pain  and  palpitations  may  be 
present ;  perhaps  only  dyspnoea  and  slight  fever  ;  or  merely  friction, 
limited  in  extent  and  found  by  chance  on  examination.  A  few  cases  show 
intense  pain,  urgent  dyspnoea,  high  fever,  sleeplessness  and  delirium.  If 
there  is  a  severe  attack  with  considerable  effusion,  we  find  an  anxious  look, 
dusky  pallor,  dilating  also  nasi,  and  dyspnoea  or  orthopncea,  a  most  important 
sign  and  out  of  all  proportion  to  the  state  of  the  lungs,  temperature  and 
pulse  rate.  It  is  partly  due  to  pain,  partly  to  congestion  of  the  lungs.  It 
may  be  so  severe  that  the  patient  assumes  weird  positions,  such  as  the 
genu-pectoral,  and  is  only  able  to  sleep  in  that  posture.  Cough  is  short, 
dry,  frequent  and  distressing.  One  patient  exhibited  constant  yawning 
and  others  have  shown  this  to  a  less  extent.    Pain  is  moderate,  occasionally 


Acquired  Heart    Disease.  497 

severe,  and  localised  over  the  cardiac  area  if  due  to  friction.  It  may  be 
induced  or  increased  by  precordial  or  epigastric  pressure,  which  may  bring 
on  nausea  or  vomiting.  It  often  decreases  as  the  effusion  increases,  and  is 
at  times  due  to  acute  dilatation.  The  large  veins  in  the  neck  may  be  much 
distended.  The  pulse  is  very  frequent,  up  to  180,  quick,  small  and  of  low 
tension,  perhaps  very  irregular  and  almost  running.  A  pulsus  paradoxus 
is  rare,  except  in  mediastino-pericarditis.  Moderate  fever,  perhaps  aphonia 
and  dysphagia,  and  the  usual  signs  of  general  malaise  are  present.  Delirium 
is  fairly  common  in  rheumatic  cases  with  hyperpyrexia.  Acute  mania  has 
been  noted. 

A  purulent  effusion  is  suggested  by  symptoms  unusual  in  the  course  of 
acute  lung  disease,  pleurisy  or  empyema.  Its  course  is  acute,  subacute  or 
chronic,  varying  with  the  nature  of  the  illness.  It  may  come  on  quite  in- 
sidiously during  the  convalescent  stage  of  pneumonia.  The  chief  signs  are 
serious  illness,  lividity  or  livid  pallor,  panting,  dyspnoea,  orthopncea,  very 
frequent  pulse  and  syncopal  attacks,  and  irregular  attacks  of  fever  with 
feeble  heart  action.  The  temperature  is  not  characteristic.  It  is  generally 
irregular,  with  sudden  falls  below  normal  and  attacks  of  collapse.  The  pulse 
rate  is  often  150-180,  out  of  proportion  to  the  discomfort  and  distress,  and 
varies  with  the  rate  of  breathing.  Flabbiness,  wasting,  cyanosis,  and 
oedema  of  the  legs  and  feet  may  be  present.  Friction  is  usually  absent. 
At  times  there  is  neither  cardiac  nor  respiratory  distress,  and  the  signs  may 
be  limited  to  increased  cardiac  dulness  and  decreased  loudness  of  heart 
sounds.  The  heart  sounds  are  not  always  enfeebled.  Nor  is  cardiac  dulness 
invariably  increased  for  the  amount  of  effusion  may  be  small,  and  is  rarely 
large  in  young  children.  In  small  effusions  the  apex  may  be  normally 
situated.  In  chronic  cases  there  may  be  merely  wasting  and  asthenia  ; 
sometimes  vomiting  and  diarrhoea  ;  or  cough,  pleural  pain  and  wasting. 
In  young  infants  a  small  purulent  effusion  may  only  be  suggested  by  severe 
cardiac  weakness  of  no  apparent  causation. 

Diagnosis. — Increased  dulness  suggests  effusion  or  dilatation.  The 
chief  difficulty  is  in  differentiating  acute  dilatation  from  effusion,  especially 
when  they  are  conjoined  or  if  the  dilatation  is  associated  with  pleural 
effusion,  with  or  without  pneumonia.  The  position  of  the  apex  beat  is  a 
most  valuable  diagnostic  point.  Orthopncea,  weak  apex  beat,  feeble  sounds 
and  increased  dulness  are  the  chief  signs  of  effusion.  Peritonitis  may  be 
suspected,  if  the  pain  is  referred  to  the  abdomen.  Mediastinal  tumours 
and  pneumonia  are  occasional  sources  of  difficulty.  The  nature  of  the  fluid 
can  be  definitely  settled  by  exploration.  Haernorrhagic  effusions  are  due 
to  purpura,  scurvy  and  other  blood  affections,  and  to  tuberculosis.  Under 
4  years  of  age  the  effusion  is  likely  to  be  purulent  because  of  the  liability 
to  pneiimococcal  infection,  pneumonia,  empyema  and  pyaemia.  Later  in 
life  it  is  more  apt  to  be  fibrinous  or  sero-fibrinous.  A  scanty  purulent 
effusion  may  give  rise  to  no  special  signs  or  symptoms.     It  should  always 

2  K 


498  Chapter  XLII. 

be  suspected  in  a  child  dying  from  empyema.  A  large  one  may  be  so 
extensive  as  to  simulate  empyema  and  be  opened  under  that  impression. 
Pus  is  also  indicated  by  the  serious  general  condition  of  the  patient, 
attacks  of  lividity  or  collapse,  and  the  presence  of  some  source  of  pyeemic 
infection.  In  the  absence  of  hyperpyrexia,  the  occurrence  of  delirium  and 
maniacal  symptoms  is  to  my  mind  suggestive  of  pus  ;  and  other  signs 
are  progressive  anaemia,  wasting,  and  acute  tenderness  over  the  whole  lower 
end  of  the  sternum.  In  spite  of  these  iudications,  it  is  by  no  means  un- 
common for  the  existence  of  pyo-pericardium  to  be  only  recognised  at  the 
autopsy.  On  account  of  the  absence  of  a  murmur  attention  is  not  drawn 
to  the  heart ;  and  the  presence  of  serious  disease  explaining  the  illness  leads 
to  the  effusion  being  overlooked.  Bronchitis  and  patches  of  purulent 
pleurisy  may  be  mistaken  for  broncho-pneumonia,  although  pyo-pericardium 
is  present.  Its  occurrence  in  marasmic  infants  is  frequently  ascribed  to 
tuberculosis. 

Prognosis. — A  simple  rheumatic  pericarditis  is  not  often  fatal,  for  it 
rarely  leads  to  copious  effusion  in  children.  The  prognosis  is  serious  for 
complete  recovery  is  rare.  It  is  often  associated  with  endocarditis,  or  myo- 
carditis which  may  end  fatally  ;  or  results  in  adhesions,  in  which  case  the 
prognosis  is  that  of  adherent  pericardium.  The  frequent  pulse  and 
respiration,  anaemia,  wasting  and  vomiting  are  bad  signs,  due  to  myo- 
carditis rather  than  pericarditis.  Purulent  pericarditis  is  almost  invariably 
fatal,  sometimes  from  empyema  or  meningitis.  A  few  cases  have  recovered 
after  treatment  by  incision  and  drainage. 

Treatment. — In  dry  pericarditis  and  rheumatic  infection  salicylates  are 
given.  Small  doses  of  tr.  opii,  quartis  horis,  relieve  the  excited  action  of 
the  heart.  Apply  to  the  precordium  cold,  mesotan,  methyl-salicylate, 
lin.  iodi,  turpentine  stupes  or  a  mustard  leaf.  Small  flying  blisters  and 
even  leeches  are  occasionally  permissible  in  older  children.  The  pro- 
duction of  blisters  or  local  soreness  interferes  with  examination  of  the 
heart.  General  treatment  consists  of  absolute  rest  in  the  recumbent 
posture,  avoidance  of  all  exertion  and  excitement,  light  diet,  and  stimulants 
if  there  is  much  interference  with  the  heart's  action.  Stimulants,  such  as 
alcohol,  strychnia  and  ether,  are  necessary  in  effusion.  Avoid  digitalis  for 
it  prolongs  diastole,  permits  dilatation  of  the  cavities,  and  adds  to  the 
difficulties  of  a  heart  already  hampered  in  its  action  by  the  mechanical 
effects  of  effusion.  Diuretics  and  purgatives  are  of  little  value  in  its  relief. 
The  question  of  aspiration  or  drainage  arises  if  there  is  much  fluid.  It  is 
rarely  necessary  in  rheumatic  pericarditis,  though  it  is  probable  that  it 
could  be  used  more  freely  with  advantage.  The  indications  for  operation 
are  a  large  effusion,  marked  cyanosis,  great  dyspnoea  and  a  frequent,  weak, 
irregular  pulse. 

Exploration  must  not  be  undertaken  lightly.  It  is  quite  easy  to  wound 
the  heart,  an  injury  recognised  at  once  by  the  movement  of  the  needle. 


Acquired   Heart    Disease.  499 

Fortunately  this  is  not  a  serious  blunder.  In  fact  the  ventricle  has  been 
aspirated  with  distinct  advantage  in  dilatation.  A  slight  injury  to  the 
ventricle  is  soon  closed,  owing  to  the  peculiar  arrangement  of  the  muscular 
fibres.  A  wound  of  the  auricle  may  cause  uncontrollable  haemorrhage  and 
death  from  hoemo-pericardium.  Sudden  death  has  also  resulted  from 
inhibition.  Other  risks  are  the  wounding  of  a  large  vessel  and  infection 
of  the  pleura  by  septic  material  from  the  pericardium.  Simple  paracentesis 
may  prove  negative  from  a  diagnostic  point  of  view,  although  a  small 
amount  of  pus  is  present. 

It  is  sometimes  advised  that  the  exploring  needle  should  not  be  used 
and  that  incision  and  resection  must  be  adopted  even  for  diagnosis.  This 
is  a  counsel  of  timidity.  With  reasonable  care  exploration  is  safe  and 
satisfactory,  and  can  be  used  in  circumstances  which  would  not  justify 
recourse  to  the  more  serious  operation.  For  exploration  or  aspiration  only 
a  local  anaesthetic  is  needed  ;  for  intercostal  incision,  resection  and  drainage 
a  general  one  is  required.  Use  a  small  needle  1|  in.  long,  attached  to  a 
rubber  tube  and  syringe.  The  safest  place  for  its  insertion  is  between  the 
apex  and  the  extreme  limit  of  dulness  in  the  axilla  (S.  West)  although  the 
pleura  is  punctured.  Avoid  the  site  of  friction.  Push  the  needle  in  slowly 
and  stop  as  soon  as  the  heart  is  felt.  Drain  off  fluid  slowly  by  syphonage, 
attaching  a  larger  tube. 

In  choosing  the  site  of  operation  bear  in  mind  the  position  of  the 
heart,  for  it  may  float  up  in  approximation  with  the  chest  wall.  Consider 
too  the  position  of  the  internal  mammary  artery  and  that  the  relations  of 
the  right  pleura  to  the  thoracic  walls  are  not  altered  by  pericardial  effusion. 
It  extends  well  to  the  middle  of  the  sternum,  perhaps  to  the  left  edge.  The 
site  depends  partly  on  the  physical  signs.  Some  surgeons  recommend  the 
fourth  or  fifth  left  space,  as  close  to  the  sternum  as  possible,  trying  the  fifth 
first,  and  if  both  fail  then  trying  1|  in.  from  the  left  edge  of  the  sternum  ; 
or  the  fourth  and  fifth  right  spaces,  although  the  pleura  is  certain  to  be 
punctured  ;  or  the  sixth  space  in  the  nipple  line  below  the  apex  if  it  is 
palpable. 

The  site  of  incision  should  be  chosen  with  a  view  to  securing  efficient 
drainage  at  the  time  and  when  the  sac  contracts.  There  is  no  serious 
•objection  to  draining  through  the  pleural  cavity,  for  the  pericardium  rapidly 
becomes  adherent  after  the  evacuation.  Cases  opened  as  empyemata  have 
done  well.  The  incision  should  extend  from  the  middle  of  the  sternum  over 
the  fifth  left  costal  cartilage  to  its  junction  with  the  rib  ;  the  cartilage  is 
•excised,  and  the  internal  mammary  vessels  ligatured  in  two  places  and 
•divided  ;  the  fibres  of  the  triangularis  sterni  are  separated,  and  the  pleura 
identified  and  pushed  aside  ;  the  pericardium  exposed,  and  an  incision  made 
•downward  and  outward  from  the  sternum  ;  the  edges  of  the  incision  are 
stitched  to  the  soft  parts.  Or  a  vertical  incision  is  made  and  the  sixth 
•cartilage,  perhaps  the  seventh  also  or  the  seventh  and  part  of  the  gladiolus, 


500  Chapter  XLII. 

is  removed.  Others  recommend  an  incision  in  the  fourth  left  space, 
beginning  1  in.  from  the  sternum  and  reaching  to  the  apex.  West  advises 
incision  in  the  apex  region  and  no  resection  ;  and  probably  this  is  the  safest 
and  best  mode  of  operation.  A  large  rubber  tube  is  inserted.  The  cavity 
is  irrigated  daily  with  warm  fluid,  provided  there  is  a  free  exit  for  the  fluid,, 
and  the  patient  is  turned  on  the  side  or  face,  if  not  too  ill,  to  facilitate  drain- 
age. The  tube  is  removed  in  3-4  days  if  the  effusion  is  serous.  The  mortality 
is  about  60  per  cent.  It  depends  on  the  cause  ;  is  least  in  pneumococcal 
cases  and  highest  in  pyemic  ones,  even  though  the  pericardium  becomes- 
adherent  a  few  days  after  the  operation.  Aspiration  is  much  more  dan- 
gerous than  open  incision. 

Mediastino-pericarditis  was  described  by  Griesinger  in  1854.  Cases. 
have  been  reported  under  the  names  of  indurative  mediastino-pericarditis, 
obliterative  pericarditis  with  ascites,  pericarditic  pseudo-cirrhosis  of  the 
liver,  polyserositis,  and  "  zuckergussleber  "  (Curschmann).  It  is  a  chronic- 
inflammation  of  the  pericardium  and  mediastinum,  insidious  in  onset,  and 
septic,  rheumatic  or  tuberculous  in  origin.  Tuberculosis  of  the  pericardium 
is  described  above  (p.  487).  The  inflammation  may  spread  from  the  glands 
to  the  mediastinum  and  thence  to  the  pericardium,  or  be  primary  in  the 
pericardium  and  not  necessarily  followed  by  mediastinitis.  Tuberculous 
cases  have  been  reported  at  the  age  of  15  months  (Sequeira)  and  2  years 
(Ashby).  Others  have  followed  specific  fevers,  notably  measles,  and 
rheumatic  pericarditis. 

The  pericardium  may  be  merely  adherent.  More  generally  it  is  very 
greatly  thickened,  fibrous  or  almost  cartilaginous.  In  a  girl,  aged  13,  it 
contained  large  calcareous  deposits  (Bennion).  It  is  universally  adherent. 
to  the  heart,  sometimes  irregularly  adherent  with  saccules  of  purulent  fluid  ; 
adherent  to  both  layers  of  the  pleura  and  the  sternum  ;  and  the  inflam- 
mation spreads  upward  around  the  great  vessels.  The  anterior  and  pos- 
terior mediastinal  tissues  are  much  thickened  and  adherent  to  the  peri- 
cardium. The  fibrous  tissue  slowly  contracts,  interferes  with  the  growth 
of  the  heart,  and  leads  to  mechanical  obstruction  to  the  return  of 
blood  to  the  heart,  enlargement  of  the  liver,  ascites,  anasarca  of  the  legs. 
and  cyanosis.  The  other  serous  membranes,  especially  the  peritoneal 
covering  of  the  liver,  may  be  involved.  The.  pathological  changes  in  the 
liver,  spleen  and  kidneys  are  those  of  venous  engorgement.  The  ventricles 
are  dilated  and  hypertrophied,  and  the  valves  usually  healthy. 

Cough,  shortness  of  breath,  giddiness  and  debility  may  be  the  first 
symptoms.  In  early  stages  the  child  is  pale  but  looks  healthy,  has  a  clean 
tongue,  and  no  undue  frequency  of  pulse  or  breathing.  Later  on  it  develops, 
swelling  of  the  face  and  legs,  coldness  and  blueness  of  the  extremities, 
persistent  cyanosis  which  is  marked  in  the  lips  and  ears,  distension  of  the 
veins  in  the  neck,  much  enlargement  of  the  liver  and  perhaps  of  the  spleen, 
increasing  ascites  and  oedema  of  the  abdominal  wall.    Inspiratory  collapse. 


Acquired   Heart    Disease.  501 

of  the  veins  in  the  neck  is  a  noticeable  sign.  The  pulse  is  frequent,  and  a 
pulsus  paradoxus  is  more  common  in  this  than  any  other  disease,  but  may 
be  present  in  acute  pericarditis  and  even  in  health.  The  symptoms  are 
chiefly  those  of  cardiac  dilatation  or  abdominal  in  character.  Alternating 
attacks  of  diarrhoea  and  constipation,  abdominal  pain,  and  pleurisy  are  not 
uncommon.  Dyspnoea  is  marked.  Albuminuria  is  usually  absent,  except 
in  late  stages.  Ascites  may  appear  before  the  anasarca.  The  heart  is  not 
always  enlarged  and  generally  presents  no  adventitious  sounds.  The 
signs  of  enlargement  may  be  present  and  extend  upward  along  the  great 
vessels,  to  the  level  of  the  second  rib  of  the  left  side. 

The  course  is  chronic.  Bosanquet's  3  patients,  boys  aged  6,  8  and  15 
years,  lived  2-3  years.  The  usual  duration  is  2-6  months.  Death  results 
from  asthenia,  diarrhoea,  broncho-pneumonia  or  other  complication.  The 
outlook  is  most  hopeful  in  cases  of  rheumatic  origin. 

It  is  liable  to  be  mistaken  for  tuberculous  peritonitis  or  cirrhosis  of  the 
liver.  Stress  must  be  laid  on  the  dilated  veins  and  their  inspiratory  collapse, 
pulsus  paradoxus,  oedema  and  ascites,  and  the  absence  of  valvular  disease. 
Hepatic  enlargement  with  persistent  pleural  effusion  in  children,  without 
obvious  cause,  is  suggestive.  The  large,  tense,  tender  liver  is  out  of  pro- 
portion to  the  venous  stasis.  Treatment  is  directed  to  symptoms.  Possibly 
potassium  iodide  may  do  good.  Paracentesis  may  be  needed  for  the  relief 
of  ascites  or  pleural  effusion. 

Adherent  Pericardium. — The  simple  form  of  adherent  pericardium, 
commonly  of  rheumatic  origin,  must  be  distinguished  from  the  preceding 
condition  of  mediastino-pericarditis,  though  there  is  no  strict  line  of  demar- 
cation. It  is  often  associated  with  adhesions  to  the  chest  wall  and  diaphragm, 
perhaps  pleurisy  and  mediastinitis.  It  has  been  found  in  the  newborn  and 
at  3  months  of  age,  but  is  rare  before  7  years.  It  is  liable  to  occur  whenever 
there  has  been  pericardial  friction  heard  in  the  course  of  illness. 

It  must  be  suspected  in  cases  of  marked  cardiac  hypertrophy,  when  the 
valvular  mischief  does  not  seem  sufficient  to  account  for  the  degree  of 
•enlargement ;  in  the  presence  of  ascites  and  anasarca,  associated  with  a 
valvular  lesion,  when  the  cardiac  impulse  is  forcible  and  the  heart  sounds 
seem  good  ;  and  in  cases  of  "  quiet  "  ascites,  in  which  hepatic  cirrhosis, 
tuberculous  peritonitis  and  malaria  can  be  excluded.  Except  the  first, 
these  conditions  are  rather  those  of  mediastino-pericarditis  than  simple 
adherent  pericardium.  Hypertrophy  due  to  chronic  interstitial  nephritis 
must  not  be  forgotten. 

The  orthodox  signs  are  often  conspicuous  by  their  absence,  and  the 
condition  may  be  quite  unsuspected  and  only  found  after  death.  It  is  on 
account  of  the  difficulty  in  excluding  mediastino-pericarditis  that  differen- 
tial diagnosis  between  the  two  affections  is  so  great.  One  of  the  most 
valuable  signs  is  an  abnormally  frequent  pulse.  If  it  remains  very  frequent 
in  spite  of  treatment,  more  frequent  than  any  cardiac  murmur  present  will 


502  Chapter  XLII. 

account  for,  and  particularly  if  there  is  no  great  hypertrophy,  it  is  almost 
certain  that  the  affection  is  present.  It  is  one  of  the  chief  causes  of 
hypertrophy  and  yet  the  large  heart  only  produces  a  frequent,  persistently 
feeble  pulse,  and  the  apex  beat  may  be  imperceptible.  Epistaxis  is  said 
by  Letulle  to  be  a  symptom. 

The  diagnosis  is  based  on  a  combination  of  some  of  the  following 
physical  signs  : — hypertrophy  of  the  heart,  weak  heart  action,  weak  and 
frequent  pulse,  marked  undulation  of  the  heart  beat,  imperceptible  apex 
beat,  absence  of  postural  changes  in  the  apex  beat,  absent  impulse  without 
increase  in  the  area  of  dulness,  and  the  usual  signs  of  cardiac  insufficiency. 
Hypertrophy  may  be  absent,  if  the  pericardium  is  universally  adherent. 
If  the  pericardium  is  adherent  to  the  chest  wall  there  is  systolic  retraction 
of  the  intercostal  spaces,  and  perhaps  the  ribs,  in  the  region  of  the  apex, 
and  even  of  the  entire  precordium.  Systolic  retraction,  limited  to  the  apex, 
is  of  no  value  for  it  occurs  in  other  affections.  There  is  no  change  in  the 
area  of  dulness  on  inspiration  or  change  of  posture,  for  the  edge  of  the 
lung  on  expansion  cannot  extend  between  the  heart  and  chest  wall.  Retrac- 
tion of  the  lower  portion  of  the  left  chest  in  the  lateral  and  posterior  aspects, 
absence  of  respiratory  movements  in  the  epigastric  triangle,  and  a  diastolic 
shock  and  rebound  may  be  present,  if  there  is  mediastinitis  and  adhesions 
of  the  pericardium  to  the  chest  wall  and  diaphragm,  for  the  diaphragm 
cannot  descend  properly.  A  presystolic  murmur  has  been  noted  in  some 
cases,  in  the  absence  of  valvular  mischief,  and  is  ascribed  to  cardiac  dila- 
tation. Other  signs,  such  as  cyanosis  of  lips  and  ears,  hepatic  enlargement 
and  ascites,  are  also  evidence  of  mediastino-pericarditis.  Thus  it  is  obvious 
how  difficult  is  the  differential  diagnosis  of  the  two  affections,  and  that 
many  of  the  signs  commonly  ascribed  to  adherent  pericardium  are  those 
of  the  more  extensive  disease. 

It  is  by  no  means  invariable  for  pericarditis  to  be  followed  by  adherent 
pericardium,  at  any  rate  not  to  an  extent  which  interferes  with  growth  and 
development.  I  have  known  a  most  prolonged  and  serious  case  apparently 
clear  up  entirely,  and  the  girl,  6  years  later,  aged  15  and  well  grown,  showed 
no  sign  of  cardiac  mischief.  Good  nutrition  and  growth  are  favourable 
signs.  Nevertheless  the  outlook  is  most  grave  and  few  patients  reach  adult 
life,  dying  from  cardiac  failure  and  asthenia,  sometimes  suddenly.  It  must 
be  regarded  as  a  more  serious  sequence  of  rheumatism  than  valvular  disease. 

Treatment  is  entirely  symptomatic,  and  that  of  cardiac  failure  on  the 
lines  described  in  the  general  treatment  of  heart  disease  (p.  493).  Resection 
of  rib  cartilages  in  the  regio  cordis  has  been  recommended,  if  there  is 
strong  retraction  of  the  ribs  indicative  of  extensive  adhesion  to  the  chest 
wall.  It  lightens  the  work  of  the  heart,  but,  even  if  successful,  is  unlikely 
to  be  of  more  than  temporary  benefit. 


CHAPTER    XLTII. 

THE    BLOOD    AND    LYMPHOID    STRUCTURES. 

The  Blood — Primary  Anosmias — The  Spleen — Anosmia  Splenica  Infantum- 
—  Splenic  Anosmia — LeuJccemia  —  Chloroma — Glandular  Affections — 
Glandular  Fever — Lymphosarcoma — Lymphadenoma —  The  Thymus — 
The  Status  Lymphaticus. 

Examination  of  the  Blood. — To  obtain  a  sample,  prick  the  lower  surface 
of  the  lobule  of  the  ear  with  a  sterile  triangular  needle.  This  area  is  very 
insensitive  and  can  be  pricked  without  waking  a  sleeping  child.  Wipe 
away  the  first  few  drops  and  do  not  use  blood  obtained  by  squeezing.  Take 
the  sample  before  a  meal,  to  avoid  error  from  the  leucocytosis  of  digestion, 
which  is  well  marked  in  infants  and  children.  Make  blood-films  by  pressing 
a  minute  portion  between  two  cover-slips,  separating  them  by  a  sliding 
movement,  and  dry  them  slowly  over  a  spirit  flame.  To  make  a  fresh 
preparation,  take  up  some  staining  fluid,  0*2  per  cent,  methylene  bhie 
(Griibler)  in  40  per  cent,  alcohol,  in  a  Thoma-Zeiss  pipette.  Mix  it  gently 
with  a  largish  drop  of  blood  on  a  glass  slide,  by  blowing  the  staining  fluid 
on  to  the  blood.  The  colour  turns  deep  green.  Put  on  a  cover-slip  and  seal 
the  edges  with  vaseline.  In  this  method  the  white  cells  are  undistorted  by 
pressure.  In  addition,  make  a  fresh  preparation  by  taking  a  minute  portion 
of  blood  on  a  cover-slip  and  inverting  it  gently  on  the  slide.  Examine  this 
at  once  for  blood-plates,  rouleaux  formation  and  fibrin  strands.  A  fair 
idea  of  the  degree  of  ansemia,  poikilocytosis  and  leucocytosis  is  at  once 
obtained. 

The  red  cells  are  counted  by  means  of  a  Thoma-Zeiss  or  Gower's 
hcematocytometer.  In  examining  for  poikilocytes  fix  the  red  cells  first 
by  osmic  acid  solution  1  per  cent.,  containing  02  per  cent,  methylene  green. 
Or  use  as  a  diluting  fluid,  Toison's  solution  (methyl  violet  0025,  sod. 
chlor.  TO,  sod.  sulphat.  8-0,  neutral  glycerine  3O0,  distilled  water  160  parts), 
filtered  before  use.  Another  good  diluting  fluid  is  Edington's,  consisting 
of  neutral  sod.  citrat.  7*5,  formalin  (40  per  cent.)  2-0,  Griibler's  dahlia  0*03, 
chloroform  m5,  water  250  parts.  Count  5  fields  of  36  squares  each,  repeat 
the  process  with  three  different  drops  of  the  diluted  blood,  and  then  take 
the  average  of  the  two  results  which  most  approximate.  For  counting 
white  cells  dilute  the  blood  with  glacial  acetic  acid  solution,  0-33  per  cent, 
strength,    Toison's    or    Edington's    fluid,    or    methylene    green    or  blue 


504 


Chapter  XLIII. 


O2-04  per  cent,  in  40  per  cent,  alcohol.  Clean  the  pipette  with  distilled 
water,  sulphuric  acid,  distilled  water,  ether,  absolute  alcohol  and  hot  air 
successively. 

For  differential  staining  use  Ehrlich-Biondi  fluid,  Ehrlich's  triple  stain 
or  acid  dahlia  solution,  Jenner's  stain,  or  eosin  and  methylene  blue,  either 
separately  or  in  the  form  of  Canon's  dye.  To  estimate  percentages  count 
1000  cells. 

Yon  Fleischl's  or  Gower's  haeruoglobinorneter  is  used  for  estimating  the 
'percentage  of  haemoglobin.  They  depend  on  colorimetric  methods  and  are 
not  very  reliable.  The  specific  gravity  gives  a  fair  estimate.  It  is  obtained 
by  letting  a  drop  of  blood  fall  into  a  mixture  of  benzol  and  chloroform  of 
specific  gravity  1059,  that  of  normal  blood.  If  it  sinks  add  more  chloroform, 
if  it  rises  to  the  surface  add  benzol.  When  the  drop  floats  like  a  bead  in  the 
mixture,  the  specific  gravity  of  the  mixture  is  the  same  as  that  of  the  blood. 
The  lower  the  specific  gravity,  the  lower  is  the  percentage  of  haemoglobin, 
and  vice  versa.  The  colour-index  is  represented  by  a  fraction,  with  numerator 
the  percentage  of  haemoglobin  and  denominator  the  percentage  of  red  cells. 
The  red  cells  are  erythrocytes,  macrocytes,  microcytes  or  poikilocytes 
according  as  they  are  normal,  larger  than  normal,  smaller  than  normal,  or 
irregular  in  shape.  Nucleated  red  cells  or  hsematoblasts  are  divisible 
according  to  size  into  normoblasts,  megaloblasts  and  microblasts.  Megalo- 
blasts  are  found  in  foetal  marrow  and  grave  forms  of  anaemia.  Microblasts 
are  rarer.  Normoblasts  resemble  ordinary  erythrocytes,  except  for  con- 
taining a  nucleus.  They  are  present  in  marrow  in  small  numbers  ;  after 
haemorrhage,  in  large  numbers.  They  are  usually  regarded  as  immature 
erythrocytes. 

The  white  corpuscles  are  non-granular  or  granular.  Their  protoplasm 
does  not  stain  with  methylene  green.  The  non-granular  cells,  usually  known 
as  Lymphocytes  or  mononuclears,  stain  with  basic  dyes.  They  are  usually 
regarded  as  the  youngest  form  of  leucocyte  and  are  divided  into  : — (1) 
■Small  lymphocytes,  consisting  of  a  round  nucleus  about  the  size  of  an  ery- 
throcyte, surrounded  by  a  narrow  zone  of  faintly  staining  protoplasm. 
The  smaller  the  nucleus,  the  more  deeply  it  stains.  They  are  said  to  grow  by 
increase  in  protoplasm  and  nucleus  into  the  next  variety.  (2)  Large 
lymphocytes  or  large  hyaline  cells,  about  twice  the  size  of  the  small  type  and 
much  paler.  The  nucleus  is  large,  stains  feebly,  and  is  surrounded  by  a 
bigger  zone  of  protoplasm.  (3)  Transitional  or  intermediate  forms  occupy  a 
position  between  the  other  two.  Some  are  large  and  oval.  Some  have  an 
indented  or  horseshoe-shaped  nucleus. 

The  granular  cells  include  : — (1)  Polymorphonuclear  cells,  sometimes 
called  polymorphs  or  polynuclears,  neutrophiles,  or  finely  granular  oxy- 
philes.  The  granules  stain  faintly  with  acid  and  neutral  dyes,  the  latter 
being  really  faintly  acid.  They  are  regarded  as  the  full-grown  type  of 
leucocyte.      They  are  intermediate  in   size    between  a   small   and  large 


The  Blood  and  Lymphoid  Structures.  505 

lymphocyte,  and  contain  many  fine  granules  and  an  irregular  or  multipartite 
nucleus,  situated  in  the  centre  of  the  cell  and  staining  deeply  but  unevenly 
with  basic  dyes.  The  granules  surround  the  nucleus,  and  neither  the 
protoplasm  nor  the  granules  stain  with  methylene  blue.  (2)  Eosinophils, 
cells  resembling  the  last  variety  except  in  the  granules.  They  are  coarsely 
granular,  oxyphile  cells,  regarded  as  old  or  overripe  leucocytes.  The 
granules  are  large  and  stain  with  Ehrlich-Biondi  fluid,  eosin,  acid  fuchsin 
and  other  acid  dyes,  and  greenish  with  methylene  blue.  The  protoplasm 
is  stained  by  the  last  dye.  Eosinophilia  is  found  in  infants,  bronchitic  asthma, 
some  skin  diseases,  and  at  times  in  leukaemia,  bone  disease,  worms,  gonor- 
rhoea and  at  puberty  in  girls.  (3)  Mast-cells  are  basophilic  and  resemble 
eosinophiles  but  are  much  smaller,  about  the  size  of  small  lymphocytes. 
The  granules  are  large  and  not  numerous.  They  stain  deeply  with  methy- 
lene blue,  but  in  specimens  stained  with  Ehrlich-Biondi  fluid  they  appear  as 
clear  white  spots.  The  protoplasm  stains  mauve  or  purple  with  methylene 
blue.  These  cells  are  few  in  number  or  absent.  (4)  Myelocytes  or  marrow 
cells  can  be  recognised  on  staining  with  Ehrlich-Biondi  fluid.  They  are  like 
large  lymphocytes  but  contain  a  great  many  granules  ;  and  the  nucleus 
almost  fills  and  is  in  close  contact  with  the  wall  of  the  cell,  being  large, 
spherical  or  egg-shaped,  and  eccentric,  instead  of  centrally  placed.  On 
staining  with  Jenner's  dye  they  are  subdivisible  into  neutrophilic  or  ordinary 
myelocytes,  the  granules  of  which  stain  blue  ;  and  a  few  eosinophilic  ones, 
the  granules  of  which  stain  red.  The  relative  proportion  does  not  appear 
to  have  any  special  significance.  The  granules  are  small,  as  in  the  poly- 
morphs. These  cells  possess  no  amoeboid  movement.  They  are  supposed 
to  be  an  intermediate  stage  between  the  large  lymphocytes  and  the  poly- 
morphs, though  they  are  usually  larger  than  both  varieties. 

Myelocytes,  many  eosinophilic,  are  normally  present  in  the  marrow. 
They  are  occasionally  found  in  the  blood  of  the  newborn  and  are  rarely 
entirely  absent  during  the  first  few  weeks  of  life.  In  various  conditions  of 
ansernia  and  splenic  enlargement  they  are  found  in  quantities  from 
1-20  per  cent,  of  the  total  number  of  white  cells.  They  are  often 
present  in  congenital  syphilis,  rickets,  tuberculosis,  pneumonia  and 
entero-colitis.  Their  presence  is  due  to  the  introduction  of  toxins,  and  it  is 
doubtful  whether  they  have  any  diagnostic  or  prognostic  significance. 
They  are  apt  to  be  more  abundant  in  the  younger  infants  on  account  of 
the  tendency  of  the  blood  to  revert  to  the  more  infantile  type  in  the  course 
of  illness. 

The  reaction  of  the  blood  is  valueless  for  clinical  purposes  at  present. 
It  is  practically  neutral,  and  not  alkaline  in  the  sense  that  sodium  hydrate 
is  alkaline.  The  salts  are  mainly  carbonates  and  phosphates  of  the  alkalies. 
The  bicarbonate  and  phosphate  of  soda  are  really  acid  salts  with  an  alkaline 
reaction  to  many  reagents.  It  is  extremely  difficult  to  make  the  blood  either 
more  or  less  alkaline. 


505 


Chapter   XLIII. 


The  Origin  of  Blood  Cells. — Up  to  a  certain  stage  of  embryonic  life 
the  blood  cells  are  developed  from  a  primitive  mesoblastic  cell,  an  original 
"  indifferent "  cell  of  a  lymphoid  type  with  a  large  oval  nucleus  and 
basophile  non-granular  protoplasm.  According  to  a  classification  by 
Treadgold  (1908)  three  varieties  of  cells  are  derived  from  the  primitive  one. 

The  first  passes  through  the  stages  of  megaloblast  and  normoblast  into 
the  red  cell  or  erythrocyte.  The  second  develops  eventually  into  the 
lymphocytes  of  lymph  glands,  thymus  and  spleen.  And  from  the  third  is 
formed  the  basophilic  lymphocyte  of  the  early  embryonic  circulation  from 
which  arises  the  large  mononuclear  cell  (amphoblast).  This  gives  birth  to 
lymphocytes  and  myelocytes,  and  from  the  various  types  of  myelocytes  are- 
developed  the  polymorphs,  eosinophiles  and  mast  cells.  Treadgold's- 
classification  may  be  tabulated  in  an  abbreviated  form  as  follows  : — 


Large  mononuclear 
Megaloblast 

Normoblast 

I 
Erythrocyte. 


The  Development  of  Blood  Cells. 
Lymphoid  Cell 


Lymphocytes  of 

glands,  spleen  and 

thymus. 


Leucoblast, 
or  large  lymphocyte 

Lymphocyte. 


Basophilic  lymphocyte 

I 

Amphoblast, 

large  mononuclear 

cell. 

i 


Myelocyte 
fine  gramdes 
neutrophile 


Myelocyte  Myelocyte- 

coarse  granules 
eosinophile  basosphile- 


Polymorph.        Eosinophile. 


Mast  cell. 


Before  birth  the  lymphadenoid  and  myeloid  tissues  become  differen- 
tiated and  the  granular  cells  arise  from  the  marrow,  the  non-granular  cells 
from  the  lymphoid  tissue.  The  marrow  contains  foci  of  lymphadenoid 
tissue,  so  some  of  the  non-granular  cells  arise  from  the  marrow  though 
not  from  myeloid  tissue.  Possibly  on  a  reversion  to  foetal  conditions,  or  a 
more  infantile  blood  formation,  as  the  result  of  illness,  the  origin  of  the 
non-granular  and  granular  cells  may  be  reversed  or  take  place  in  both 
ways.  In  infancy  there  is  a  great  amount  of  lymphoid  tissue  and  its 
activity  is  much  increased  during  ill-health.  Its  function  is  doubtful. 
Possibly  it  is  the  chief  agent  for  the  destruction  of  toxins,  while  the  micro- 
organisms are  destroyed  by  cells  which  take  their  origin  from  the  bone 
marrow. 

The  bone  marrow  contains  two  varieties  of  red  cells,  non-nucleated 
blood  cells  and  nucleated  red  marrow  cells.  The  white  cells  are  non- 
granular and  granular.  Of  the  non-granular  ones  50-70  per  cent,  are 
faintly  basophilic,  lymphoid  or  primitive  cells,  the  size  of  erythrocytes 
and  1  per  cent,  are  giant  or  mother  cells,  faintly  neutrophilic  and  containing 


The  Blood  and  Lymphoid  Structures. 


507 


many  nuclei.  The  granular  cells  are  the  ordinary  myelocytes,  finely 
granular  oxyphile  or  neutrophile  (30-40  per  cent.)  ;  the  eosinophil 
myelocytes,  coarsely  granular  oxyphile,  the  most  constant  and  typical ; 
basophile  myelocytes,  like  the  eosinophile  ones  except  in  the  nature  of 
the  granules  ;    and  polymorphs  from  the  blood  (C.  P.  Jones,  1905). 

The  Blood  in  the  Newborn. — The  amount  of  blood  is  proportionally  to 
the  weight  less  than  in  the  adult,  unless  the  reserve  blood  is  pressed  out  of 
the  placenta  before  the  cord  is  tied.  The  reaction  is  alkaline  to  litmus, 
and  the  colour  rather  darker  during  the  first  few  days  of  life  than 
later.     The  chief  differences  are  best  shown  in  the  form  of  a  table. 


The  Characters  of  the  Blood. 


AT  BIRTH. 

AT  6  MONTHS. 

ADULT. 

Specific  gravity 

1062-66 

1048-52 

1058-62 

Hsemoglobin 

110 

70 

100 

Red  cells  per  c.mm. 

5-6,000,000 

4,500,000 

5,000,000 

White  cells  do. 

20,000 

15,000 

10,000 

Percentages — 

Small  lymphocytes 

llfi-05i 

50-70 

20-30 

Large  lymphocytes 

riu  V/t^~j 

4-8 

5-15 

Polymorphonuclears 

73-4 

20-40 

60-75 

Eosinophiles 

— 

1-10 

0-5-4 

Mast  cells 

few  or  absent 

up  to  0-5 

The  differential  count  for  leucocytes  in  the  newborn  is  that  obtained  by 
Carstangen  on  the  first  day  of  life.  The  "  leucocytosis  of  the  newborn  " 
is  one  of  polynuclear  cells.  The  number  of  these  cells  falls  by  the  end  of  the 
first  week  to  a  level  which  remains  fairly  constant  throughout  life.  After 
the  first  week  there  is  a  relative  lymphocytosis.  No  adequate  explanation 
of  the  leucocytosis  of  the  newborn  has  been  put  forward.  During  the  early 
days  of  life  and  throughout  childhood  the  percentage  varies  greatly  and  the 
"leucocytosis  of  digestion"  is  marked.  The  adult  type  of  blood  is  not 
fully  attained  until  the  fifth  year,  possibly  not  until  the  eighth. 

In  the  third  year  of  life  the  percentages  of  lymphocytes  and  polymorphs 
are  about  equal.  A  leucocytosis  is  normal  in  infancy  but  indicates  disease 
in  later  life.  Similarly,  lymphocytosis  is  characteristic  of  infancy,  but  after 
3  years  of  age  it  is  abnormal.  In  all  disease  conditions  the  blood  reverts  to 
a  more  infantile  type  and  the  blood  is  like  that  of  a  younger  child.  The 
characters  of  the  blood  vary  as  the  development  of  the  child  and  causes, 
which  retard  development,  have  a  retarding  effect  on  the  blood. 


508  Chapter  XLIII. 

The  percentage  of  hemoglobin  is  high  at  birth  and  falls  steadily  for 
6  months,  then  remains  stationary  up  to  2  years  of  age,  and  slowly  rises  to 
the  adult  level  in  the  sixth  year.  Sometimes  it  falls  to  the  minimum  level 
in  the  first  few  weeks  of  life,  remains  stationary  until  the  sixth  month  and 
then  slowly  rises.  It  is  generally  lower  in  children  than  in  adults,  and  higher 
in  boys  than  girls.  The  red  cells  are  in  excess  at  birth  and  perhaps  for  a  few 
days  after.  They  diminish  during  the  first  few  months  and  then  increase 
to  the  normal  level  by  about  the  eighth  year.  Microcytes  are  more  numer- 
ous, the  cells  more  spherical  and  with  less  tendency  to  rouleaux  formation, 
and  "  shadow  corpuscles  "  are  more  plentiful  for  the  haemoglobin  is  less 
closely  combined  with  the  protoplasm.  Oxygen  seems  to  be  more  firmly 
combined.  Milne  Murray  found  that  it  required  seven  times  as  much 
reducing  agent  to  get  a  reduced  spectrum.  Normoblasts  and  megaloblasts 
are  present  in  foetal  blood,  and  are  often  found  in  considerable  number 
on  the  first  day  of  life,  especially  in  the  premature.  They  disappear  by  the 
end  of  the  fourth  day.  Coagulation  is  incomplete.  Scherenziss  states  that 
there  is  only  one-third  the  amount  of  fibrinogen  present  compared  to  that 
in  adult  blood.  There  are  more  sodium  and  less  potassium  salts  than  in 
adults.  The  most  important  differences  are  the  deficiency  of  haemoglobin, 
a  relative  chlorosis,  and  the  excess  of  lymphocytes.  These  cells  vary  more 
in  size  and  many  are  larger  than  in  adults.  Leucocytosis  and  grave  anaemia 
are  produced  by  much  more  trivial  causes. 

Leucocytosis  is  of  value  for  diagnostic  purposes.  It  is  normal  in  the 
newborn,  after  cold  baths,  massage  and  exercise,  during  digestion,  and 
sometimes  in  the  dying.  It  is  present  in  gastro-enteritis,  appendicitis, 
septic  peritonitis,  bronchitis,  pneumonia,  pleurisy,  pericarditis,  rheumatic 
fever,  septic  and  cerebrospinal  meningitis,  advanced  phthisis,  scarlatina, 
variola,  diphtheria,  tonsillitis,  whooping  cough,  erysipelas,  osteomyelitis, 
septic  and  pyaemic  conditions,  rickets,  leukaemic  affections,  and  some 
diseases  of  the  skin,  liver  and  kidney..  It  is  absent  in  early  phthisis,  miliary 
tuberculosis,  tuberculous  meningitis,  enteric  fever,  measles,  rotheln, 
mumps,  influenza  (generally),  malaria,  and  some  varieties  of  pleurisy, 
pericarditis  and  peritonitis.  Thus  it  is  present  in  most  septic  and  febrile 
disorders.  It  may  also  be  induced  by  antipyrin,  pilocarpin,  salicylates, 
large  doses  of  quinine,  thyroid  extract  and  tuberculin  injections. 

It  is  present  in  inflammation,  if  the  intensity  of  the  infection  can  excite 
reaction  and  if  the  patient's  resistance  is  capable  of  reaction.  Hence  the 
degree  of  leucocytosis  is  of  value  in  prognosis,  provided  that  the  toxaemia 
is  not  so  intense  as  to  prevent  reaction.  In  febrile  disorders  it  may  occur 
before  the  fever,  and  bears  no  relation  to  its  severity.  In  pneumonia  a 
"  blood  crisis  "  may  precede  the  temperature  crisis. 

Leucopenia  may  be  found  in  some  of  the  affections  in  which  leucocytosis 
is  absent,  e.g.,  enteric  fever,  measles,  influenza  and  uncomplicated  tuber- 
culosis ;    also  in  malnutrition  and  starvation. 


The  Blood  and  Lymphoid  Structures,  509 

Anaemia. — The  classification  of  the  various  anaemias  into  primary, 
secondary  and  intermediate  varieties  is  unsatisfactory  and  of  no  assistance 
in  understanding  the  pathological  changes.  Anaemia  is  due  to  a  multi- 
plicity of  causes.  A  few  cases  are  congenital  in  origin,  dependent  on  syphilis, 
tuberculosis,  malaria,  delicacy  or  general  malnutrition  in  the  mother. 
Usually  it  is  symptomatic,  a  secondary  result  of  improper  feeding,  a  pro- 
longed diet  of  cooked  milk,  insufficient  protein  or  deficiency  of  iron  con- 
taining foods  ;  gastro-enteric  derangements,  tuberculosis,  fevers,  suppura- 
tions, renal  disease,  haemorrhage  and  haemorrhagic  affections,  such  as 
purpura,  scurvy  and  haemophilia  ;  and  poisons,  e.g.,  lead,  mercury,  chlorate 
of  potash  and  coal  tar  products.  Intestinal  toxins  can  only  cause  haemolysis 
and  anaemia,  if  they  escape  destruction  in  the  liver  and  pass  into  the  blood. 
Their  effect  on  lymphoid  tissue  is  to  produce  lymphocytosis.  On  the  marrow 
the  effect  is  first  an  increased  production  of  polymorphs  and  eosinophiles  ; 
and  later  the  production  of  myelocytes,  due  to  the  failure  of  their  con- 
version into  more  matured  cells.  The  red  cells  are  destoyed  in  the  blood ; 
haematoblasts  appear  ;  and  the  spleen  becomes  enlarged  in  order  to  dispose 
of  the  red  cells  and  leucocytes.  Probably  other  toxins  act  in  a  similar 
manner.  There  may  be  a  deficiency  of  haemoglobin,  as  in  scurvy  ;  destruc- 
tion of  red  cells,  as  in  diphtheria  ;  or  both,  as  in  rheumatic  and  infective 
fevers. 

Examination  of  the  blood  enables  us  to  estimate  the  severity  of  the 
process.  In  mild  cases  the  percentage  of  haemoglobin  is  decreased  and  the 
blood  assumes  the  chlorotic  type.  Its  specific  gravity  is  lowered.  In  more 
severe  ones  the  red  cells  are  reduced  in  number,  and  poikilocytes  and 
haematoblasts  appear  in  varying  degree.  This  is  a  striking  feature  in  early 
life.  The  field  for  blood  formation  cannot  be  increased  in  area  and  over- 
stimulation leads  to  imperfection  of  its  products.  Leucocytosis  may  be 
present  as  the  result  of  the  primary  or  of  coincident  disease.  The  per- 
centage of  the  different  cells  is  unaltered  or  the  polymorphs  are  in  excess.. 
Except  in  mild  cases  without  leucocytosis  the  spleen  is  almost  always 
enlarged.  Put  shortly,  the  greater  the  degree  of  anaemia  the  greater  is  the 
reduction  in  the  specific  gravity  (down  to  1035)  ;  the  more  the  reduction 
in  red  cells  (down  to  2  million)  and  the  percentage  of  haemoglobin  (down  to 
30  per  cent.)  ;  the  more  marked  the  poikilocytosis  and  polychromatophilia  ; 
the  greater  the  number  of  normoblasts  and  megaloblasts  ;  and  the  greater 
the  leucocytosis.    A  few  myelocytes  may  be  present. 

The  symptoms  are  pallor,  fretfulness  and  irritability,  shortness  of 
breath  on  exertion,  digestive  troubles,  constipation,  headache,  insomnia 
and  muscular  debility. 

The  diagnosis  depends  on  the  characteristics  of  the  blood  and  the 
recognition  of  the  cause.  Splenic  hyperplasia  suggests  leukaemia  or  anaemia 
splenica  infantum,  etc. 


510  Chapter   XLIII. 

The  prognosis  varies  with  the  cause,  age,  extent  of  blood  changes,  and 
general  condition  of  the  patient.  Anaemia  due  to  simple  haemorrhage  is 
readily  recovered  from.  In  other  cases  it  depends  on  the  severity  of  the 
cause  and  is  often  that  of  the  primary  disease.  In  a  few  instances  an 
apparently  mild  type  develops  into  a  fatal  one.  Death  is  usually  due 
to  intercurrent  disease. 

Chlorosis,  sometimes  called  "  oligosideraemia,"  is  rare  in  early  life 
and  in  breast-fed  infants.  The  age  of  most  recorded  cases  is  from  11  months 
to  3  years.  One  infant,  seen  in  consultation,  was  only  8  months  old.  He 
was  born  in  the  eighth  month  of  pregnancy  and  only  weighed  3  lb.  9  oz.  at 
birth.  He  had  been  brought  up  on  peptonised  milk  and  then  on  boiled 
milk,  cream  and  water.  When  seen,  he  was  profoundly  anaemic  and 
weighed  14  lb.  6  oz.  Six  months  later  there  was  no  anaemia.  Another  case 
was  also  one  of  twins,  one  month  premature.  At  9  months  of  age  he  had 
acute  summer  diarrhoea  and  at  16  months  was  profoundly  anaemic.  This 
affection  is  most  often  found  in  twins  and  premature  infants  fed  on 
prolonged  milk  diet.  According  to  Bunge  reserve  iron  is  stored  up  in  the 
liver  in  utero,  and  it  is  stated  that  this  accumulation  takes  place  in  the 
last  three  months  of  pregnancy.  Thus  a  premature  infant  is  likely  to  have 
an  inefficient  store  and  cannot  obtain  sufficient  from  a  milk  diet. 

The  complexion  is  a  pale  yellow,  often  greenish  tint.  The  mucous 
membranes  are  pale.  The  child  is  puffy,  soft,  flaccid,  under  weight  and 
costive.  Sometimes  there  are  diarrhoea  and  digestive  troubles  which  yield 
readily  to  treatment.  Apathy,  mental  dulness  and  haemic  murmurs  are 
present.  The  spleen  is  not  enlarged.  The  percentage  of  haemoglobin  falls 
to  50  and  the  blood  shows  poikilocytes  and  polychromatophilia,  but  is 
otherwise  normal. 

Pernicious  Anaemia  is  almost  unknown  in  childhood.  Of  240  cases 
collected  by  Ehrlich  only  1  was  under  10  years  of  age.  Some  of  the  recorded 
cases  will  not  bear  strict  investigation,  and  are  really  secondary  anaemias.  It 
is  a  primary  anaemia  which  exhibits  definite  blood  changes,  progresses 
rapidly  and  almost  invariably  ends  fatally.  A  fatal  anaemia  is  not  necessarily 
pernicious  anaemia.  In  view  of  the  theory  that  the  disease  is  caused  by 
septic  infection  plus  a  specific  heemolytic  poison  and  that  the  infection  is 
commonly  buccal  in  origin,  it  is  remarkable  that  more  cases  are  not  seen 
in  children  for  they  are  particularly  liable  to  mouth  affections  and  almost 
constantly  possess  one  or  more  carious  teeth. 

The  blood  is  watery,  dirty  pink,  reddish  brown  or  coffee-coloured. 
It  clots  feebly  and  does  not  form  rouleaux.  The  red  cells  fall  to  \-2  millions 
per  c.rnm.,  haemoglobin  to  15-25  per  cent.,  and  the  specific  gravity  to  1030. 
The  colour  index  is  normal  or  high,  never  subnormal  as  in  secondary  anaemia. 
The  other  blood  changes  include  poikilocytosis,  polychromatophilia,  a 
preponderance  of  megalocytes,  microcytes,  shadow  corpuscles,  megalo- 
Tblasts  and  normoblasts,  karyokinesis  of  the  nuclei  of  red  cells,  perhaps  a  few 


The  Blood  and  Lijmphoid  Structures.  511 

myelocytes,  and  a  normal  number  or  deficiency,  rarely  an  excess,  of  white 
cells.    A  relative  lymphocytosis  has  been  found  in  bad  cases. 

Iron  is  deposited  in  the  liver  and  intestinal  mucosa,  and  is  in  excess  in 
the  kidneys  and  spleen.  The  spleen  may  exhibit  some  enlargement  from 
fibrous  hyperplasia.  The  bone  marrow  is  embryonic  in  type,  and  contains 
many  megaloblasts  and  normoblasts.  Warthin  states  that  the  prevertebral 
lymph  glands,  especially  the  cervical,  thoracic  and  retro-peritoneal  ones, 
are  affected. 

The  symptoms,  course  and  prognosis  are  the  same  as  in  adults.  An 
insidious  onset  is  followed  by  profound  anaemia  and  prostration,  without 
emaciation.  Headache,  fainting  attacks,  cardiac  dilatation,  haemic  murmurs, 
oedema,  and  sometimes  fever,  are  present.  Anorexia,  nausea  and  vomiting 
are  common  ;  diarrhoea  not  infrequent.  The  spleen  may  be  palpable. 
Haemorrhages  take  place  from  the  nose,  subcutaneously,  into  the  retina, 
from  the  stomach,  bowel,  lungs,  etc.  The  prognosis  increases  in  gravity 
as  the  megaloblasts  exceed  the  normoblasts  in  number.  It  ends  fatally 
in  a  few  months  to  a  year. 

The  Spleen. — The  spleen  is  one-tenth  the  weight  of  the  liver  at  birth  ; 
-|-|  oz.,  varying  from  J-2  ozs.  It  doubles  its  weight  in  a  year,  trebles  it  in 
3-7  years,  and  quadruples  it  in  7-14  years.  It  is  not  essential  to  life  and  its 
functions  are  not  clearly  understood.  Probably  it  acts  as  a  filter  for  the 
removal  of  foreign  particles  from  the  blood,  e.g.,  debris  of  red  and  white 
cells,  and  is  consequently  enlarged  in  diseases  which  lead  to  blood  destruc- 
tion. It  is  lymphogenic,  producing  non-granular  lymphocytes,  and 
perhaps  contains  indifferent  cells  which  can  develop  according  to  the  body 
needs. 

It  is  much  enlarged  in  myelogenic  leukaemia,  anaemia  splenica  infantum, 
infective  endocarditis,  malaria,  and  some  cases  of  hepatic  cirrhosis,  typhoid 
fever  and  infarction.  It  is  enlarged  to  a  less  extent  in  the  early  stages  of 
these  diseases  and  in  lymphatic  leukaemia,  amyloid  disease,  congenital 
syphilis,  rickets,  portal  obstruction  and  backward  cardiac  pressure.  To  a 
certain  extent  it  is  enlarged  in  all  fevers.  Occasionally  the  increase  in  size 
is  due  to  abscess,  hydatid,  caseous  masses,  gummata  or  traumatism. 

A  moderate  enlargement  causes  a  little  increase  in  the  splenic  area  of 
dulness  and  a  palpable  lump,  felt  below  the  costal  arch  on  inspiration.  If 
the  spleen  is  very  large  it  causes  bulging  on  the  left  side  in  the  hypochon- 
drium,  and  a  distinct  tumour,  which  moves  on  respiration,  is  close  to  the 
costal  margin,  and  has  a  sharply  defined  edge  with  a  notch.  The  inner  edge 
may  stand  up  as  a  well-marked  ridge  and  the  notch  be  visible  through  the 
thin  abdominal  wall.  The  percussion  note  is  dull  in  front,  except  perhaps 
over  the  lower  anterior  edge  if  a  coil  of  intestine  happens  to  become  inter- 
posed between  the  abdominal  wall  and  the  spleen.  In  the  left  loin  it  is 
resonant,  for  the  tumour  is  covered  by  the  descending  colon. 


512  Chapter  XLIII. 

It  has  to  be  diagnosed  from  renal  and  adrenal  tumour  and  abscess, 
tuberculous  peritonitis,  masses  of  enlarged  glands,  faeces,  ovarian  cysts, 
pancreatic  cysts  and  tumours,  and  malignant  disease  of  the  glands,  splenic 
flexure,  stomach  or  omentum. 

Anaemia  Splenica  Infantum. — Syn.  :  Anaemia  Infantum  Pseudo- 
leukcemica  (von  Jaksch),  Ancemia  splenica  infettiva  dei  bambini,  Splenic 
ancemia. — In  this  affection  anaemia  and  enlargement  of  the  spleen  are 
combined,  without  any  characteristic  changes  in  the  blood.  There  is  no 
definite  evidence  of  a  primary  cause  and  yet  there  are  sufficient  grounds  for 
looking  upon  it  as  a  disease  sui  generis,  rather  than  a  secondary  anaemia. 
Possibly  it  is  due  to  some  toxin  which  gives  rise  to  both  the  anaemia  and  the 
splenic  enlargement ;  the  hyperplasia  not  being  due  to  the  anaemia,  nor 
the  anaemia  a  secondary  effect  of  the  hyperplasia,  for  both  can  occur 
independently.  It  affects  both  sexes  equally,  and  is  most  common  at 
6  months  to  2  years  of  age.  Twins  are  particularly  liable.  Much  argument 
has  been  devoted  to  its  connection  with  rickets  and  syphilis.  No  doubt 
both  these  affections  can  cause  splenic  hyperplasia  and  possibly  anaemia, 
but  the  disease  under  consideration  is  found  sometimes  quite  independently 
of  the  least  evidence  of  either  affection.  Pickets  is  not  a  cause  of  anaemia 
and  the  degree  of  rickets,  when  present,  bears  no  proportionate  relation 
to  the  blood  changes  or  the  size  of  the  spleen.  It  is  coincident, 
not  causative.  The  same  factors  concerned  in  the  production  of  splenic 
anaemia  may  induce  rickets.  In  my  experience  there  is  rarely  a  family 
history  or  direct  evidence  of  syphilis.  The  disease  is  more  common 
among  Jews,  especially  Polish  Jews,  than  Gentiles.  Yet  syphilis  is 
said  to  be  less  common  among  Jews  and  more  of  their  children  are 
breast  fed.  It  is  most  frequent  in  hand-fed  infants  brought  up  on 
proprietary  foods  and  condensed  milk.  Often  there  is  a  past  history  of 
alimentary  disturbance  and  bad  hygienic  surroundings.  Possibly  these 
are  concomitant  factors  or  the  primary  cause  is  a  toxin  of  intestinal 
origin.  There  is  no  doubt  that  many  varieties  of  anaemia,  usually 
secondary,  in  which  the  spleen  is  enlarged,  have  been  described  under  this 
heading,  but  there  is  a  definite  residuum  of  cases  which  we  are  justified  in 
regarding  as  a  distinct  entity. 

Morbid  Anatomy. — There  are  no  special  anatomical  changes  peculiar 
to  this  disease.  The  spleen  is  large,  often  enormous,  and  has  a  firm  rounded 
edge.  Its  size  bears  no  relation  to  the  number  of  red  cells  or  the  degree  of 
leucocytosis,  if  any.  The  enlargement  is  a  simple  hyperplasia  without  any 
leukaemic  infiltration  ;  and  similar  changes  are  found  in  both  rickets  and 
congenital  syphilis.  The  degree  of  fibrosis  depends  on  the  duration  of  the 
disease.  The  liver  is  generally,  but  not  always,  larger  than  normal  and  its 
size  in  no  way  depends  on  that  of  the  spleen.  It  may  not  be  at  all  enlarged 
though  the  spleen  is  enormous.  Microscopically  it  is  normal,  fatty,  or  may 
show    foetal    characteristics.       In  about    half    the    cases    there    is    some. 


The  Blood  and  Lymphoid  Structures.  513 

hyperplasia  of  the  lymph  glands.     No  characteristic  changes  are  found  in  the 
marrow  and  there  are  no  leukaemia  changes  throughout  the  body. 

Symptoms. — The  onset  and  course  are  insidious,  the  pallor  being  the 
most  striking  feature.  The  complexion  is  waxy,  with  a  tinge  of  olive  green. 
Shortness  of  breath,  dilatation  of  the  heart  and  hsemic  murmurs  are  present. 
Sometimes  the  enlarged  spleen  is  present  before  the  anaemia.  The  child 
often  remains  plump,  though  the  anaemia  and  debility  steadily  increase. 
Occasionally  there  is  marked  emaciation.  One  boy,  8  months  old,  had 
dusky  gums  but  no  other  signs  suggestive  of  scurvy.  The  chief  gastro- 
intestinal symptoms  are  anorexia,  vomiting  and  the  passage  of  undigested 
food.  Jaundice  may  result  from  duodenal  catarrh.  The  abdomen  is  pro- 
tuberant and  tympanitic,  its  enlargement  being  mainly  due  to  the  spleen 
which  may  extend  as  low  as  the  left  iliac  fossa.  Occasionally  a  bruit  is 
heard  over  the  tumour.  Perisplenitis  sometimes  occurs  and  attacks  of 
paroxysmal  colicky  pain  in  the  left  hypochondrium,  due  to  traction  on  the 
sympathetic  plexus  or  twisting  of  the  peritoneal  attachments.  The  liver 
usually  extends  an  inch  or  two  below  the  costal  margin.  The  lymph  glands 
attain  the  size  of  a  pea  or  small  bean  in  half  the  cases.  Haemorrhages  are 
not  frequent,  though  epistaxis  and  petechias  are  liable  to  break  out  in  the 
course  of  the  disease  and  gastro-intestinal  bleeding  in  late  stages.  The  urine 
may  contain  a  trace  of  albumin.  Pyrexia  is  variable,  irregular,  and  com- 
monly set  up  by  complications. 

The  blood  shows  the  changes  found  in  chlorosis  and  polymorphism. 
The  number  of  red  cells  is  usually  reduced  to  2-3  million,  or  even  to  800,000. 
The  percentage  of  haemoglobin  falls  to  30  or  lower,  and  is  more  reduced 
than  the  number  of  red  cells.  The  colour  index  is  low.  There  are  many 
microcytes,  megalocytes,  poikilocytes  and  polychromatophilia.  Megalo- 
blasts  and  normoblasts  are  present.  Karyokinesis  is  common  and  regarded 
by  some  observers  as  of  diagnostic  importance.  The  number  of  white  cells 
is  very  variable.  Leucocytosis  is  probably  due  to  some  complication.  These 
cells  exhibit  great  variety  in  size,  sbape  and  staining  properties  ;  the 
variation  being  more  marked  in  the  polymorphs  than  the  lymphocytes. 
Eosinophiles  are  decreased,  normal  or  increased  in  number.  Mast  cells 
are  often  found  and  myelocytes  in  small  numbers,  and  in  even  large  numbers 
in  late  stages.  There  is  generally  a  relative  lymphocytosis,  such  as  is 
common  in  all  infantile  ailments,  unless  there  are  complications.  Thus 
the  blood  picture  is  that  of  chlorosis  and  a  reversion  to  a  more  infantile 
type. 

Diagnosis. — A  pure  case  is  one  with  no  history  or  evidence  of  syphilis 
or  rickets.  Anaemia  and  splenic  hyperplasia  are  rarely  great  in  congenital 
syphilis  and  commonly  found  under  6  months  of  age.  The  blood  picture 
affords  comparatively  little  reliable  assistance  but  a  certain  amount  of 
stress  can  be  lain  on  the  presence  of  a  large  number  of  haematoblasts, 
karyokinesis,  poikilocytes,  polychromatophilia,  leukopenia  and  a  relative 

2    L 


514  Chapter   XLIII. 

lymphocytosis.  I  think  leucocytosis  is  merely  a  sign  of  coincident  disease. 
The  changes  in  the  red  cells  occur  in  any  form  of  grave  anaemia,  and 
leucocytosis  is  also  often  present  in  such  affections.  The  presence  of  a 
large  number  of  myelocytes  may  lead  to  an  erroneous  diagnosis  of  true 
leukaemia,  but  this  disease  is  very  rare  in  infancy  and  there  is  no  evidence 
that  it  is  ever  a  sequel  of  the  milder  affection. 

The  prognosis  is  uncertain  for  cases  are  chronic  and  apt  to  be  lost  sight 
of.  They  tend  to  relapse,  but  on  the  whole  the  outlook  is  good  and  pro- 
bably about  75  per  cent,  recover.  Some  patients  remain  stationary  or 
even  get  gradually  worse  for  2  or  3  months,  and  then  suddenly  take  a  turn 
for  the  better  and  rapidly  recover.  No  case  is  hopeless.  Gastro-intestinal 
complications  increase  the  gravity  of  the  prognosis.  CEdema  of  the  feet 
and  petechial  haemorrhages  on  the  abdomen  and  trunk  are  bad,  though  not 
necessarily  fatal  indications.  Death  is  usually  due  to  intercurrent  disease, 
notably  bronchitis,  broncho-pneumonia  or  miliary  tuberculosis.  It  may 
result  from  marasmus  and  simple  asthenia.  The  percentage  of  leucocytes 
is  of  no  value  in  prognosis  for  a  progressive  increase  may  occur  in  fatal  cases 
or  leucopenia  be  present  throughout.  In  a  boy,  aged  13  months,  extremely 
ill,  a  large  number  of  myelocytes  were  found  yet,  in  spite  of  the  profound 
blood  changes,  he  eventually  recovered.  It  is  probable  that  the  presence  of 
myelocytes  in  any  large  number  is  an  unfavourable  sign.  The  number  of 
haematoblasts  is  no  measure  of  the  severity.  In  cases  which  recover,  the 
spleen  may  contract  to  its  normal  size.  Possibly  some  terminate  in  the 
splenic  anaemia  of  later  life.    It  does  not  develop  into  true  leukaemia. 

Splenic  Anaemia  in  older  children  is  closely  allied  to  anaemia  splenica 
infantum.  It  is  characterised  by  splenic  enlargement,  leucopenia,  blood  of  a 
chlorotic  type,  no  glandular  hyperplasia,  and  a  prolonged  course  with 
liability  to  haemorrhages,  especially  from  the  gastro-intestinal  tract.  A 
case  of  this  nature  was  a  girl,  seen  in  consultation  with  Dr.  Macintosh  of 
Hampstead.  At  5  years  of  age  she  had  haematemesis.  At  9  years,  when  she 
came  under  Dr.  Macintosh's  care,  she  was  anaemic  and  had  an  enlarged 
spleen.  Next  year  she  had  haematemesis  and  melaena,  and  the  spleen 
reached  the  umbilicus.  The  blood  showed  considerable  reduction  in  red 
cells,  marked  leucopenia  (about  2000)  and  a  relative  lymphocytosis  of  small 
cells  (55  per  cent.). 

Similar  cases  have  been  recorded  in  more  than  one  member  of  a  family  : 
6  cases  in  2  generations,  two  of  them  children  7  and  10  years  old,  had 
anaemia,  leucopenia,  and  enlarged  spleen  but  no  haemorrhages  ;  splenectomy 
was  successful  in  two  (Springthorpe  and  Stirling,  1904)  ;  6  cases  of  enlarged 
spleen  in  3  generations  (Claud  Wilson),  and  others.  Some  of  these  are 
described  under  the  name  of  "  family  splenomegaly  "  and  are  associated 
with  dwarfing,  infantilism,  clubbing  of  the  fingers,  sometimes  hepatic 
enlargement  and  skin  pigmentation.  In  family  acholuric  jaundice  (p.  136) 
the  spleen  is  generally  enlarged. 


The  Blood  and  Lymphoid  Structures.  515 

Banti  (1881)  differentiated  a  special  variety  under  the  name  of  pro- 
gressive ancemia  or  ancemia  ganglionare.  Its  features  are  a  progressive 
anaemia,  disturbance  of  organic  functions,  irregular  fever,  haemorrhages 
from  the  stomach  and  bowels,  splenic  enlargement,  and  a  fatal  termination. 
Both  the  liver  and  spleen  show  fibrosis,  and  there  is  a  black  or  steely  grey 
pigmentation  of  the  skin.  The  course  of  events  is  first  a  primitive  spleno- 
megaly with  no  disturbance  of  health ;  a  stage  of  splenic  anaemia,  secondary 
anaemia  and  leucopenia  ;  and  a  final  stage  of  hepatic  cirrhosis,  jaundice  and 
ascites.  The  affection  has  been  regarded  by  Bolleston  as  a  special  entity 
due  to  endothelial  proliferation  in  the  spleen.  Most  of  the  cases  are  more 
probably  atrophic  cirrhosis  with  splenic  enlargement,  syphilitic  cirrhosis 
of  the  liver  and  spleen,  or  of  cirrhosis  occurring  in  the  course  of  splenic 
anaemia. 

Lymphatic  Ancemia  was  described  by  Alex  MacGregor  (1901)  as  a 
special  variety  of  anaemia.  Of  23  cases  from  3-16  years  old,  18  were  under 
11  years.  The  glands,  chiefly  in  the  groins  and  cervical  triangles,  are 
enlarged,  small  and  hard.  The  spleen  is  usually  enlarged.  The  symptoms 
are  anaemia,  clean  tongue,  poor  appetite,  constipation,  loss  of  flesh  and 
cough,  worst  at  night.  The  blood  is  deficient  in  red  cells  and  haemoglobin  ; 
and  shews  a  lymphocytosis  of  large  cells  : — small  lymphocytes  12-13,  large 
lymphocytes  20-40,  polymorphs  41-63,  eosinophiles  2-7  per  cent.  Further 
observations  are  required  before  this  can  be  separated  as  a  special  disease. 
All  the  cases  recovered.    It  is  probably  a  variety  of  secondary  anaemia. 

Leukaemia  was  formerly  divided  into  lymphatic  and  splenic  types. 
Subsequently  the  importance  of  the  bone  marrow  was  recognised  in  the 
splenic  type  and  it  was  named  spleno-medullary,  and  later  on  medullary 
or  myelogenic  leukaemia.  More  recently  it  has  been  realised  that  it  cannot 
be  sharply  differentiated  in  this  manner.  Lymphatic  cases  occur  in  which 
the  lesions  are  limited  to  the  bone  marrow  ;  and  myelogenous  changes  have 
been  found  in  adenoid  tissue  in  myelocytic  cases.  The  development  of 
lymphoid  cells  from  adenoid  tissue  and  of  granular  cells  from  the  bone 
marrow  is  not  strictly  limited,  and  vicarious  action  takes  place. 

Clinically  it  is  useful  to  recognise  a  Lymphocytic  or  lymphoid  variety, 
and  a  Myelocytic  or  mixed  cell  type,  although  the  classification  is  based  on 
the  blood  picture  only.  The  lymphocytic  type  is  called  Lymphcemia  or 
Lymphocythcemia,  and  the  myelocytic  is  known  as  Myelcemia  or  Myelocy- 
thcemia.  Both  may  occur  in  the  so-called  spleno-medullary  form  of  the 
•disease.  Myelaemia  can  occur  without  either  glandular  or  splenic  enlarge- 
ment ;  and  lymphaemia  may  be  present  without  enlarged  glands  but  with 
an  enormous  spleen.  The  bone  marrow  is  always  involved  and  the  glandular 
system  may  escape  entirely.  The  essential  features  of  leukaemia  generally 
are  leucocytosis,  a  relative  alteration  in  the  percentages  of  normal  cells  or 
the  presence  of  abnormal  ones,  and  changes  in  the  bone  marrow,  spleen 
and  lymph  glands. 


516  Chapter   XLIII. 

Acute  Lymphcemia  is  the  variety  of  leukaemia  seen  most  often  in 
children,  though  it  is  quite  a  rare  disease.  Only  about  25  cases  are  on 
record.  Emerson  (1907)  recognised  4  different  varieties  : — (1)  An  acute 
infectious  type,  like  an  acute  streptococcal  pyaemia  but  without  streptococci ; 
(2)  Cases  like  chronic  leukaemia  but  more  acute ;  (3)  Haemorrhagic ; 
(4)  Acute  cachectic  cases.  Its  etiology  is  doubtful.  Possibly  it  is  due  to 
toxaemia  or  acute  infection.  Although  streptococci  have  been  found  in  some 
cases  they  were  probably  a  terminal  infection.  The  enlargement  of  the 
spleen  is  not  an  essential  feature,  and  probably  neither  the  spleen  nor  the 
glands  are  primarily  involved.  The  glands  are  generally  enlarged.  The 
bone  marrow  shows  lymphadenoid  degeneration,  a  reversion  to  the  foetal 
condition,  and  lymphaemia  may  be  intense  when  the  spleen  and  glands  are 
unaffected.  Hence  the  lymphaemia  may  be  due  in  some  cases  to  prolifera- 
tion of  the  non-granular  cells  in  the  marrow,  and  in  others  to  over- 
stimulation of  lymphoid  tissues  throughout  the  body.  The  evidence  is. 
in  favour  of  it  being  a  primary  disease  of  the  bone  marrow. 

The  onset  is  insidious  with  pallor  and  languor.  Anaemia  is  progressive. 
The  haemorrhagic  tendency  may  be  present  from  the  first  or  follow  profound 
anaemia  and  general  glandular  enlargement.  Infective  purpura  is  possibly 
an  acute  leukaemia.  Some  cases  simulate  scurvy,  because  of  the  pre- 
dominance of  mouth  symptoms.  Usually  the  glands,  liver  and  spleen  show 
some  enlargement,  varying  during  the  course  of  the  disease  ;  and  often 
there  is  slight  albuminuria.  The  temperature  is  generally  raised  and 
irregular  in  acute  stages. 

Leucocytosis  is  commonly,  but  not  always,  present  and  may  be  extreme  ,* 
occasionally  there  is  leucopenia.  The  lymphocytosis  is  one  of  large  cells, 
rarely  of  small  cells,  and  is  absolute  or  relative.  With  extreme  leucocytosis 
the  small  lymphocytes  may  in  rare  cases  predominate  ;  otherwise  the  large- 
lymphocyte  is  in  excess.  A  differential  count  shows  as  many  as  97  per  cent, 
lymphocytes,  few  polymorphs,  rarely  eosinophiles.  Haematoblasts  and 
myelocytes  have  been  found  in  small  numbers  in  most  recent  cases.  The 
number  of  red  cells  drops  to  1-2  millions  and  the  haemoglobin  index  may  be 
above  or  below  normal. 

These  patients  die  in  a  few  days  to  6  weeks.  Post-mortem  examination 
shows  general  lymphocytic  infiltration,  haemorrhages,  a  pale  liver  and 
much  enlargement  of  the  kidneys.    The  marrow  is  affected  as  in  myelaemia. 

Chronic  Lymphcemia  shows  general  glandular  enlargement,  excessive 
leucocytosis,  and  predominance  of  the  small,  rarely  of  the  large  lymphocytes. 
It  is  still  more  rare  than  the  acute  type.    Mixed  varieties  may  occur. 

Myelcemia  is  acute  or  chronic.  Hirsch  and  Cabot  have  recorded  acute 
cases.  About  7  cases  of  the  chronic  type  have  been  found  in  children. 
The  spleen  is  large  and  contains  an  excess  of  lymphoid  tissue.  The  liver 
shows  similar  changes.  The  mesenteric  glands  are  enlarged  but  the  others 
are  little  or  not  at  all  affected.    The  marrow,  especially  of  the  long  bones,. 


The  Blood  and  Lymphoid  Structures.  517 

is  of  the  "  red  currant  jelly  "  appearance  or,  more  rarely,  gelatinous  and 
puriform.  It  contains  haematoblasts,  myelocytes  and  all  sorts  of  red  cells. 
The  thymus  is  generally  large.  The  blood  contains  20-60  per  cent,  mye- 
locytes, many  polymorphs  and  few  lymphocytes.  Mast  cells  are  present.  It 
resembles  cafe  au  lait,  and  serous  and  visceral  haemorrhages  are  often  present. 
The  symptoms  are  progressive  weakness  and  increasing  pallor ;  increase 
in  the  size  of  the  spleen  and  liver  ;  shortness  of  breath,  perhaps  paroxysmal 
dyspnoea;  dyspepsia  and  attacks  of  diarrhoea;  fainting  attacks;  bleeding 
from  the  nose,  stomach,  bowel,  gums,  lungs,  kidneys,  etc. ;  anasarca  and 
ascites  in  late  stages ;  moderate  irregular  pyrexia ;  albumin  and  casts  in 
the  urine,  and  occasionally  attacks  of  colic  due  to  the  deposition  of  uric 
acid  in  the  kidneys.  The  prognosis  is  worse  in  lymphaemia  than  in 
myelaemia.  In  adults  myelaemia  sometimes  runs  a  very  slow  course. 
Insufficient  cases  have  been  recorded  in  children  to  enable  an  approximate 
duration  of  life  to  be  fixed.  Few  cases  of  lymphaomia  are  likely  to  live 
longer  than  3  months.  Life  may  be  more  prolonged  in  the  other  type  and 
death  is  often  due  to  intercurrent  disease. 

Chloroma  is  a  rare  disease  in  many  respects  allied  to  acute  leukaemia. 
It  was  described  by  Alan  Burns  in  1823,  and  first  diagnosed  during  life 
by  Melville  Dunlop  in  1901.  About  50  cases  are  on  record,  over  three-fifths 
in  males.  Some  of  these  were  in  children  3  and  4  years  of  age.  The  affection 
is  most  common  before  puberty.  The  characteristic  features  are  severe 
anaemia,  prominent  eyes  or  exophthalmos,  one  or  more  tumours  with  a 
greenish  tinge  in  the  orbits,  temporal  fossae  and  cranial  periosteum,  and  a 
marked  lymphocytosis  of  large  cells.  Some  cases  are  ushered  in  with 
facial  paralysis  ;  pain  in  the  forehead,  top  of  the  head  or  mastoid  region  ; 
exophthalmos,  proptosis,  chemosis,  and  perhaps  optic  neuritis  and  retinal 
haemorrhage ;  dilatation  of  the  veins  of  the  eyelids  and  temples ;  oedema 
of  the  eyelids,  face  and  forehead;  and  semi-fluctuating  swellings  in  the 
temporal  regions  or  hard  immovable  tumours  here,  in  the  mastoid  region 
and  other  situations.  The  child  has  a  peculiar  yellowish  or  greenish  pallor, 
and  gradually  gets  weaker  and  dies  from  exhaustion  in  a  few  weeks  or 
months.  The  symptoms  vary  with  the  size  and  distribution  of  the  tumours. 
Drowsiness,  semi-coma,  epistaxis,  petechial  haemorrhages,  bleeding  from 
the  orbit,  destruction  of  the  cornea  and  the  formation  of  a  fungating  tumour, 
and  other  cutaneous  and  mucous  haemorrhages  have  been  noted.  The 
spleen  and  glands  are  at  times  enlarged. 

Post  mortem,  the  growths  have  been  found  arising  from  the  peri- 
cranium, over  the  outer  surface  of  the  dura  mater,  in  the  basal  fossae,  in  the 
ethmoido-facial  region  of  the  skull,  beneath  the  periosteum  on  the  under 
surface  of  the  sternum,  spine  and  ribs.  The  bone  marrow,  spleen  and 
glands  are  infiltrated.  Metastases  are  present  in  numerous  places,  e.g., 
liver,  kidneys  and  ovaries.  The  tumours  are  greenish  in  colour,  from  a 
colour  like  that  of  turtle  fat  up  to  bright  green.     Some  of  them  are  not 


518  Chapter  XLIII. 

coloured.  The  cause  of  the  green  tint  is  not  known.  The  disease  appears 
to  start  in  the  red  marrow  of  a  cranial  bone  and  less  often  in  that  of  a 
vertebra,  rib  or  the  sternum. 

Clinically  these  cases  are  very  much  like  those  of  sarcomata  of  the 
skull,  orbits  and  adrenals  (p.  211).  Microscopically  the  structure  is  that  of 
an  infiltrating  round-celled  sarcoma.  The  blood  picture  is  that  of  lymph- 
aemia.  Possibly  the  large  mononuclear  cells  found  are  really  modified 
myeloblasts  ;  and  the  disease  is  a  variety  of  myelogenous  leukaemia. 
Treadgold  (1908)  suggests  there  are  three  stages  or  three  different  affections, 
viz.,  Sarcoma  of  bone;  Chloroma,  a  tumour  of  myeloblasts,  arising  primarily 
in  the  marrow,  remaining  focal  for  a  time  and  producing  metastases ;  and 
Acute  Lymphaemia,  a  tumour  also  of  bone  marrow,  consisting  of  ampho- 
blasts,  leucoblasts  or  mixed  cells. 

Treatment  of  Anamiia  and  Allied  Affections. — Diet  and  hygiene  are 
necessary  and  the  primary  cause,  if  discoverable,  must  be  treated.  In 
severe  cases  rest  in  bed  is  essential.  Iron  and  arsenic  are  the  best  drugs. 
Iron  can  be  given  in  organic  forms  in  yolk  of  egg,  bone  marrow,  raw  meat 
and  raw  meat  juice,  potatoes,  spinach  and  other  foods  (p.  34)  ;  or  in 
inorganic  preparations  (p.  81).  One  gm.  of  inorganic  iron  is  present  in 
reduced  iron  1,  saccharated  carbonate  of  iron  10,  tr.  ferri.  chlor.  28,  iron 
somatose  50,  carniferrin  3-3,  triferrin  4-5,  ferratin  15*4,  hsematogen  1420, 
haemoglobin  233,  hcemogallol  359  gms.,  and  in  5  Blaud's  pills.  Arsenic  is 
useful  in  pernicious  anaemia,  when  given  in  full  doses,  and  is  often  beneficial 
in  leukaemia,  in  which  it  may  reduce  the  number  of  white  cells  without 
increasing  the  erythrocytes. 

Sea  air  and  high  altitudes  are  not  as  good  as  country  air.  Avoid  chills, 
loss  of  body  heat,  exposure  to  the  direct  rays  of  the  sun  and  sea  bathing, 
Moderate  massage  can  be  used  to  replace  exercise. 

The  removal  of  the  spleen  in  anremia  splenica  infantum  is  unnecessary 
and  useless  ;  in  leukaemia  it  is  soon  fatal.  In  the  family  form  of  spleno- 
megaly and  Banti's  disease  it  may  be  followed  by  recovery.  Harris  and 
Hertzog  (1901)  collected  19  cases  of  which  4  died.  After  the  operation  there 
is  some  temporary  fever  and  leucocytosis  and  the  blood  condition  improves. 
A  gradual  compensation  has  taken  place  during  the  course  of  the  disease, 
so  that  the  operation  is  not  very  serious.  The  treatment  of  leukaemic 
cases  by  exposure  of  the  enlarged  spleen  to  the  action  of  X-rays  has 
occasionally  proved  beneficial. 

The  Lymph  Glands  consist  of  adenoid  tissue  and  lymph  sinuses. 
According  to  Warthin  (1902)  haemolymph  glands,  containing  blood  sinuses 
instead  of  lymph  sinuses,  are  found  in  the  prevertebral  retro-peritoneal 
tissue,  usually  near  the  great  vessels  ;  less  often  in  the  mediastinum  ;  and 
frequently  near  the  parathyroids.  Possibly  they  are  compensatory  to  the 
bone  marrow  and  spleen  in  function.  Of  these  the  splenolymph  glands  are 
the  more  common,  and  may  be  mistaken  for  secondary  spleens.     Their 


The  Blood  and  Lymphoid  Structures.  519 

lymphadenoid  tissue  contains  small  and  large  lymphocytes,  transitionals 
and  polymorphs  ;  rarely  mononuclear  eosinophiles  and  mast  cells.  The 
sinuses  are  lined  by  endothelium  and  contain  red  and  white  cells.  They  are 
chiefly  hemolytic  and  partially  leucocyte-forming  organs.  The  marrow 
lymph  glands  contain  blood  sinuses  filled  with  a  coarse  reticulum  through 
which  the  red  cells  filter.  Masses  of  lymphoid  tissue  are  arranged  between 
the  sinuses  but  there  are  no  true  follicles.  Many  scattered  fat  cells  are 
present.  The  lymphadenoid  tissue  contains  mononuclear  eosinophiles, 
polymorphs,  occasionally  myelocytes  of  bone  marrow  type,  erythrocytes 
and  deposits  of  hyaline  material.  Their  function  is  the  formation  of 
leucocytes  and  they  take  little  part  in  haemolysis. 

Glandular  Enlargement  is  caused  by  proliferation  of  the  lymphadenoid 
and  connective  tissues.  It  varies  in  consistency,  and  may  be  very  hard  or 
may  undergo  softening,  caseation  and  suppuration.  It  is  induced  by  the 
irritation  of  toxins  or  micro-organisms  which  reach  the  gland  through  the 
lymphatics  or  blood  stream,  commonly  the  former.  Adenitis  causes  leucocy- 
tosis  of  polymorphs  and  sometimes  eosinophilia.  Always  seek  for  some  local 
source  of  irritation,  bearing  in  mind  the  distribution  of  the  lymphatics 
running  to  the  affected  gland.  In  many  instances  the  enlargement  is  pro- 
tective and  a  measure  of  the  activity  of  the  lymphocytes  in  the  gland  in 
destroying  the  microbes  or  toxins  which  reach  its  meshes.  The  glands  in 
this  way  act  as  a  barrier  to  the  spread  of  the  infection  into  the  system. 
Sometimes  the  process  is  very  acute,  the  poison  strong,  and  the  infection  one 
by  pyogenic  organisms,  so  that  the  gland  undergoes  suppuration. 

According  to  the  situation  of  the  glands  there  are  different  causes 
of  enlargement.  Some  causes  produce  general  lymphatic  hyperplasia,  e.g., 
Hodgkin's  disease  and,  to  a  less  extent,  specific  fevers,  and  the  continued 
toxaemia  of  prolonged  tuberculous  or  septic  affections.  More  usually  the 
enlargement  is  limited  to  a  group  of  glands,  especially  those  in  the  cervical 
regions,  not  a  surprising  fact  when  the  numerous  sources  of  infection  about 
the  scalp,  ears,  face,  nose  conjunctivae,  mouth,  teeth  and  throat  are  taken 
into  account.  Occasionally  no  definite  cause  can  be  found,  as  in  those  cases 
which  follow  exposure  to  cold  and  in  the  so-called  glandular  fever.  Possibly 
some  of  these  are  due  to  the  rheumatic  poison.  Cervical  adenitis  has  been 
noted  in  cases  of  erythema  nodosum,  and  this  has  sometimes  been  thought 
a  rheumatic  manifestation,  though  it  is  much  more  probably  toxaemic. 

Cervical  adenitis  from  throat  and  mouth  affections  differs  in  its 
location.  The  submaxillary  lymph  nodes  are  affected  as  the  result  of 
carious  teeth,  if  the  gums  are  inflamed  ;  and  later  on  the  gland  below  and 
behind  the  angle  of  the  jaw  is  attacked.  This  is  distinguished  from  the 
submaxillary  lymph  node  by  being  more  movable  posteriorly.  It  is  the 
one  which  becomes  enlarged  in  affections  of  the  faucial  tonsil ;  and  subse- 
quently the  lower  deep  cervical  glands  may  become  enlarged.  In  diseases 
of  the  pharyngeal  tonsil  the  glands  just  beneath  the  posterior  border  of  the 


520  Chapter   XLIII. 

sterno-mastoid  are  first  attacked,  then  those  under  the  muscle,  and 
lastly  those  in  front  of  it,  causing  a  diffuse  swelling  of  the  upper  part  of  the 
muscle. 

Tuberculosis  is  one  of  the  most  common  causes  of  adenitis,  and  is 
particularly  liable  to  follow  enlargement  from  other  causes.  The  vitality 
of  the  gland  is  lowered  and  the  tubercle  bacillus  finds  in  it  a  suitable  nidus 
for  its  growth  and  development.  Tuberculosis  of  glands  is  therefore  due  to 
primary  infection  of  a  patient  unduly  susceptible  to  tuberculous  disease  ; 
to  secondary  infection  of  a  gland  of  lowered  vitality  ;  or  to  a  mixed  infec- 
tion by  pyogenic  organisms  in  addition.  In  the  last  case  there  is  a  great 
tendency  to  suppuration.  The  effect  of  tuberculous  infection  is  first 
hyperemia  and  swelling  ;  secondly,  proliferation  of  the  adenoid  reticulum  ; 
and  finally  destruction  or  conversion  of  lymphoid  cells  and  caseation. 
Sometimes  there  is  merely  hyperplasia.  The  tubercle  bacilli  may  be  found 
in  involution  forms,  known  as  "  Schron's  capsules."  Several  glands  are 
generally  affected.  In  the  early  stages  they  are  hard  and  freely  movable 
on  themselves  and  the  surrounding  tissues.  Later  they  become  adherent 
to  each  other  and  to  the  skin,  and  often  break  down.  Softening  is  due  to 
caseation  or  pyogenic  infection.  The  skin  becomes  involved,  inflamed, 
thin  and  perforated,  and  the  pus  and  caseous  matter  are  discharged. 
Occasionally  the  tuberculosis  starts  as  an  acute  process.  Much  more  often 
it  begins  quietly,  remains  more  or  less  stationary  for  some  time,  and  then 
undergoes  rapid  exacerbation  and  breaks  down.  For  this  reason  it  is 
imperative  to  keep  such  cases  under  close  observation,  as  the  time  for 
operation  is  before  the  skin  and  subcutaneous  tissues  have  become  involved. 
Tuberculous  supracondylar  glands  are  due  to  strumous  dactylitis  and  the 
inguinal  glands  may  become  infected  by  circumcision. 

Generalised  Tuberculous  Adenitis. — A  few  cases  have  been  described 
in  which  many  glands  are  acutely  involved,  possibly  as  the  result  of  a  general 
infection  of  the  glands  with  the  tubercle  bacillus.  They  run  a  short  course 
and  exhibit  anaemia,  irregular  fever  with  exacerbations,  and  polymorpho- 
nuclear leucocytosis.     The  spleen  is  little  or  not  at  all  enlarged. 

Tuberculous  Thoracic  Glands. — The  bronchial,  anterior  and  posterior 
mediastinal  glands  may  be  enlarged  separately  or  simultaneously,  almost 
always  from  tuberculous  infection.  Very  considerable  enlargement  is 
needed  to  produce  symptoms  ;  and  hyperplasia,  caseation,  fibrosis  and 
calcification  can  occur  without  any  evidence  thereof.  Enlargement  of  the 
anterior  mediastinal  glands  may  be  so  great  as  to  cause  dulness  on  per- 
cussion over  the  manubrium.  According  to  Durham  these  glands  are 
commonly  the  first  affected  in  peritonitis,  for  they  are  the  most  important 
drain  of  the  peritoneum.  If  so,  it  is  curious  that  they  are  not  more  con- 
stantly involved  in  tuberculous  peritonitis.  Enlargement  of  the  posterior 
mediastinal  glands  may  produce  bronchophony,  bronchial  breathing  and 
then  dulness  high  up  in  the  interscapular  region. 


The  Blood  and  Lymphoid  Structures.  521 

The  tracheo-bronchial  glands  are  those  situated  about  the  root  of  the 
lungs,  between  the  divisions  of  the  bronchi.  They  are  usually  all  affected  ; 
more  especially  the  "  pre-tracheal  gland,"  the  one  at  the  bifurcation  of  the 
trachea.  If  the  disease  is  unilateral,  it  is  i  or  5  times  more  common  on  the 
right  side  than  on  the  left,  possibly  because  the  right  bronchus  is  greater 
than  the  left.  The  tuberculous  infection  is  conveyed  to  the  bronchial 
glands  by  the  inspired  air  ;  by  the  pharyngeal  lymphatics  from  the  pharynx, 
tonsils  and  adenoids,  via  the  cervical  and  mediastinal  glands,  thoracic 
duct  and  right  side  of  the  heart ;  from  the  intestines,  mesenteric  and  retro- 
peritoneal glands  ;  and  occasionally  from  the  oesophagus,  lungs,  carious 
vertebra?  or  by  the  blood  stream.  In  quite  three-fourths  of  all  cases  of 
miliary  tuberculosis  and  tuberculous  meningitis  in  early  life  the  oldest 
tuberculous  lesion  is  in  the  tracheo-bronchial  glands,  generally  in  the  pre- 
tracheal gland,  and  it  is  exceptional  to  find  evidence  of  a  cervical 
adenitis.  This  is  an  important  point  for  it  is  an  argument  against  the 
entrance  of  the  tubercle  bacillus  into  the  system  through  the  mucous 
membrane  of  the  mouth  and  throat. 

The  symptoms  depend  on  the  degree  of  engorgement  and  the  situation 
of  the  affected  glands,  and  may  be  equivocal  or  even  temporary.  A  rise  of 
temperature  in  the  evening  is  not  infrequent  and  the  child  may  waste,  be 
easily  tired,  complain  of  pain  under  the  manubrium  and  have  a  troublesome 
cough.  The  cough  is  due  to  pressure  or  irritation  of  the  recurrent  laryngeal 
nerve.  It  is  spasmodic,  paroxysmal,  suggestive  of  but  more  constant  than 
pertussis,  and  occasionally  ends  in  vomiting.  Pressure  on  the  trachea  or 
bronchus  may  cause  dyspnoea  on  slight  exertion  and  stridor.  If  on  a  bron- 
chus, it  may  render  the  breath  sounds  weaker  over  the  corresponding  lung. 
The  irritation  from  pressure  may  set  up  bronchitis,  broncho-pneumonia 
and  bronchiectasis.  Occasionally  the  gland  ulcerates  through  into  the 
trachea  or  bronchus  and  causes  sudden  death  from  asphyxia,  or  severe  and 
fatal  haemorrhage,  a  small  circular  ulcer  being  found  after  death.  Some- 
times the  caseous  material  is  coughed  up  and  the  child  gets  well.  Ulceration 
into  the  air  passages  gives  rise  to  offensive  breath.  The  pericardium  may  be 
invaded  and  ulceration  into  the  aorta  has  occurred. 

Pressure  on  the  oesophagus  is  indicated  by  dysphagia.  The  pre-tracheal 
gland  is  apt  to  perforate  the  oesophagus.  A  girl  died  from  hemorrhage, 
blood  and  air  being  brought  up,  after  an  illness  of  9  months  with  wasting, 
•diarrhoea  and  vomiting,  and  offensive  breath.  The  stomach  was  full  of 
blood  and  a  small  circular  ulcer  of  the  oesophagus  was  found.  It  had 
smooth,  sloping  edges,  and  was  secondary  to  an  abscess  of  the  pre-tracheal 
gland  which  opened  also  into  the  lower  lobe  of  the  right  lung.  Similar 
•cases  are  on  record  and  others  in  which  the  gland  had  only  ulcerated  into 
the  oesophagus.  Eupture  into  the  lung  is  generally  followed  by  extensive 
caseous  pneumonia  and  general  dissemination.  In  children  it  is  not  very 
uncommon  to  find  tuberculous  infection  spreading  backward   along   the 


522  Chapter  XLIII. 

lymphatics  running  into  the  gland,  causing  a  definite  triangular  patch  of 
consolidation  in  the  lower  lobe.  Occasionally  the  gland  ruptures  into  the 
pleura  and  sets  up  empyema.  In  a  child,  aged  4  years,  there  were  signs  of 
enlargement  of  the  anterior  mediastinal  glands,  dulness  and  bronchial 
breathing  over  the  manubrium.  Gradually  the  dulness  extended  until  the 
note  over  the  whole  right  upper  lobe  was  impaired.  Exploration  high  up 
in  the  axilla  revealed  the  presence  of  pus.  The  abscess  was  opened  and  a 
probe  could  be  passed  upward  and  inward,  between  the  upper  and  middle 
lobes,  in  the  direction  of  the  manubrium  for  3  ins.  The  child  recovered. 
Tuberculosis  of  the  lungs,  especially  of  the  lower  lobes,  in  children  is  com- 
monly a  sequel  of  tuberculous  adenitis.  The  caseous  glands  may  become 
inflamed  as  the  result  of  non- tuberculous  disease  and  then  produce  general 
dissemination. 

Physical  signs  are  sometimes  well  marked.  They  are  generally  due  to 
pressure  on  veins  and  to  the  size  of  the  enlargenient.  Pressure  on  the 
vena  cava  superior  causes  dilatation  of  the  veins  in  the  neck  and  on  the 
cheeks,  temples  and  front  of  the  chest ;  puffiness  of  the  face  and  eyelids  ; 
oedema  and  cyanosis  ;  headache  and  attacks  of  giddiness.  These  signs  may 
be  unilateral,  if  the  innominate  vein  alone  is  compressed.  A  continuous- 
venous  hum,  heard  over  the  manubrium  when  the  head  is  thrown  back, 
has  been  ascribed  by  Eustace  Smith  to  pressure  on  the  vena  cava  superior 
or  the  left  innominate  vein.  It  is  not  always  present  and  may  occur  though 
no  enlarged  glands  are  found  after  death.  Enlarged  glands  under  the 
manubrium  cause  dulness  which  extends  laterally,  especially  to  the  right,. 
and  bronchial  or  tracheal  breathing.  Enlargement  of  the  posterior  medias- 
tinal glands  causes  dulness  on  either  side  of  the  spine,  from  the  second  to 
the  fifth  dorsal  vertebra,  prolonged  expiration,  bronchial  or  amphoric 
breathing,  and  bronchophony,  notably  on  the  right  side.  Normally  the 
bronchial  tone  stops  at  the  seventh  cervical  spine.  If  the  glands  are 
enlarged,  it  may  extend  lower,  even  down  to  the  fourth  dorsal  spine. 
X-ray  examination  may  show  an  increase  in  size  and  density  of  the  shadow 
at  the  root  of  the  lung.  Lymphocytosis  is  sometimes  present.  The  sub- 
clavicular and  episternal  lymph  glands  may  be  enlarged.  Undue  hairiness- 
of  the  chest  has  been  noted.  Anaemia,  anorexia,  night  sweats,  epistaxis, 
fever  and  haemoptysis  may  occur. 

Tuberculous  Mesenteric  Glands. — The  name  of  "tabes  mesenterica "" 
should  be  limited  to  the  rare  cases  in  which  the  mesenteric  glands  are- 
tuberculous,  apart  from  peritonitis.  It  is  a  rare  disease  in  that  it  is  not 
often  diagnosed  unless  the  peritoneum  is  also  involved.  A  movable  tumour 
in  a  child's  abdomen  is  much  more  likely  to  be  a  faecal  mass  than  an  enlarged 
gland.  In  the  early  stages,  before  general  infection  or  peritonitis  occurs,, 
the  condition  is  not  found  for  no  attention  is  attracted  to  the  abdomen. 
These  lumps  are  found  in  children  admitted  to  hospital  for  general  ill- 
health,    abdominal   distension,    slight   fever,    anorexia   and   constipation.. 


The  Blood  and  Lymphoid  Structures.  523 

They  are  due  to  primary  infection  or  tuberculous  enteritis  ;  and  probably 
the  cause,  but  not  the  result  of  tuberculous  peritonitis.  The  glands  may 
calcify,  become  caseous,  set  up  caseous  peritonitis,  and  rarely  suppurate. 
Whitworth  (1908)  reported  a  case  of  ulceration  into  the  superior  mesenteric 
artery.  Adhesions,  intestinal  obstruction  and  local  peritonitis  may  ensue. 
The  most  common  situation  is  to  the  right  of  and  a  little  above  the  level  of 
the  umbilicus,  or  below  and  to  the  right,  and  less  often  below  and  to  the 
left  of  the  navel. 

Symptoms  may  be  absent.  Occasional  signs  are  anaemia,  pain  and 
vomiting  ;  colicky  pains  and  loose  stools  ;  wasting  and  jaundice,  due  to 
pressure  or  of  toxic  origin  ;  and  enlargement  of  the  liver.  They  must  be 
diagnosed  from  subacute  intussusception,  faecal  masses,  hydatids,  new 
growths  and  caseous  peritonitis.  Caseous  masses  are  included  among 
adherent  gut  and  are  little,  if  at  all,  movable. 

Treatment  of  Adenitis. — In  the  treatment  of  all  visible  or  palpable 
glands  it  is  essential  to  remove  or  treat  any  local  exciting  cause  of  irritation 
such  as  carious  teeth,  alveolar  abscess,  adenoids,  enlarged  tonsils,  throat 
affections,  ear  troubles  and  skin  lesions.  If  there  is  evidence  of  tuberculosis 
rely  on  general  treatment  by  sea  air,  hygiene,  etc.,  and  give  cod-liver  oil, 
maltine,  syr.  fer.  iodidi,  ichthyol  and  ferri-ichthyol.  Friction  with  ointments 
is  not  advisable  for  it  may  cause  irritation  and  induce  suppuration.  Paint- 
ing with  iodine  is  useless.  An  ointment  of  ung.  hydragyri,  ung.  belladonnae 
and  olive  oil,  p. a.,  may  be  smeared  on.  Operate  before  the  glands  become 
adherent  or  break  down,  provided  that  they  are  undoubtedly  tuberculous. 
Little  scarring  is  left.  The  removal  of  tuberculous  cervical  glands  is  not  an 
operation  to  be  undertaken  lightly  for  many  more  glands  will  be  found 
affected  than  can  be  felt,  and  they  must  all  be  thoroughly  and  carefully 
removed.  The  removal  of  those  chiefly  affected  is  rapidly  followed  by 
enlargement  of  others  left  behind,  and  further  operation  is  needed.  To 
incise  and  scrape  a  tuberculous  gland  is  bad  treatment.  A  sinus  is  almost 
certain  to  be  left  which  heals  with  difficulty,  and  the  skin  and  surrounding 
tissues  may  become  infected.  It  is  doubtful  whether  it  is  ever  advisable  to 
attempt  the  removal  of  tuberculous  mesenteric  glands,  though  it  has  been 
carried  out  successfully.    Most  cases  get  well  under  medical  treatment. 

For  inflammatory  enlargements  use  hot  or  cold  applications,  bella- 
donna and  glycerine,  or  mercury  and  belladonna  ointments.  Local  treat- 
ment must  be  applied  gently. 

Glandular  Fever. — Syn.  :  Driisenfieber  (Pfeijfer),  Febrile  Polyadenitis, 
Fievre  Ganglionare. — Pfeiffer  (1889)  suggested  the  possible  existence 
of  glandular  fever  as  a  distinct  entity,  and  many  cases  of  this  type  have 
been  recorded  since.  It  is  an  infectious  disease,  running  through  a  household 
and  especially  affecting  the  younger  members.  It  occurs  at  any  age,  com- 
monly 4-12  years,  and  is  infrequent  after  puberty.  Both  sexes  are  equally 
liable.    The  incubation  period  is  stated  by  Byers  to  be  5-7  days. 


524  Chapter   XLIII. 

The  onset  is  sudden,  often  with  headache,  abdominal  pain  and  vomiting, 
perhaps  with  convulsions  or  rigors.  The  temperature  rises  to  101-104°  F. 
In  24-48  hours  the  glands  at  the  angles  of  the  jaws  and  behind  the  sterno- 
mastoid  muscles,  forming  a  regular  chain,  are  enlarged.  They  are  tender, 
painful,  hard,  movable,  of  the  size  of  large  beans,  and  cause  discomfort 
and  stiffness  of  the  neck,  and  perhaps  dysphagia.  They  may  even  reach 
the  size  of  a  pigeon's  egg.  The  skin  is  rarely  reddened.  The  adenitis  may 
not  commence  until  the  third  or  fourth  day,  and  may  be  unilateral.  It 
continues  for  a  few  days  to  a  week,  gradually  subsides  in  7-10  days,  and 
may  last  4  weeks.  The  fever  is  from  1-2°  F.  lower  in  the  morning  than  the 
evening,  and  is  of  short  duration.  With  it  are  associated  from  the  onset 
headache,  foul  tongue,  anorexia,  nausea,  sometimes  vomiting  and  con- 
stipation. In  mild  cases  there  may  be  diarrhoea.  Abdominal  pain  is  a 
prominent  symptom  but  may  be  absent.  The  face  is  flushed  in  the  febrile 
stage  and  afterwards  unduly  pale.  The  liver  and  spleen  are  enlarged  in 
about  three-quarters  of  the  cases  in  some  outbreaks.  The  mesenteric, 
axillary  and  occasionally  the  inguinal  glands  are  enlarged.  Undue  redness  of 
the  fauces  and  pharynx  has  been  found  sometimes,  even  sorethroat  at  the 
onset,  but  no  definite  pharyngitis  or  tonsillitis. 

The  chief  complications  are  epistaxis  and  hsemorrhagic  nephritis  ; 
simple  albuminuria  ;  the  passage  of  urine  containing  hyaline,  epithelial 
and  granular  casts  ;  or  simple  hematuria  without  any  evidence  of  nephritis. 
In  two  boys  hematuria  was  the  main  sign  ;  in  another,  who  had  just 
escaped  operation  for  the  removal  of  glands  because  albumin  was  found  in 
the  urine,  a  relapse  a  few  days  later  was  accompanied  by  hsematuria.  The 
glands  do  not  suppurate. 

The  disease  is  mild  if  the  temperature  does  not  rise  above  102°  F., 
and  severe  if  it  reaches  104°  F.  Death  is  a  rare  event  and  due  to  some 
complication.  The  fever  lasts  from  3-7  days  and  may  end  by  crisis  and 
sweating  ;  or  the  illness  may  last  from  a  few  days  to  a  fortnight  with 
irregular  pyrexia.  The  adenitis  subsides  slowly.  The  renal  complications 
in  cases  under  my  care  have  invariably  cleared  up  entirely.  Convalescence 
is  prolonged  and  characterised  by  anaemia,  debility  and  depression. 

At  the  onset  the  illness  simulates  influenza  or  a  specific  fever,  notably 
aberrant  typhoid,  or  some  throat  affection.  Mumps  can  be  excluded,  for 
the  parotid  glands  are  unaffected  and  there  is  no  pain  on  eating.  Local 
sources  of  adenitis  must  be  looked  for  and  tuberculosis,  Hodgkin's  disease 
and  the  early  stage  of  acute  leukaemia  borne  in  mind.  It  is  doubtful 
whether  we  are  justified  in  regarding  this  as  a  specific  disease  though  it  is 
very  convenient  to  do  so.  The  course,  symptoms,  complications  and 
delayed  convalescence  are  very  suggestive  of  a  microbial  infection  of  the 
throat  or  pharynx,  perhaps  post-nasal.  Pneumococci  and  streptococci 
have  been  found.  The  treatment  consists  of  cold  compresses,  belladonna 
fomentations,   or  belladonna  and  glycerine  locally  ;    mild  purgation  by 


The  Blood  and  Lymphoid  Structures.  525 

calomel ;    phenacetin,  salicin,  quinine  or  a  mild  febrifuge  ;    bed  and  light 
diet;  tonics,  iron  and  sea  air  during  convalescence. 

Lymphosarcoma. — This  is  a  malignant  disease  of  the  glands,  sometimes 
seen  in  children  from  2-15  years  of  age.  It  begins  in  mediastinal  glands, 
generally  the  posterior  ones,  and  spreads  to  cervical  glands,  in  which  it  is 
first  evident  or  possibly  at  times  primary.  In  the  earliest  stages,  when 
cervical  enlargement  is  alone  present,  the  lump  is  sometimes  called  a 
Lymphoma.  This  stage  lasts  from  one  to  several  months  without  malaise, 
pain  or  local  discomfort.  Many  glands  in  series  are  affected,  on  one  or  both 
sides  ;  and  are  firm,  of  uniform  consistence,  discrete,  movable,  and  neither 
painful  nor  tender.  The  skin  is  uninvolved.  Subsequently  the  child 
develops  anremia,  anorexia,  debility,  shortness  of  breath,  cough,  faint 
or  giddy  attacks,  and  choking  fits,  from  pressure  on  various  intra-thoracic 
structures.  The  symptoms  and  physical  signs  are  those  of  enlarged  thoracic 
glands,  as  above  described.  The  glands  tend  to  become  fused,  though  there 
is  no  sign  of  inflammation.  In  late  stages  the  spleen  may  be  enlarged,  the 
axillary  glands  rarely  involved,  and  ascites  and  oedema  develop.  The 
blood  picture  is  that  of  mild  anaemia,  with  leucopenia  or  a  relative  lympho- 
cytosis. Microscopically  the  growths  consist  of  masses  of  small  round 
cells,  like  lymphocytes,  with  large  nuclei  and  a  fine  stroma,  very  little 
vascular.  In  the  case  of  a  boy,  3  years  old,  the  growth  was  apparently  a 
round-celled  sarcoma  of  a  posterior  mediastinal  gland,  no  cervical  or  other 
glands  being  affected.  It  compressed  without  invading  the  right  lung, 
which  was  practically  airless.  The  tumour  had  broken  down  in  the  peri- 
pheral portion,  forming  a  large  irregular  cavity  filled  with  blood  and  clot. 
It  was  adherent  to  the  diaphragm  and  chest  wall,  except  over  the  upper 
lateral  and  anterior  portions.  In  another  3-year  old  boy,  who  died  during 
an  attack  of  dyspnoea  and  cyanosis  from  tracheal  pressure,  the  growth  was 
retro-pleural  and  had  apparently  started  in  the  left  oesophageal  or  posterior 
aortic  glands  in  the  upper  part  of  the  mediastinum.  The  duration  of  these 
cases  is  very  variable.  From  the  time  that  symptoms  due  to  the  intra- 
thoracic growth  develop  to  the  fatal  termination,  the  illness  lasts  from  a  few 
weeks  to  several  months. 

Lymphadenoma  or  Hodgkin's  Disease  differs  from  lymphosarcoma  in 
that  it  affects  all  the  lymphoid  tissues  and  the  glands  remain  distinct.  It 
is  rare  in  infancy  and  childhood.  Many  of  the  cases  described  under  this 
name  are  probably  really  instances  of  lymphosarcoma,  multiple  tuberculous 
adenitis  and  possibly  syphilis.  Out  of  43  cases  10  were  under  10  years  of 
age  (Mitchell  Clarke,  1901).  Hutchison  (1904)  states  that  it  is  rare  under 
5  years  of  age.    Greig  (1907)  says  that  it  occurs  after  30  years  of  age. 

The  signs  are  anaemia  and  progressive  hyperplasia  of  the  lymph  nodes. 
The  liver  and  spleen  are  usually  enlarged  and  contain  lymphoid  masses 
resembling  secondary  growths,  and  similar  masses  may  be  found  in  other 
organs.  Limited  to  one  group  of  glands  it  may  be  spoken  of  as  a  Lymphoma. 
Acute  cases  show  moderate  fever  and  a  haernorrhagic  tendency,  suggestive 


526  Chapter   XLIII. 

of  an  infectious  origin.  "When  generalised  it  resembles  chronic  lymphatic 
leukaemia  clinically,  except  in  its  blood  picture.  At  first  the  blood  is  normal. 
Later,  it  shows  the  usual  characteristics  of  secondary  anaemia.  Polynuclear 
leucocytosis  may  be  present  from  secondary  infection,  and  a  few  myelocytes 
and  haematoblasts  in  advanced  cases.  The  glands  are  firm,  movable,  non- 
adherent, and  do  not  break  down  unless  there  is  secondary  infection.  They 
are  found  in  the  neck,  axillae,  groins,  mediastinum  and  mesentery. 

Greenfield  (1877)  recognised  hard  and  soft  types,  due  to  chronic 
inflammation  of  the  fibrous  stroma  of  the  glands.  Andrewes  (1902)  stated 
that  the  distinction  between  the  cortex  and  medulla  is  abolished,  the 
stroma  hyperplastic,  lymphocytes  decreased,  eosinophiles  generally 
increased,  and  the  endothelial  cells  large  and  multinucleated  (lymph- 
adenoma  cells).  D.  M.  Keed  (1902)  found  proliferation  of  endothelial  cells 
and  dilatation  of  blood  vessels,  and  that  the  spaces  were  filled  with  these 
cells  and  masses  of  lymphoid  cells  in  early  stages  ;  the  fibrosis  being  a  later 
development. 

Lymphadenoma  is  sometimes  differentiated  from  Hodgkin's  disease. 
It  is  probable  that  some  of  the  cases  are  identical  therewith  and  others 
are  lymphosarcomata.  Rolleston  and  Latham  found  the  stomach  of  a 
boy,  18  months  old,  covered  with  numerous  smooth  white  polypoid  growths 
of  lymphoid  tissue,  enlarged  anterior  mediastinal  glands,  large  spleen,  and 
a  blood  picture  of  myelogenous  leukaemia.  It  was  supposed  to  be  secondary 
to  ear  disease.  In  a  boy,  14  months  old,  with  otitis  media,  masses  of 
enlarged  non-adherent  glands  were  present  on  both  sides  of  the  neck  and 
the  spleen  reached  the  crest  of  the  ilium.  The  blood  count  yielded  red 
cells  7,470,000,  whites  60,000,  small  lymphocytes  14-4,  large  lymphocytes 
31*5,  polymorphs  53-9  per  cent,  and  a  few  eosinophiles.  The  autopsy  showed 
many  cervical  glands  breaking  down  from  secondary  infection,  enlarged 
mesenteric  glands,  a  mass  behind  the  sternum  and  at  the  root  of  the  lung, 
fatty  liver,  fibrosis  of  the  spleen,  no  leucocytic  infiltration,  and  giant  cells 
in  the  liver,  spleen  and  lungs.  The  glands  in  lymphadenoma  seem  specially 
prone  to  secondary  tuberculous  infection.  Cases  of  the  above  type  indicate 
that  the  differentiation  into  distinct  groups  is  difficult  and  that  there  are 
probably  intermediate  varieties  or  mixed  infections.  It  is  not  uncommon 
for  Hodgkin's  disease  to  start  as  a  secondary  process,  after  a  primary 
disease  of  the  ear  with  glandular  infection.  Tuberculosis  may  be  a  further 
complication.  Moreover  tuberculosis  is  not  a  rare  sequence  of  anaemia 
splenica  infantum,  and  secondary  tuberculous  adenitis  or  a  lymph- 
adenomatous  condition  in  the  course  of  this  disease  would  give  rise  to 
grave  difficulty  in  diagnosis. 

The  prognosis  is  bad  except  when  the  mischief  is  limited  to  one  group 
of  glands.  Leucocytosis,  due  to  secondary  infection,  may  suggest  the  onset 
of  acute  leukaemia,  an  occasional  termination.  The  treatment  is  on  the 
.same  lines  as  that  of  other  types  of  anaemia. 

The  Thymus. — The  thymus  is   a    ductless  gland  found   in   all  true 


The  Blood  and  Lymphoid  Structures.  527 

vertebrates  and  demonstrated  bySchaffer  in  marsipobrancb.iatefisb.es.  It  is 
reddisb-grey  in  colour,  situated  in  tbe  anterior  mediastinum  just  above  tbe 
pericardium,  and  extends  upward  to  about  2  cm.  above  tbe  sternum  and 
2  cm.  below  tbe  tbyroid,  lying  between  tbe  innominate  and  left  carotid 
arteries.  It  is  thickest  bebind  tbe  manubrium  and  tbere  covers  part  of  the 
vena  cava  superior,  tbe  innominate  veins  and  tbe  arcb  of  tbe  aorta,  and 
extends  backward  to  tbe  tracbea.  Lower  down  it  is  partially  covered  by  tbe 
anterior  edges  of  tbe  lungs.  In  transverse  section  of  an  infant  it  may 
occupy  as  large  an  area  as  tbat  of  tbe  left  lung.  It  may  cause  marked 
dulness  on  percussion,  continuous  witb  tbe  cardiac  dulness,  and  extending 
more  to  tbe  left  tban  tbe  right.  It  receives  blood  from  the  inferior  thyroid 
arteries  and  its  nerve  supply  from  the  sympathetic. 

It  is  somewhat  flat,  composed  of  two  lobes,  usually  asymmetrical  and 
united  by  an  isthmus,  and  covered  by  a  fibrous  capsule  from  which  septa 
pass  inward  dividing  it  into  lobules  and  follicles.  Each  follicle  is  more 
or  less  polyhedral,  and  consists  of  a  dense  cortical  and  a  looser  medullary 
portion,  dependent  on  the  number  of  lymphoid  cells.  In  the  medullary 
parts  are  seen  the  concentric  corpuscles  of  Hassall,  protoplasmic  masses 
with  a  nucleated  granular  centre  surrounded  by  flattened  cells.  They  are 
the  remains  of  original  epithelial  outgrowths.  Eosinophiles  are  fairly 
numerous.  The  size  and  weight  of  the  gland  are  very  variable  in  different 
infants  and  at  different  ages.  It  varies  in  the  young  of  the  same  litter, 
is  rarely  absent  except  in  acephalic  twins,  and  is  often  large  in  monsters. 
It  is  normally  largest  shortly  after  birth,  remains  about  the  same  size  for 
2-5  years,  and  then  slowly  atrophies.  The  avian  thymus  does  not  undergo 
regressive  changes.  As  it  atrophies  it  is  converted  into  fibrous  tissue,  and 
may  be  infiltrated  with  fat  after  puberty.  The  weight  is  no  reliable  guide  to 
the  functional  capacity.    No  constant  ratio  to  body  weight  can  be  made  out. 

The  weight  in  grammes  at  birth  is  said  to  be  3-5  by  several  observers, 
8-12  (Haugbsted),  13-20  by  others.  On  the  whole  it  is  probable  that  the 
lower  figures  are  the  more  reliable,  and  that  the  other  ones  are  due  to 
including  exceptional  weights.  Similarly  I  think  we  may  accept  5-7  gms. 
as  an  average  weight  during  the  first  5  years  of  life  and  regard  glands  of 
greater  weight  as  to  some  extent  abnormal. 

Its  functions  are  somewhat  uncertain.  The  gland  is  bypoblastic  in 
origin,  being  developed  from  the  epithelium  of  the  third  pouch  of  the 
gut-tract,  and  acquires  its  infantile  type  in  the  third  month  of  foetal  life. 
Kolliker  regards  it  as  the  parent  source  of  leucocytes.  For  a  relatively  long 
time  the  blood  only  contains  nucleated  red  cells  and  at  the  period  when 
leucocytes  first  appear  there  is  no  spleen,  rectal  gland  or  caecum,  and  the 
thymus  is  represented  by  small  pieces  of  modified  epithelium.  Beard 
suggests  that  the  first  leucocytes  are  formed  by  modification  of  these 
epithelial  cells  and  that  the  thymus  is  the  parent  of  all  leucocytes.  Bryce, 
however,  states  (1904)  that  he  has  found  leucocytes  in  the  blood  of 
Lepidosiren   before   any  trace   of   a   thymus   could   be   detected.      Blood 


528  Chapter   XLIII. 

pressure  experiments  with  extracts  of  the  gland  seem  to  show  that  it  has 
no  direct  vasomotor  influence.  Extirpation  causes  muscular  weakness  and 
progressive  debility  in  frogs  (Abelous  and  Billard,  1896)  ;  changes  in  the 
blood,  disturbance  of  growth  of  bone,  nervous  symptoms  and  profuse 
sweating,  a  condition  like  rickets  (Friedleben) ;  no  ill  effects  in  dogs, 
except  temporary  weakness  and  erythropenia  in  young  ones  (Tarulli  and 
Lo  Monaco,  1858).  In  some  way  the  gland  exercises  an  influence  on 
nutrition  and  haemopoiesis. 

Atrophy  is  noted  in  various  conditions.  The  gland  may  be  absent  in 
the  mentally  defective.  It  is  atrophied  in  marasmus  from  any  cause  and 
the  weight  is  a  fair  measure  of  the  nutrition  in  infancy.  In  moderate  atrophy 
the.  cortex  and  medulla  are  not  easily  distinguished.  In  severe  wasting 
there  is  much  fibrosis  of  the  capsule, trabecular  and  about  the  bloodvessels. 
The  endothelial  cells  undergo  proliferation  and  the  lymphoid  cells  are 
decreased.  Small  giant  cells,  somewhat  like  those  seen  in  the  glands  in 
lymphadenoma,  have  been  found  by  Dudgeon.  Hassan's  corpuscles  stain 
bright  yellow  or  orange  with  Van  Gieson's  fluid,  perhaps  from  hyaline 
degeneration.  In  many  illnesses  the  gland  is  atrophied  and  shows  fibrosis 
and  hyaline  degeneration,  often  infiltration  with  adipose  tissue.  Atrophy 
of  the  thymus  is  part  of,  but  not  the  cause  of,  the  malnutrition. 

Hypertrophy  is  present  in  many  cases  of  sudden  and  unexpected  death 
in  infants,  thymic  asthma,  the  status  thymicus  or  lymphaticus,  in  most 
acute  conditions  in  which  there  is  leucocytosis,  in  leukaemia  and  lympha- 
denoma, in  many  cases  of  acromegaly  and  gigantism,  and  sometimes  in 
exophthalmic  goitre,  chlorosis,  epilepsy  and  myasthenia  gravis ;  and  after 
castration  in  rabbits  (Calzolari). 

Other  affections  are  rare.  Miliary  tubercles  and,  less  often,  tuberculous 
nodules  are  found.  Primary  inflammation  has  been  recorded  and  pysemic 
abscesses.  Multiple  minute  haemorrhages  are  present  in  asphyxia  neona- 
torum, and  scattered  haemorrhages  in  most  lung  diseases.  Minute  collec- 
tions of  a  thick,  yellowish- white,  semi-purulent  material  can  sometimes 
be  squeezed  out  on  section.  They  are  not  abscesses,  but  are  due  to  softening 
of  normal  lymphoid  tissue  and  are  not  pathological.  Gummata  are  very 
uncommon. 

Status  Thymicus  vel  Lymphaticus,  or  Lymphatism. — As  long  ago  as 
1614  Felix  Plater  found  the  thymus  enlarged  in  cases  of  sudden  death  from 
dyspnoea  in  3  children  of  one  family.  That  it  may  be  a  family  peculiarity 
is  shown  by  its  occurrence  in  more  than  one  child,  e.g.,  in  3  nurslings 
(Weber),  in  3  children  (Barrock),  and  in  5  out  of  9  children  (Hedinger,  1905), 
an  autopsy  on  the  fifth,  aged  5  years,  showing  the  status  lymphaticus. 
Perrin  reported  that  9  out  of  11  children  in  one  family  died  suddenly,  but 
the  cause  was  not  ascertained.  In  1889  and  1890  Paltauf  collected  a  large 
number  of  such  cases  in  adults  and  named  the  affection  "  the  lymphatico- 
chlorotic  constitution."    He  regarded  it  as  a  morbid  entity,  a  condition  of 


The  Blood  and  Lymphoid  Structures.  529 

hyperplasia  of  the  thymus  and  lymphatic  apparatus  generally,  including 
the  spleen.  With  it  is  associated  an  abnormal  predisposition  to  sudden  or 
unexpected  death  in  infants  and  adults.  A  large  thymus  may  give  rise,  by 
compression  of  the  trachea  or  in  other  ways,  to  dyspnoea,  stridor,  asphyxia 
and  even  sudden  death.  This  was  named  by  Millar  "  Thymic  Asthma" 
a  title  which  might  be  reserved  for  those  cases  in  which  there  is  definite 
evidence  of  compression  or,  in  addition,  those  in  which  attacks  of  dyspnoea 
are  the  chief  symptom. 

Clinically  there  are  three  types  of  these  cases  in  which  sudden  death 
occurs.  In  one  the  child  is  apparently  healthy  and  no  other  cause  is 
discoverable.  In  the  second  it  is  associated  with  the  presence  of  other 
disease,  adequate  or  inadequate  to  produce  the  fatal  issue.  In  the  third 
a  definite  cause  of  death  is  present  but  one  which  is  insufficient  to  produce 
it  in  a  normal  child.  Such  cases  are  those  due  to  intense  excitement  or  fear, 
a  sudden  cold  plunge,  the  introduction  of  a  tongue  spatula,  the  injection 
of  serum,  and  the  action  of  anaesthetics.  Possibly  some  still-births  and 
deaths  from  overlaying  depend  on  this  peculiarity  of  the  constitution.  The 
mode  of  death  varies.  It  takes  the  form  of  sudden  syncope  or  collapse, 
cyanosis  followed  by  pallor,  or  mild  epileptiform  convulsions.  In  thymic 
asthma  dyspnoea,  cyanosis  and  distress  may  precede  a  sudden  termina- 
tion by  several  hours.  Other  infants  have  laboured  breathing  and 
attacks  of  grunting  and  lividity  ;  symptoms  of  croup  ;  or  attacks  of 
suffocation  with  cyanosis  and  recession  (Siegel).  A  common  termination 
is  for  the  child  to  sit  up  in  its  cot,  turn  pale  or  livid,  and  fall  back  dead. 
One  child  was  playing  quietly  when  he  suddenly  ran  to  his  nurse  and 
died.  Perhaps  while  suckling  or  drinking  out  of  a  cup  the  head  is  thrown 
back  and  death  occurs  without  a  cry,  convulsion  or  movement  of 
any  sort. 

McCardie  (1908)  collected  30  fatal  cases  after  anaesthetics  :  chloroform 
17,  ether  6,  C.  and  E.  5,  nitrous  oxide  2  (doubtful  cases)  ;  1  after  injection 
of  morphine  and  2  after  local  anaesthesia.  Other  cases  have  been  reported 
since.  The  average  age  of  35  cases  was  16  years ;  7  under  10  years,  and 
14  from  10-20  years  of  age.  The  sexes  were  about  equal.  Death  in 
anaesthetic  cases  is  always  sudden;  with  facial  pallor,  dilated  pupils  and 
cardiac  failure,  and  occasionally  preceded  by,  or  simultaneous  with, 
respiratory  failure  and  cyanosis. 

The  signs  of  lymphatism  are  most  indefinite.  Many  patients  seem 
to  enjoy  perfect  health  but  they  are  very  subject  to  infectious  disease. 
Usually  the  complexion  is  pale  or  pasty,  the  skin  thin  and  pallid,  and  there 
is  excess  of  subcutaneous  fat.  In  addition  to  the  enlarged  thymus  there 
may  be  found  evidence  of  rickets,  enlarged  cervical  and  axillary  glands, 
hyperplasia  of  the  circumvallate  papillae,  the  tongue,  the  tonsils  and  the 
adenoid  tissue  of  the  pharynx,  enlargement  of  the  spleen  and  perhaps 
lymphocytosis.     The  heart  sounds  are  weak,  the  fisart  often  dilated,  pulse 

2   M 


530  Chapter   XLIII. 

soft,  and  blood  pressure  low.  The  pupils  are  large,  and  there  is  a  tendency  to 
cedema. 

Morbid  Anatomy. — The  anatomical  changes  are  those  of  hyperplasia  of 
lymphoid  tissues  throughout  the  body.  In  two  infants,  9  weeks  and 
9  months  old,  under  my  care,  who  died  suddenly  from  no  apparent  cause, 
the  solitary  follicles  and  Peyer's  patches  were  so  much  enlarged  as  to 
suggest  the  early  stage  of  typhoid  fever  ;  and  the  mesenteric  glands  were 
also  swollen.  The  mesenteric  and  retro-peritoneal  glands  are  especially 
large.  Sometimes  proliferation  of  the  endothelial  cells  along  the  tra- 
becule of  the  thymus  has  been  found  ;  and  proliferation,  with  slight  degen- 
erative changes  in  the  proliferated  cells,  in  the  spleen,  lymph  glands,  tonsils 
and  intestinal  lymph  masses. 

Pathogeny. — Death  is  ascribed  to  mechanical  pressure,  cardiac  par- 
alysis, or  toxaemia.  Tamassia  states  that  it  requires  a  weight  of  180  gms. 
to  compress  the  trachea,  and  Scheele  puts  the  weight  at  750-1000  gms. 
Certainly  there  is  a  very  narrow  space,  2-3  cm.  in  nurslings,  between  the 
manubrium  and  the  spinal  column,  and  this  can  be  further  decreased 
by  throwing  the  head  back.  Cases  are  on  record  in  which  the  symptoms 
have  been  cured  by  removal  of  part  of  the  gland,  and  the  trachea  has  been 
found  flattened.  Evidence  of  compression  is  often  absent  after  death, 
perhaps  because  the  trachea  is  elastic  and  resumes  its  normal  shape  when  the 
sternum  is  removed.  It  is  clear  that  there  is  a  small  group  of  cases  in  which 
an  enlarged  thymus  does  actually  compress  the  trachea  arid  that  it  gives 
xise  to  attacks  of  dyspnoea  and  cyanosis,  and  inspiratory  and  expiratory 
stridor,  mainly  expiratory.  The  attacks  are  sudden,  violent,  and  not 
relieved  by  intubation  or  tracheotomy.  There  is  no  evidence  of  com- 
pression of  the  heart,  blood  vessels  or  nerves. 

Cardiac  paralysis  is  undoubtedly  the  cause  in  some  cases,  but  the 
predisposing  factor  is  probably  a  lympho-toxeemia,  not  necessarily  constant 
in  action. 

The  diagnosis  of  thymic  asthma  is  difficult  for  it  varies  in  type.  It 
may  be  fatal  in  the  first  attack  or  series  of  attacks.  Sometimes  there  is 
regular  sighing  respiration  ;  attacks  of  subacute  asphyxia,  ascribed  to 
glottic  spasm ;  or  cyanosis  and  crowing,  suggestive  of  laryngospasm, 
followed  by  unconsciousness,  loss  of  reflexes,  rigidity,  cyanosis,  and  gradual 
cessation  of  the  heart  and  breathing.  Or  it  may  end  in  an  inspiratory  crow. 
In  other  instances  the  breathing  is  rapid,  cyanosis  and  dilatation  of  the  veins 
in  the  neck  develop,  and  the  child  dies  in  a  few  minutes  from  suffocation. 
Gradually  increasing  inspiratory  dyspnoea  is  due  to  pressure  on  the  trachea. 

The  diagnosis  of  enlargement  of  the  thymus  is  based  on  the  dulness 
on  light  percussion  over  the  manubrium.  It  is  roughly  triangular  in  shape, 
with  the  base  upward  and  a  somewhat  cone-shaped  apex  at  a  level  with 
the  second  ribs.  It  extends  a  little  beyond  the  manubrium,  more  to  the 
left  than  the  right.    The  thyroid  gland  is  enlarged  in  about  half  the  cases. 


The  Blood  and  Lymphoid  Structures.  531 

Sudden  death  may  occur  from  numerous  other  causes,  e.g.,  coryza  in  the 
mewborn  and  pertussis,  causing  "  swallowing  of  the  tongue,"  it  being  drawn 
upward  and  backward  and  preventing  the  entrance  of  air  ;  asphyxia 
irom  overlaying  ;   glottic  spasm,  etc.  (p.  102). 

No  treatment  is  available,  except  partial  or  entire  removal  of  the 
.gland  if  there  is  distinct  evidence  of  tracheal  pressure. 


Chapter  XLIV. 

DISORDERS    OF    THE    BLOOD    AND    LYMPH. 

Urticaria — Erythema  Nodosum — Purpura —  Haemophilia^ 

Urticaria. — Syn.  :  Nettle  Rash —  Urticaria  papulosa — Lichen  urticatus- 
— Strophulus — Prurigo. — Many  varieties  are  included  under  the  title 
of  urticaria,  differing  in  pathology,  so  it  is  important  to  understand  what 
is  meant  by  the  term.  In  all  these  affections  there  is  a  characteristic 
eruption  of  lumps,  sometimes  called  "  heat  bumps,"  "  water  blisters,"' 
"  hives,"  etc.,  closely  resembling  those  due  to  nettle  stings  or  aggregated 
into  wheals  of  similar  character.  At  first  the  bumps  are  white  and  raised,, 
involving  the  skin  and  subjacent  connective  tissue.  In  the  young  they 
quickly  subside  and  leave  small,  itching,  hard  papules.  The  papules  are 
most  common  on  the  lower  limbs,  forearms,  wrists,  hands  and  palms, 
feet  and  soles,  buttocks  and  trunk,  in  order  of  frequency  ;  especially  on  the 
extensor  surfaces.  Sometimes  they  are  vesicular  at  the  apices  (  Urticaria 
vesiculosa),  and  become  pustular  (  U.  varicelliformis),  or  they  may  be 
hsemorrhagic  (  U.  hemorrhagica),  or  form  large  bulla;  (  U.  bullosa).  Itching 
is  severe  and  induces  scratching  of  the  parts  within  reach,  the  papules 
being  then  covered  with  blood  crusts  or  scabs.  If  the  rash  becomes  infected, 
it  assumes  a  pustular  or  ecthymatous  appearance. 

Giant  Urticaria  is  an  angioneurotic  oedema  (p.  458).  There  is  a  rare 
form,  epidemic  in  character,  but  the  rash  does  not  itch.  Factitious  Urticaria 
and  Dermatographism,  "writing  on  the  skin,  can  be  produced  in  neuropathic 
and  hysterical  subj  ects  in  consequence  of  vasomotor  instability.  Mechanical 
Urticaria  is  the  result  of  external  irritation  by  plants,  such  as  nettles  and 
the  primula  obconica,  insects  and  hairy  caterpillars,  notably  the  "  woolly 
bear."  This  variety  is  of  particidar  interest  in  that  it  shows  the  eruption 
can  be  caused  by  poisonous  substances  which  set  up  a  vasomotor  dis- 
turbance of  the  cutaneous  vessels. 

Pathology. — Some  toxin,  possibly  a  by-product  of  protein  or  carbo- 
hydrate digestion,  is  absorbed  from  the  alimentary  tract.  It  irritates  the- 
nerve  endings  and  causes  a  rapid  effusion  of  serum.  There  is  a  vasomotor 
disturbance  of  cutaneous  vessels.  The  injection  of  diphtheria  antitoxin 
frequently  produces  the  rash.  In  acute  cases  the  coagulability  of  the- 
blood  is  often  diminished.  The  itching  is  due  to  irritation  of  the  nervfr 
endings  by  toxin  or  by  the  pressure  of  swollen  papillae.  A  curious  idio- 
syncrasy in  respect  of  quite  common  articles  of  food  is  not  infrequent.    Thua 


Disorders  of  the  Blood  and  Lymph.  533 

an  attack  of  acute  urticaria  may  follow  the  ingestion  of  shell-fish,  eggs, 
cheese,  strawberries,  bananas,  etc.  Hingston  Fox  (1908)  suggested  that 
the  symptoms  of  egg-poisoning  arise  because  eggs,  like  shell-fish,  contain 
a  powerful  decalcifying  agent,  chiefly  in  the  outer  membrane.  This 
passes  from  the  stomach  to  the  blood  and  precipitates  calcium  salts,  thus 
causing  diminished  coagulability  and  transudation.  Interesting  cases  of 
•egg-poisoning  are  on  record  as  early  as  the  fifth  month  of  age,  the  rash 
appearing  in  6-8  minutes  (Bendix).  Egg  produced  acute  urticaria,  alarming 
collapse,  swollen  head  and  loss  of  radial  pulse  in  an  infant  13  months  old  ; 
a  second  attack  2  weeks  later  ;  and  a  third,  after  custard,  with  severe 
vomiting  and  diarrhoea,  1  month  later.  Egg  caused  erythema  exudativum 
bullosa  in  a  child  from  the  first  to  fifth  year  of  life  (Albu).  So  far  I  am 
unaware  of  the  presence  of  a  decalcifying  agent  in  bananas  which  in  my 
experience  are  sometimes  the  cause  of  acute  and  chronic  attacks.  A  few 
•cases  are  due  to  intestinal  parasites. 

Acute  Urticaria. — The  typical  attack  is  seen  after  the  ingestion  of. 
various  articles  of  diet  and  shell-fish,  notably  mussels,  the  poison  being 
probably  located  in  the  liver.  Mussel  poisoning  gives  rise  to  three  different 
types  of  poisoning  : — (1)  Vomiting  and  diarrhoea  shortly  after  ingestion, 
or  after  a  varying  incubation  period  with  fever  ;  (2)  An  acute  peripheral 
paralysis  resembling  the  effects  of  curare.  It  is  ushered  in  with  nausea, 
vomiting,  constipation  and  dyspnoea.  The  face  may  be  swollen  and  livid, 
and  psychical  excitement  marked.  The  onset  is  variable,  usually  rapid 
and  even  within  30  minutes,  beginning  with  "pins  and  needles"  in  the 
extremities.  It  varies  in  severity  and  duration,  and  may  be  quite  tran- 
sitory. All  the  muscles  may  be  involved  and  death  result  from  respiratory 
paralysis  without  loss  of  consciousness.  Incoordination  and  spasm  of  the 
arms  have  been  noted.  It  is  treated  by  lavage,  saline  purgatives,  and 
cardiac  and  respiratory  stimulants.  (3)  Erythema  or  Urticaria,  with 
headache  and  malaise. 

In  acute  attacks  the  rash  appears  in  a  few  hours  and  rapidly  involves 
the  whole  body.  It  may  be  very  marked  on  the  face  and  head,  causing 
great  swelling  of  the  subcutaneous  tissues  and  a  striking,  swollen,  bloated, 
blotchy  appearance.  The  child  feels  very  ill,  and  often  vomits  or  quickly 
develops  diarrhoea.  The  alimentary  symptoms  depend  greatly  on  the 
nature  of  the  poison.  It  runs  its  course  in  a  few  hours  and  is  rarely  pro- 
longed beyond  2  or  3  days ;  occasionally  as  many  weeks.  The  chief  com- 
plications are  dyspnoea,  due  to  serous  effusion  into  the  larynx  or  pharynx; 
albuminuria  and  hsematuria  ;  vomiting  and  colic.  Most  cases  rapidly 
yield  to  treatment  by  an  emetic,  if  the  food  has  been  recently  taken  and  not 
vomited,  saline  purgatives,  and  bran  or  oatmeal  baths.  Sedatives  are 
sometimes  required. 

Lichen  Urticatus  is  a  much  more  troublesome  affection,  for  it  may 
be  prolonged    for    years  in  recurrent  outbreaks.       The  appearance   and 


534  Chapter  XLIY. 

distribution  of  the  rash  are  very  suggestive  of  scabies,  so  careful  examination 
must  be  made  for  cuniculi.  The  presence  of  wheals  and  irritability  of 
the  skin  are  signs  of  urticaria.  Flattened  patches  are  rather  like  lichen 
planus.  Prurigo  is  a  similar  condition  in  older  children,  but-the  urticarial 
patches  are  absent  and  the  neighbouring  lymph  glands  are  enlarged.  It- 
may  be  mild  or  severe. 

Lichen  urticatus  is  most  common  under  2  years  of  age.  It  may  begin 
in  the  third  month  or  even  earlier.  It  tends  to  disappear  in  the  third  and 
fourth,  but  may  continue  up  to  the  tenth  year.  It  is  most  common  in 
summer  and  in  the  worst  cases  comes  out  in  winter  as  well.  It  is  chiefly 
associated  with  gastric  and  intestinal  troubles,  rickets  and  teething,  and 
may  follow  varicella,  measles,  or  other  infections  which  increase  the 
susceptibility  of  the  skin.  It  causes  chronic  irritation,  loss  of  sleep,  mal- 
nutrition and  glandular  enlargement,  if  there  is  secondary  infection. 

Treatment. — It  is  most  difficult  to  cure.  Change  of  air  is  sometimes 
needed.  The  garments  next  the  skin  should  be  of  linen,  silk  or  other 
unirritating  material.  The  diet  must  be  carefully  supervised.  For  infants 
it  is  generally  advisable  to  reduce  the  amount  of  milk  and  butter,  prohibit 
eggs  and  raw  fruit,  reduce  sugars,  and  give  fewer  meals,  and  more  soups, 
vegetables  and  starchy  foods.  For  older  children  prohibit  oatmeal  foods. 
and  reduce  or  omit  starches  and  cane  sugar.  In  the  worst  cases  an 
exclusive  milk  diet  may  be  beneficial.  As  a  rule  it  is  best  to  give  a  mixed 
diet  of  fresh  foods,  digestible  and  well  cooked,  at  regular  intervals.  I  have 
not  found  fresh  fruit  deleterious  and  am  quite  convinced  that  it  is  necessary 
to  avoid  foods  which  are  liable  to  set  up  intestinal  fermentation.  It  is  very 
common  to  find  these  patients  taking  an  excess  of  malted  foods,  cane  sugar 
or  oatmeal  preparations.  In  many  instances  it  is  best  to  start  with  a 
simple  mixed  diet  and  to  alter  it  in  accordance  with  the  progress  of  the 
case.  One  is  not  justified  at  present  in  assuming  that  the  cause  is  invariably 
the  same. 

The  child  must  have  a  warm  bath  at  bedtime  containing  bran,  oatmeal, 
boric  acid  or  "  emollient  bath  powder  "  ;  or  liq.  carbonis  detergens  or  ol. 
betulee  alb,  dr.  1-8  to  water  2  gallons.  Soda  or  sulphur  baths  are  occasion- 
ally useful.  In  some  cases  warm  baths  must  be  avoided.  For  the  relief 
of  itching  dab  on  weak  vinegar  or  eau  de  Cologne  and  water  ;  an  alkaline 
or  calamine  lotion,  alone  or  with  carbolic  acid  1-2  per  cent. ;  lead  or  cyllin 
lotion;  acidi  carbolici  dr.  |-1  in  cotton  seed  oil  oz.  6  ;  or  liq.  carb.  deterge 
plumb,  acetat.,  glycerin,  aa  dr.  2,  water  ad  oz.  6  ;  menthol  gr.  2  ad  water 
oz.  1  ;  ichthyol  5,  glycerin.  5,  water  ad  100  parts,  applied  twice  daily. 
Dust  freely  with  talc  or  starch  powder  afterwards.  Ointments  of  ichthyol 
1  per  cent.,  b-naphthol  1-2  per  cent.,  sulphur,  resinol,  tar  and  diachylon 
p. a.,  are  sometimes  beneficial.  Carbolic  acid  preparations  must  be  used 
with  caution.  Internal  medication  is  primarily  directed  to  the  intestinal 
tract.     Give  an  occasional  dose  of  calomel  or  grey  powder  at  night  and  a 


Disorders  of  the  Blood  and  Lymph.  535 

morning  saline  draught.  Or  a  preliminary  dose  of  rhubarb  and  soda,  grey- 
powder  night  and  morning  for  two  days,  and  then  salol  grs.  2-3  with 
mucilage  and  aniseed,  t.d.s.  On  the  whole  grey  powder  every  other  night 
and  a  mixture  of  rhubarb,  gentian  and  soda,  t.d.s.,  give  as  good  results  as 
most  drugs.  Sometimes  large  doses  of  pot.  citrat.  are  efficacious.  Wolff 
claims  a  cure  in  24  hours  by  giving  sod.  phosphate,  gr.  10-60,  every  3  hours 
or  after  each  meal,  if  the  mischief  is  of  gastro-intestinal  origin.  Ichthyol 
m.  1-2,  in  glycerine  and  syrup,  t.d.s.,  or  a  10  per  cent,  aqueous  solution  in  doses 
of  m.  10.,  is  said  to  relieve  itching  and  restore  vasomotor  tone.  Bromide  and 
chloral  are  required  for  insomnia.  Quinine  gr.  1£  for  each  year  of  age  at 
bedtime  (E.  Smith),  atropin  and  phenazone  in  moderately  large  doses  (Holt), 
and  suprarenal  extract  (Meachin)  have  been  recommended.  A  course  of 
intestinal  antiseptics  and  tonics  may  be  required.  Calcium  salts  are  of 
little  value. 

Urticaria  pigmentosa  usually  begins  at  birth  or  in  the  first  months  of 
life  as  a  series  of  attacks  of  nettle  rash,  leaving  stains  which  fade  in  the 
course  of  a  few  months.  It  is  either  an  urticaria  with  a  sero-sanguineous 
exudation  or  an  infiltration  of  the  tissues  wTith  peculiar  granular  cells  known 
as  "  mast  "  cells.  Some  of  the  cases  recorded  under  this  name  are  really 
U.  hemorrhagica  leaving  stains.  In  a  girl,  aged  18  months,  the  rash  con- 
sisted of  squamous,  brownish,  subcutaneous  spots  on  the  thighs,  buttocks 
and  lower  part  of  the  abdomen.  They  had  followed  an  attack  of  varicella. 
At  the  onset  the  patches  are  dark  red  or  reddish  brown,  somewhat  infiltrated , 
the  size  of  peas,  and  may  cover  the  entire  face  and  body.  They  may  look 
like  insect  bites  or  urticaria,  but  they  do  not  itch.  Later  on  they  become 
sepia  brown  or  yellowish  in  colour.  They  disappear  towards  the  twentieth 
year  but  may  last  longer.  These  children  are  often  neurotic.  Dermato- 
graphism  may  be  present.  Lime,  arsenic  and  salicylates  are  the  drugs 
usually  given.     Local  applications  are  useless. 

Erythema  Nodosum  ( Nodal  Fever)  is  an  acute  specific  febrile  disorder 
with  an  incubation  period,  prodromata,  a  stage  of  eruption,  and  a  period  of 
convalescence.  It  occurs  in  its  most  characteristic  form  in  childhood.  It  is 
rare  under  3  years  and  in  extreme  old  age.  The  youngest  case  under  my 
notice  was  18  months  old.  About  one-fifth  of  the  cases  occur  in  the  first 
decade,  two-fifths  in  the  second,  and  one-fifth  in  the  third  decade  of  life. 
Under  10  years  of  age  two  females  are  affected  to  one  male  ;  and  the  relative 
preponderance  of  the  female  sex  increases  with  advancing  years,  the  reverse 
of  what  holds  good  in  rheumatic  fever.  It  is  said  to  occur  with  about  equal 
frequency  in  each  quarter  of  the  year  and  does  not  exhibit  the  autumnal 
rise  of  rheumatic  fever.  In  my  experience  it  is  most  frequent  in  May  and 
comparatively  rare  in  July  and  August.  Three-fourths  of  my  cases  began 
in  the  first  6  months  of  the  year.  It  may  affect  more  than  one  in  a  family 
and  sometimes  assumes  an  epidemic  prevalence.  It  is  liable  to  occur  in 
the  convalescence  of  scarlet  fever. 


536  Chapter  XLI  V. 

Its  pathology  is  doubtful.  The  onset  and  course  are  in  favour  of  micro- 
bial infection,  but  so  far  no  organism  has  been  recovered  from  the  blood  or 
the  serum  of  artificial  blisters. 

Probably  it  is  closely  allied  to  Urticaria.  At  times  the  two  diseases 
are  present  in  the  same  patient  and  dermatographism  may  be  marked. 
Many  attacks  are  ushered  in  by  gastro-intestinal  disturbance,  and  it  is 
likely  that  the  disease  is  the  result  of  toxic  absorption  from  the  alimentary 
canal  or  perhaps  from  the  tonsils.  Formerly  it  was  supposed  to  be  a  sign 
of  rheumatism  and  in  favour  of  this  were  urged  the  similarity  of  the  age 
incidence,  the  special  liability  of  girls  aged  10-15,  epidemic  occurrence, 
a  suspicion  of  contagion,  the  liability  to  arthritis,  tonsillitis,  and  endocar- 
ditis, and  the  occurrence  of  erythema.  On  the  other  hand  it  is  only  half  as 
frequent  as  rheumatism  in  the  first  decade,  and  is  much  more  frequent  in 
females.  It  is  least  prevalent  in  the  third  quarter  of  the  year,  when  acute 
rheumatism  is  most  common,  and  is  uninfluenced  by  salicylates.  In  my 
experience  girls  of  5-10  are  more  liable  than  girls  of  10-15  years  of  age. 
The  character  of  arthritis  is  different.  No  family  history  of  rheumatism 
was  obtained  by  Lenden  in  63  cases  and  only  2  had  a  past  history  of 
rheumatic  fever.  On  the  other  hand  I  obtained  such  a  history  in  10  cases 
out  of  25  and  a  personal  history  in  only  1. 

Symptoms. — There  is  an  indefinite  prodromal  period  of  variable  severity 
for  1-4  weeks  during  which  the  child  is  ailing,  dyspeptic,  feverish,  and 
suffers  with  headache  and  pains  in  the  limbs.  Sometimes  there  is  tonsillitis 
or  an  attack  of  diarrhoea.  One  child  had  an  attack  of  epistaxis  on  the 
day  before  the  rash.  The  onset  may  be  severe  and  accompanied  by  vomiting 
or  gastro- enteritis.  The  temperature  rises  and  in  a  day  or  two  the  rash 
appears.  Fever  may  be  present  for  some  days  before  the  rash  and  rarely 
reaches  104°  F.  It  subsides  by  lysis  in  the  second  week.  Occasionally  it 
last  for  some  weeks,  being  intermittent  or  irregularly  remittent  in  character 
and  uninfluenced  by  salicylates.  Cases  vary  much  in  type  and  severity. 
In  rare  instances  the  constitutional  symptoms  are  severe  with  much 
prostration,  mental  depression,  and  little  rash.  Or  the  rash  may  be 
extensive  and  the  symptoms  slight.  Frequently  both  rash  and  symptoms 
are  trivial,  with  no  sense  of  illness  and  little  pain.  Delirium  and  coma  may 
occur  from  hyperpyrexia  and  occasionally  are  due  to  salicylates. 

The  rash  appears  in  1-5  days.  It  is  chiefly  distributed  on  the  front 
and  sides  of  the  shins.  In  more  extensive  cases  it  comes  out  on  the  knees, 
thighs  and  forearms,  mainly  the  extensor  surfaces,  and  on  the  buttocks. 
The  characteristic  nodes  are  raised,  somewhat  conical  swellings,  varying  in 
colour  from  a  bright  or  dusky  red  to  a  dull  purple.  The  purplish  colour 
is  most  in  evidence  when  the  limbs  are  cold  and  the  rash  fading.  The 
nodes  are  hot,  painful  and  exquisitely  tender.  Frequently  only  a  few  are 
present.  Sometimes  there  is  a  polymorphic  rash  of  papules,  diffused 
blotches,  and  even  circinate  or  annular  patches. 


Disorders  of  the  Blood  and  Lymph.  537 

Arthritis  is  uncommon  or  slight,  and  takes  the  form  of  pain  in  the 
joints  with  slight  tenderness  on  movement  but  no  redness  and  swelling,  such 
as  are  seen  in  acute  rheumatism  in  adults  though  analogous  to  the  type  of 
rheumatic  joint  affection  of  early  life.  Occasionally  the  joints  are  swollen, 
red  and  cedematous,  as  in  gout ;  or  may  simulate  the  appearances  of 
gonorrheal  rheumatism  or  osteo-arthritis.  S.  Mackenzie  (1897)  stated  that 
17  out  of  108  cases  at  all  ages  had  arthritis  and  another  17  had  rheumatic 
pains,  while  no  less  than  23  had  or  developed  signs  of  endocarditis.  This  is 
quite  contrary  to  my  experience  in  children.  Though  a  murmur  is 
■occasionally  found,  it  disappears  during  convalescence  and  is  no  doubt  due 
to  cardiac  dilatation. 

The  rash  subsides  slowly.  The  nodes  become  less  hot  and  tender, 
Jess  painful,  more  dusky  in  colour,  and  in  late  stages  may  be  a  little 
cedematous.  The  oedema  of  the  legs  quickly  disappears,  but  will  return 
if  the  child  is  allowed  up  too  soon.  Eelapses  are  uncommon  and  recurrence 
rare.  Occasional  complications'  are  angina,  bronchitis,  pleurisy,  endocar- 
ditis and  nephritis.  Phlyctenules  are  quite  frequent.  Convalescence  is 
somewhat  slow,  and  characterised  by  weakness  out  of  proportion  to  the 
.severity  of  the  attack  and  much  anaemia.  The  prognosis  is  excellent. 
Serious  and  dangerous  cases  are  associated  with  endocarditis,  and  are 
probably  of  septic  origin  and  different  in  character.  There  is  no  special 
prevalence  of  cardiac  affections  in  these  children. 

The  diagnosis  is  easy  when  the  rash  is  out.  Before  this  the  febrile  state 
may  be  mistaken  for  influenza,  gastritis,  rheumatism,  typhoid  fever,  or  even 
meningitis  if  the  constitutional  symptoms  are  severe.  Neither  a  febrile 
arthritis  nor  endocarditis  is  a  proof  of  acute  rheumatism,  for  they  both 
occur  in  other  diseases.  A  cardiac  murmur  is  not  necessarily  due  to 
endocarditis. 

Treatment. — Keep  the  child  in  bed  until  the  nodes  have  subsided 
and  there  is  no  fear  of  secondary  swelling  from  cardiac  weakness.  In  the 
•erect  posture  the  legs  swell  and  are  more  painful.  Apply  cold  compresses, 
lead  or  lead  and  opium  lotion.  Hot  fomentations  may  afford  more  relief. 
Give  a  warm  bath  daily  and  keep  the  bowels  open.  Attend  to  the  diet  and 
digestion.  During  the  febrile  stage  restrict  the  diet  to  milk  and  carbo- 
hydrate foods.  Oranges  and  lemons  can  be  given  freely.  Citrates,  citric 
acid  and  quinine  are  useful  drugs.  Iron  tonics  or  cod-liver  oil  are  valuable 
•during  convalescence.  For  2  or  3  weeks  the  heart  must  be  watched  for  fear 
of  dilatation. 

Purpura. — Syn.  :  Morbus  Macuhsus — Werlhoffs  Disease. — Purpuric 
•eruptions  of  all  kinds  are  symptomatic  rather  than  special  disease  entities 
and  great  confusion  has  arisen  from  attempts  to  define  separate  varieties. 
Bleeding  may  take  place  subcutaneously,  from  mucous  membranes  or  into 
internal  organs.  P.  simplex,  rheumatica,  hemorrhagica,  fulminans  and 
-Henoch's  purpura  are  probably  the  same  disease  varying  in  severity.    Even 


538  Chapter   XLIV. 

in  mild  cases  there  is  usually  some  joint  pain,  swelling  of  the  legs  and 
intestinal  disturbance.  These  varieties  are  classified  by  Osier  as  Essential 
Purpura  in  opposition  to  the  Symptomatic  Purpura  of  infective  diseases  ; 
due  to  toxic  causes  such  as  drugs  and  snake  venom  ;  cachexia  ;  hysteria  ; 
or  of  mechanical  origin,  as  in  pertussis.  Such  eruptions  depend  on  altered 
blood  states  and  occur  in  leukaemia,  scurvy,  haemophilia  ;  infective  endo- 
carditis, pyaemic  affections,  haemorrhagic  types  of  specific  fevers,  cerebro- 
spinal meningitis ;  diphtheria,  biliary  toxaemia  ;  marasmus ;  chronic 
nephritis  and  cardiac  troubles  causing  renal  congestion.  Purpura  may  be- 
associated  with  urticaria  and  angioneurotic  oedema.  Symptomatic  purpura, 
is  of  grave  prognostic  import  though  it  adds  nothing  to  the  severity  of  the- 
primary  disease.    No  special  treatment  is  needed. 

Purpura  Simplex  is  a  simple  purpuric  eruption  for  which  no  cause  can 
be  found  ;  frequently  associated  with  no  constitutional  symptoms  or 
merely  with  slight  fever  and  digestive  disturbance.  It  is  mild  in  character 
and  course,  and  ends  in  recovery.  Anorexia,  headache,  nausea,  apathy 
and  general  malaise  may  precede  the  eruption  by  a  few  days  to  2  weeks. 
The  rash  is  limited  to  the  skin  and  generally  appears  on  the  extensor- 
surfaces  of  the  arms  and  legs.  The  face  and  hands  often  escape.  The 
spots  are  variable  in  size  and  shape,  bright  red  in  colour,  not  confluent,, 
and  do  not  disappear  on  pressure.  In  size  they  vary  from  that  of  a  pin  head 
to  large  subcutaneous  haemorrhages,  with  the  appearance  and  undergoing 
the  changes  of  bruises.  They  last  from  1-4  weeks  and  may  come  out  in 
successive  crops.  P.  Convalescentium  is  a  simple  purpura  during  con- 
valescence from  fevers  such  as  measles,  scarlet  fever  and  diphtheria.  It  is. 
very  rare  after  diphtheria,  is  not  due  to  antitoxin,  and  must  be  distinguished 
from  haemorrhagic  diphtheria.  Occasionally  it  is  haemorrhagic  in  type  or 
fulminating  and  fatal. 

P.  Hemorrhagica,  the  true  morbus  maculosus  Werlhofjii. — The 
haemorrhage  is  not  limited  to  the  skin  ;  it  takes  place  also  from  the  mucous 
membranes.  It  is  more  severe  and  more  sudden  in  onset  than  the  previous 
variety,  with  a  temperature  of  101°-103°  F.,  anaemia  due  to  loss  of  blood,. 
gastro-intestinal  symptoms,  albuminuria  and  oedema.  The  purpuric 
spots  and  subcutaneous  exudations  in  a  limb  may  coalesce  and  give  it  an 
appearance  of  gangrene,  but  without  the  smell.  Purpuric  spots  may 
appear  in  the  oral  structures,  eyes,  ears,  intestines  and  bladder.  Epi- 
staxis  is  the  most  frequent  variety  of  haemorrhage  from  the  mucous  mem- 
brane. Occasionally  the  bleeding  is  limited  to  haematuria.  The  joints 
usually  escape.  Mild  cases  attain  a  maximum  in  about  a  week  and  then 
cease,  ending  in  recovery  in  14  days.  Relapses  are  not  uncommon.  Severe- 
attacks  may  pass  into  a  typhoid  state  and  are  then  almost  always  fatal 
in  1-6  weeks.    Rarely  it  is  chronic  and  recurrent  for  months  or  years. 

P.  Rheumatica,  sometimes  called  peliosis  rheumatica  or  Schonleins- 
disease. — Both  this  and  P.  Simplex  may  be  associated  with  other  skin 


Disorders  of  the  Blood  and  Lymph.  539 

affections  such  as  urticaria,  erythema  nodosum  and  erythema  multiforme 
exudativum.  It  has  probably  nothing  whatever  to  do  with  rheumatism 
and  is  really  a  compound  of  urticaria  and  purpura.  Thus,  an  8-year  old 
boy,  after  a  few  days  illness  with  gastric  and  intestinal  symptoms  and 
probably  a  mild  degree  of  fever,  developed  a  purpuric  rash  on  the  lower 
limbs  and  buttocks,  joint  pains  and  a  little  swelling  of  one  knee  and  ankle. 
He  had  a  fair  appetite  and  little  fever.  In  a  few  days  the  symptoms 
subsided.  After  an  interval  of  a  few  more  days  he  suddenly  developed 
oedema  of  the  penis,  especially  the  prepuce,  followed  by  hemorrhagic 
staining,  and  later  on  fresh  purpuric  spots  and  bruises.  These  signs 
cleared  up  in  another  week  and  then  again  fresh  spots  came  out  in  the 
lower  limbs. 

The  characteristic  features  of  this  variety  are  the  purpura,  painful 
joint  swelling,  oedema,  and  occasionally  haemorrhages  from  the  mucous 
membranes.  It  is  preceded  by  anaemia,  languor,  vague  pains,  vomiting  or 
diarrhoea,  and  occasionally  urticaria.  The  temperature  rises  about  2°  F., 
perhaps  5°  or  6°.  The  throat  is  sometimes  inflamed.  The  rash  is  generally 
on  the  lower  limbs,  buttocks  and  forearms.  It  is  most  common  on  the 
legs  up  to  the  knees  and  most  marked  near  the  joints.  It  may  be  scattered 
all  over  the  body,  limbs,  and  even  the  face.  Sometimes  it  resembles  an 
urticaria  with  purpura  in  the  centre  of  the  wheals.  The  purpuric  parts  may 
be  oedematous,  secondarily  to  the  rash,  especially  the  legs  when  the  patient 
is  allowed  out  of  bed  too  soon.  More  often  the  oedema  precedes  the  purpura, 
or  occurs  independently  of  it  in  the  eyelids,  face,  penis,  scrotum,  labia,  etc. 
Joint  pains  are  common  and  joint  swelling  is  not  infrequent.  The  ankles 
and  knees  are  the  most  liable,  and  are  affected  with  a  peri-articular 
rather  than  an  intra-articular  effusion.  Bleeding  may  take  place  from  the 
mucous  membranes,  e.g.,  nose  and  bowels.  Intestinal  bleeding,  associated 
with  colic  and  vomiting,  is  very  suggestive  of  Henoch's  purpura.  The  spleen 
may  be  enlarged.    The  heart  is  not  involved  and  there  is  rarely  albuminuria. 

Most  cases  recover  in  a  fortnight.  Others  have  relapses  with  rash, 
fever  and  articular  swelling  ;  and  exhibit  a  more  or  less  paroxysmal 
course,  sometimes  of  many  weeks  duration  but  ending  in  recovery. 

P.  Fulminans  is  so  called  because  of  the  sudden  violent  onset.  It  has 
followed  immersion  in  cold  water,  sea  bathing,  fright,  shock  and  scarlet 
fever.  Von  Lerber  (1904)  reported  a  case  in  a  healthy  girl,  aged  13  months, 
who  became  collapsed  after  a  restless  night.  An  hour  later  bluish-red  spots 
appeared,  the  pulse  was  cpiick  and  there  was  no  fever.  The  rash  extended 
all  over,  the -pulse  became  uncountable,  respirations  60  per  minute,  and 
death  took  place  in  coma  5  hours  after  the  onset.  In  another  case  (Haw, 
1903)  a  sturdy  healthy  boy,  after  being  nearly  drowned,  developed  epis- 
taxis,  melaena,  discrete  purpuric  spots,  insomnia,  shivering,  anorexia, 
tachycardia,  pallor,  debility,  and  splenic  enlargement.  The  epistaxis 
became   recurrent,   splenic   dulness   diminished,   general   oedema   without 


540  Chapter   XLIV. 

albuminuria  developed,  and  death  took  place  from  cardiac  failure  3  weeks 
after  the  onset. 

The  usual  signs  are  a  sudden  onset,  chill,  vomiting,  prostration  and 
high  fever.  A  rapid  and  extensive  eruption  appears,  rather  symmetrical, 
and  chiefly  on  the  extremities.  It  may  give  them  the  appearance  of 
gangrene,  with  bullae  but  no  fcetor.  Delirium,  stupor  and  coma  develop. 
The  spleen  is  generally  enlarged  and  there  is  usually  albuminuria,  and  less 
often  haemorrhage  from  mucous  membranes. 

The  signs  indicate  an  acute  infection.  It  is  usually  fatal  in  12-24  hours 
up  to  4  days.  Sometimes  it  runs  a  prolonged  course,  with  relapses,  and 
ends  in  recovery.  Visceral  haemorrhages,  e.g.,  into  the  suprarenals,  are  often 
found.  In  a  case  which  occurred  in  a  boy,  3  years  old,  on  the  eighteenth 
day  after  severe  scarlatina  and  was  fatal  in  36  hours,  the  kidneys  showed 
acute  degeneration  and  were  almost  entirely  converted  into  fat  (Biss). 
This  is  indicative  of  an  acute  toxaemia. 

Henoch's  Purpura  or  P.  abdominalis  is  a  syndrome  of  symptoms 
rather  than  a  special  entity.  It  has  been  called  by  Osier  erythema  exuda- 
tivum  multiforme  and  cases  have  been  described  as  purpura  haemorrhagica 
and  angioneurotic  oedema.  Both  sexes  are  equally  liable.  It  is  most 
common  from  3-15  years  of  age  and  occurs  in  infants.  Some  of  the  cases 
of  spontaneous  recovery  from  intussusception  are  almost  certainly  of  this 
type.  The  onset  is  sudden.  It  may  be  preceded  for  a  few  days  by  purpuric 
spots,  dyspeptic  symptoms  or  articular  pains.  The  main  feature  is  an 
abdominal  crisis,  characterised  by  severe  colic,  sometimes  tenderness, 
vomiting,  and  haematemesis  or  melaena.  The  degree  of  pain  is  a  fair 
measure  of  the  amount  of  effusion  into  the  intestinal  wall  and  the  spasm 
of  the  gut  above  the  obstruction.  The  stomach  contents  are  first  vomited, 
then  greenish  mucus,  and  finally  dark  blood.  Constipation  is  followed 
by  diarrhoea,  the  passage  of  blood  and  mucus,  and  perhaps  tenesmus. 
The  loss  of  blood  may  be  sufficient  to  produce  marked  anaemia.  The  tongue 
is  coated,  breath  foul  and  appetite  lost.  The  abdomen  is  retracted,  hard 
and  tender.  Fever  is  absent,  moderate  or  irregular.  There  is  much 
prostration,  phosphaturia  and  albuminuria.    The  spleen  may  be  enlarged. 

Purpuric  signs  may  be  absent.  Or  petechial  and  macular  haemorrhagic 
eruptions,  with  a  tendency  to  symmetry,  take  place  into  the  skin  ;  about 
the  joints,  causing  articular  and  peri-articvdar  effusions,  with  pain,  swelling 
and  stiffness  ;  and  beneath  the  periosteum.  Bleeding  may  occur  from 
the  stomach,  bowel,  nose,  gums,  mouth,  pharynx,  lungs  or  kidneys  ;  rarely 
from  the  female  genitals,  ear,  skin,  and  into  the  retina  or  choroid.  Kheu- 
matic  pains  are  not  uncommon  and  occasionally  there  is  severe  oedema. 
The  child  becomes  gravely  collapsed  and  may  present  the  abdominal  facies, 
dry  and  brown  tongue,  thirst  and  frequent  vomiting,  and  flexion  of  the 
legs  on  a  hard,  rigid,  undistended,  tender  abdomen.  The  condition  is  one 
of  partial  or  complete  obstruction,  and  the  abdomen  may  become  distended. 


Disorders  of  the  Blood  and  Lymph.  541 

Examination  reveals  resistance  and  sometimes  an  indefinite  local  swelling. 
At  operation  there  has  been  found  haemorrhagic  oedema  of  the  small  intes- 
tine or  colon.  Sutherland  states  that  in  about  75  per  cent,  the  effusion  is 
in  the  ileo-caecal  region  and  notes  that  over  70  per  cent,  of  intussusceptions 
are  found  in  this  situation. 

Recurrent  attacks  occur  in  the  same  patient  at  intervals  of  davs  or 
years.  They  vary  in  severity  and  type,  and  tend  to  become  less  severe. 
The  same  child  may  at  one  time  present  simple  purpura,  at  another  marked 
arthritic  phenomena,  and  in  a  third  attack  an  acute  abdominal  crisis. 
The  haemorrhagic  congestion  of  the  bowel  affects  one  or  all  the  coats,  and  is. 
limited  or  extensive  in  distribution.  A  limited  affection  of  the  small 
intestine  closely  simulates  a  reduced  intussusception,  but  purpuric  spots  may 
be  found  in  the  mesentery  and  on  the  peritoneum  of  other  portions  of  the. 
gut.  Superficial  ulcers  or  extensive  necrosis  of  the  mucosa  and  sub 
mucosa  may  be  present.  Acute  nephritis  has  been  noted  and  proved  fatal 
in  a  few  days.    Endocarditis  has  also  occurred. 

The  blood  has  been  found  sterile  in  the  few  cases  in  which  it  has  been 
examined.  Crawfurd  (1903)  noted  a  reduction  of  haemoglobin  to  68  and 
77  per  cent. ;  polynuclears  53  and  81  per  cent.  One  case  showed  a  leucocv- 
tosis  of  60,000  and  a  diminution  of  red  cells  ;  the  other,  neither  leucocytosis. 
nor  erythropenia.  Thus  the  blood  changes  are  not  characteristic.  In 
essential  purpura  there  may  be  found  slowing  or  absence  of  coagulation; 
reduction  in  specific  gravity,  haemoglobin,  and  number  of  red  cells  and 
blood  platelets;  megaloblasts  and  microblasts,  an  occasional  myelocyte, 
and  leucopenia,  except  perhaps  at  the  onset.  Leucocytosis  has  been  found 
in  p.  haemorrhagica.  The  changes  are  much  the  same  as  in  scurvy  and 
secondary  anaemia.  A  polynuclear  leucocytosis  is  generally  due  to  secondary 
or  symptomatic  purpura  of  infective  origin. 

General  Etiology  of  Essential  Purpura. — It  may  occur  at  all  ages, 
especially  2-12  years,  and  very  rarely  in  infancy.  Both  sexes  are  equally 
liable,  or  there  is  a  slight  preponderance  of  females.  It  is  most  frequent 
in  the  winter  months.  Bad  food,  malnutrition  and  imperfect  hygiene  are 
predisposing  factors.  Gastro-intestinal  symptoms  are  so  often  present  as 
to  suggest  that  the  cause  is  a  toxaemia  of  alimentary  origin.  In  a  few 
instances  the  antecedent  sore-throat  may  be  the  source  of  infection. 

Pathology. — Some  change  in  the  blood  permits  extravasion.  The 
disease  is  vasomotor,  toxic  or  infective  in  origin.  Henoch  regards  the 
abdominal  variety  as  a  vasomotor  neurosis.  The  symptoms  are  due  to 
effusion  into  the  wall  of  the  gut.  There  is  no  connection  with  rheumatism 
and  cardiac  lesions  are  distinctly  rare.  Joint  pains  are  due  to  haemorrhagic 
or  serous  effusion  into  or  around  the  joint.  The  similarity  of  p.  haemor- 
rbagica  to  scurvy  must  be  noted  ;  the  blood  picture  is  analogous.  The 
disease  is  closely  allied  to  urticaria,  an  auto-intoxication  by  a  vasomotor 
toxin-     The  close  connection   of  the  various  types  is  brought  out  by  the 


542  Chapter  XLI  V. 

clinical  pictures  thereof,  and  their  occurrence  in  the  same  patient.  This  in 
itself  sueeests  a  common  origin,  and  the  symptoms  and  anatomical  changes 
of  profound  toxaemia  in  fatal  cases  may  be  regarded  as  evidence  that  the 
minor  ones  have  a  similar  etiology  and  pathology.  Minute  visceral  hemor- 
rhages in  the  serous  membranes  and  omentum,  sero-sanguineous  effusions 
into  various  cavities  and  splenic  enlargement,  usually  due  to  haemorrhage, 
are  found  after  death  ;  and  sometimes  profound  degenerative  changes  in 
the  kidneys. 

Diagnosis. — The  chief  affections  to  bear  in  mind  are  scurvy,  cerebro- 
spinal fever,  malignant  infective  disorders,  intestinal  ulceration,  acute 
nephritis  and  renal  calculus.  Hematuria,  without  other  signs,  may 
not  be  recognised  as  purpuric.  Henoch's  purpura  is  apt  to  be  mistaken  for 
intussusception,  acute  colitis,  appendicitis,  peritonitis,  acute  intestinal 
obstruction  or  gastric  ulcer.  Several  cases  have  been  operated  on.  Dis- 
tension of  the  abdomen  increases  the  difficulty  of  diagnosis,  unless  some 
purpuric  spots  are  found.  An  abdominal  crisis  may  be  due  to  serous  effusion 
in  angioneurotic  oedema.  Intussusception  may  occur  in  the  course  of  the 
disease. 

Course  and  Prognosis.— It  may  get  well  in  a  few  days,  continue  for 
many  months  in  a  series  of  relapses  at  uncertain  intervals,  or  end  fatally. 
The  abdominal  type  lasts  a  few  hours  or  days  and  undergoes  gradual 
remission.  The  prognosis  is  better  in  the  older  children.  It  increases  in 
gravity  with  the  severity  of  the  symptoms  and  the  signs. of  sepsis.  No 
definite  end  to  a  case  of  medium  severity  can  be  accurately  foretold.  The 
simple  variety  is  very  rarely  fatal.  Complications  are  rare.  A  retro- 
pharyngeal blood  cyst  was  present  in  a  girl,  aged  8  months,  and  fatal 
haemorrhage  resulted  on  opening  it  (Blaker,  1904).  Sloughing  or  gangrene 
of  the  skin  and  mucous  membrane  may  occur,  and  is  generally  a  sign  of 
fatal  prognosis.  In  mild  cases  slight  injury  or  pressure  may  cause  sloughing. 
Both  the  uvula  and  prepuce  have  sloughed.  Hsematuria  is  common,  so  too 
degeneration  of  the  renal  epithelium  in  the  tubes,  but  acute  nephritis  is 
rare.  Chronic  nephritis  has  been  known  as  a  sequel.  Endocarditis  and 
pericarditis  are  unlikely  to  develop,  except  when  there  is  acute  rheumatism 
or  sepsis.  Fattv  degeneration  and  cardiac  dilatation  occur  in  prolonged 
■cases.  Meningeal  and  retinal  haemorrhages  are  uncommon.  Convalescence 
is  often  slow. 

Treatment. — Keep  mild  cases  in  bed,  because  of  the  risk  of  relapses. 
In  severe  attacks  the  horizontal  posture  is  essential.  Avoid  exposure  and 
injury.  Give  small  meals  of  simple,  nutritious,  digestible  food.  Fresh 
fruit  and  vegetables  are  most  beneficial.  Calcium  salts  may  increase  the 
coagulability  of  the  blood  and  adrenalin  can  be  applied  to  stop  local 
bleeding.  Adrenalin  and  arsenic  are  prescribed  for  haematemesis.  Keep  the 
bowels  open  with  calomel  and  use  it  as  an  intestinal  antiseptic.  For  purpura 
abdominalis,  with  pain  and  haemorrhage,  give  small  doses  of  castor  oil 


Disorders  of  the  Blood  and  Lymph.  543 

and  opium,  or  opium  alone,  an  ice  bag  to  the  abdomen,  and  atropin  gr.  -55^ 
sub  cutem.  Aromatic  sulphuric  acid  is  useful  as  a  haemostatic.  Ergot 
and  chloride  of  iron  are  of  doubtful  value.  Quinine  must  be  given  in 
infective  cases  with  fever  and  rigors.  If  the  bleeding  is  long  continued, 
recurrent  and  severe,  gelatine  should  be  given  by  the  mouth.  Fresh 
horse  serum  is  sometimes  most  efficacious  in  this  as  well  as  in  other 
haemorrhagic  diseases.  Iron,  arsenic  and  cod-liver  oil  are  needed  during 
convalescence. 

Haemophilia. — This  tendency  to  bruising  and  bleeding  is  a  congenital 
peculiarity  which  is  transmitted  through  many  generations  by  the  female 
members  and  affects  the  males.  Of  the  two  sexes  only  one-twelfth  are 
females  and  they  are  less  severely  affected.  Females  show  no  tendency  to 
excessive  bleeding  during  menstruation  or  parturition.  They  are  more 
prolific  than  normal  women  and  have  a  higher  proportion  of  daughters. 
Transmission  by  males  to  sons  and  daughters  has  been  recorded.  Thus 
6  out  of  15  cases  in  one  family  were  females  and  10  of  the  15  inherited 
through  a  male  parent  (Larrabee).  The  male  is  more  likely  to  transmit  it  if 
he  is  unaffected.  Otherwise  he  may  not  live  to  procreative  age.  Grandidier 
(1885)  found  20  cases  in  a  population  of  165  in  the  village  of  Tenna,  and  the 
diathesis  could  be  traced  back  to  1770,  and  subsequently  to  a  single  remote 
ancestor.  Osier  recorded  it  in  7  generations  of  the  Appleton-Swan  family  ; 
Muir  in  8  generations,  transmitted  from  a  male  born  in  1783  ;  and  Dunn 
collected  770  cases  in  256  families. 

The  disease  is  independent  of  race  and  climate,  but  more  common  in 
the  temperate  zones.  Some  cases  die  shortly  after  birth  from  bleeding  in 
the  first  week  of  life.  Grandidier  found  a  family  history  of  haemophilia 
in  14  out  of  228  cases  of  spontaneous  umbilical  bleeding.  Including  these 
and  one  of  his  own,  Larrabee  (1906)  collected  37  cases  of  haemophilia  in  the 
newborn,  i.e.,  a  family  history  of  the  affection  or  the  child  survived  and 
proved  a  "bleeder"  ;  males  31,  females  6;  22  fatal;  24  families  involved. 
The  bleeding  is  commonly  umbilical  but  may  occur  from  the  skin,  mucous 
membranes  or  into  joints. 

Pathology. — Recent  evidence  is  in  favour  of  the  view  that  it  is  due  to  a 
ferment  defect  in  the  blood  and  that  it  can  be  cured  by  injecting  fresh 
serum.  It  is  probably  a  primary  blood  affection  rather  than  one  of  the 
vessels,  although  fatty  degeneration  of  the  intima  has  been  found.  Possibly 
the  ovarian  secretion  renders  females  less  susceptible.  The  blood  picture 
is  that  of  severe  anaemia  and  varies  with  the  amount  of  blood  lost,  showing 
decrease  in  haemoglobin,  poikilocytes  and  haematoblasts.  The  leucocytes 
are  normal  or  slightly  decreased  in  number,  and  there  is  a  relative  lympho- 
cytosis. It  is  deficient  in  coagulability  and  in  zymoplastic  substance. 
After  bleeding  for  some  minutes  the  blood  may  coagulate  much  more  quickly 
than  normal. 


544  Chapter   XLIV. 

Fatal  cases  may  show  arterial  hypoplasia,  a  thin  right  ventricle  and 
interventricular  septum,  hypertrophy  of  the  left  ventricle,  a  large  thymus, 
and  secondary  arthritic  changes. 

Symptoms. — Bleeding  rarely  begins  in  infancy,  sometimes  in  the  first  or 
second  year,  and  only  occasionally  after  the  twenty-first.  These  subjects  are 
usually  thin,  nervous  and  intellectual,  with  transparent  skin  and  prominent 
veins.  A  spontaneous  attack  may  be  preceded  by  irritability,  restlessness, 
lassitude,  headache,  vertigo,  scanty  micturition  and  constipation  ;  and 
ushered  in  by  vasomotor  disturbance,  viz.,  flushing,  throbbing  of  the 
temples,  and  disturbances  of  sight  and  hearing,  shortness  of  breath  and 
pains  in  the  limbs.  The  bleeding  is  apparently  spontaneous  or  follows  some 
trivial  injury,  e.g.,  strain,  contusion,  scratch,  cut,  tooth  extraction,  ritual 
circumcision  or  paracentesis  of  the  tympanum.  It  is  internal,  external  or 
arthritic.  External  bleeding  takes  the  form  of  epistaxis  in  half  the  cases. 
It  may  occur  from  any  mucous  surface  and  even  beneath  the  nails.  It  is  a 
persistent  oozing,  liable  to  end  in  death  from  syncope.  Or  the  bleeding 
may  be  subcutaneous  (petechia?,  haematomata),  intramuscular,  into  serous 
cavities  or  meningeal.  It  never  affects  the  face.  Internal  haemorrhage 
is  variable  in  rapidity  of  development.  It  causes  severe  pain,  rapid  pulse 
and  rise  of  temperature. 

Arthritic  haemorrhage  is  spontaneous  or  due  to  injury.  It  may  be  the 
first  sign  and,  if  so,  the  joint  is  liable  to  be  opened  for  supposed  acute 
arthritis.  It  is  rare  under  7  years  of  age.  Swelling,  stiffness  and  slight 
fever,  with  no  external  discoloration,  are  present.  In  order  of  suscep- 
tibility come  the  knee,  hip,  elbow,  ankle,  wrist  and  shoulder.  The  fluid  is 
more  or  less  rapidly  absorbed,  except  in  the  rare  instances  in  which  it 
persists  for  months  and  causes  permanent  stiffness,  the  result  of  secondary 
synovitis,  changes  in  the  cartilages  and  bone,  and  partial  or  complete 
anchylosis.  Osteophytic  changes  follow  recurrent  attacks.  An  affected 
knee  closely  resembles  tuberculous  disease.  Often  there  is  more  than  one 
joint  involved.  It  is  treated  by  rest,  splints  and  pressure.  Puncture  may 
possibly  be  justifiable  ;    incision  never. 

Course  and  Prognosis. — Litten  states  that  60  per  cent,  die  under  7, 
and  89  per  cent,  under  10  years  of  age.  Haemoptysis,  haematemesis,  melaena 
and  haematuria  are  very  rarely  fatal.  Death  is  uncommon  in  a  first  attack 
of  bleeding.  Recurrent  attacks  with  arthritic  symptoms,  like  rheumatism, 
are  somewhat  periodical  in  character.  The  severity  of  the  bleeding  varies 
in  different  children  and  the  tendency  is  less  as  age  advances.  Complications 
are  rare.  Gangrene  of  the  skin  and  Yolkmann's  contracture,  after  intra- 
muscular haemorrhage,  have  been  recorded.  The  blood  in  internal 
haemorrhage  is  generally  reabsorbed  but  the  clot  may  persist  and  become 
calcified. 

Treatment. — The  female  members  of  haemophilic  families  should  not 
bear  children.     The  affected  children  must  live  a  quiet  sedentary  fife,  in 


Disorders  of  the  Blood  and  Lymph.  545 

warm  climates,  play  no  boisterous  games,  take  no  alcohol  and  live  on  simple 
diet.    Vaccination  is  not  dangerous.    Teeth  must  not  be  extracted. 

For  capillary  oozing  apply  a  pad  of  gauze  soaked  in  sterilised  gelatine 
or  calcium  chloride  2  per  cent,  solution,  adrenalin  1  in  1000,  or  salt  solution. 
Apply  local  pressure  and  elevate  the  part.  The  actual  cautery  may  be 
necessary.  Internally  give  large  doses  of  calcium  lactate,  gelatine,  adrenalin 
or  ergotin.  These  are  all  useless  (Sahli).  Emile  Weil  (1907)  recommends 
the  subcutaneous  injection  of  fresh  rabbit's  serum,  to  prevent  or  stop 
bleeding.  It  increases  the  coagulability  of  the  blood.  The  serum  of  man 
and  horse,  or  antidiphtheritic  serum,  not  more  than  2  weeks  old,  can  be 
used,  and  possibly  it  will  prove  efficacious  when  given  internally  or  per 
rectum.  Thyroid  and  ovarian  extract  have  also  been  credited  with  success. 
The  subcutaneous  injection  of  gelatine  is  useful  but  not  very  safe  (p.  130). 
Morphia  is  given  for  internal  bleeding,  if  there  is  much  pain.  Calcium  salts 
are  given  at  intervals  to  maintain  blood  coagulability.  Arsenic,  iron  and 
dilute  sulphuric  acid  help  to  preserve  the  general  health. 


2  N 


CHAPTER    XLV. 

THE     URINARY     SYSTEM. 

The  Urine  —  Normal  and  Abnormal  Constituents  —  Albuminuria — 
Hoematuria  —  Hcemoglobinuria  —  Micturition  —  Diabetes  Insipidus — 
Enuresis —  Affections  of  the  Bladder. 


The  Urine  can  be  obtained  in  infancy  by  passing  a  No.  2  catheter  ; 
by  pressure  on  the  bladder  from  above  downwards  after  an  interval  of 
sleep  ;  by  sitting  the  child  on  a  cold  pot  every  15  minutes  and  applying 
cold  or  heat  to  the  hypogastrium  ;  by  means  of  a  condom  fixed  to  the 
penis,  the  insertion  of  the  penis  in  a  bottle  between  the  thighs,  or  a  special 
rubber  apparatus  ;  by  a  small  cup  over  the  vulva  and  between  the  thighs  ; 
by  means  of  a  sponge  or  pad  of  absorbent  wool,  or  a  macintosh  arranged 
so  that  the  urine  runs  into  a  receptacle  beneath  the  bed  ;  or  by  giving  a 
suppository  or  clyster,  and  collecting  the  urine  which  is  rarely  passed 
simultaneously  with  the  faeces. 

Quantity. — In  early  life  the  amount,  specific  gravity,  and  percentage 
of  the  different  constituents  vary  from  time  to  time  to  a  much  greater 
extent  than  in  adults  and  are  more  readily  affected  by  slight  causes.  The 
newborn  child  passes  ^-f  oz.  at  each  evacuation.  The  amount  varies  in  the 
first  few  days  with  the  ingestion  of  fluid.  Very  little  may  be  passed  for 
3  days.  On  the  fourth  day  the  quantity  reaches  200  c.c,  and  on  the  seventh 
day  300  c.c.  ;  about  two-thirds  of  the  amount  of  milk  taken.  The 
following  table  shows  marked  variations  : — 


QUANTITY    OF   URINE    (REUSING). 

Day  of  Life. 

No.  of  c.c. 

Day  of  Life. 

No.  of  c.c. 

1 

2-61 

5 

22-222 

2 

11-145 

6 

70-280 

3 

13-171 

7 

93-338 

4 

17-179 

8 

100-331 

The  quantity  increases  but  does  not  correspond  exactly  with  the 
fluid  taken.  It  is  greater  in  the  bottle-fed.  Proportionately  to  weight  it  is 
4-5  times  the  amount  passed  by  the  adult.    From  1  month  to  2  years  of  age 


The    Urinary  System.  547 

the  quantity  is  200-600  c.c,  an  average  being  about  10-12  oz.  Towards 
the  end  of  the  first  year-  68  c.c.  of  urine  is  equivalent  to  100  gms.  of  nourish- 
ment (Camerer).  A  rough  scale  is  10-15  oz.  in  the  second  year  and  an 
additional  1-1^  oz.  for  each  year  of  life  up  to  the  twelfth.  These  amounts 
are  often  exceeded. 

The  specific  gravity  depends  on  the  fluid  taken  and  the  amount  of 
urea.  It  is  1008-1012  during  the  first  3  days  ;  falls  to  1003-1004  and 
remains  low  for  some  months  ;  and  throughout  childhood  is  much  lower 
than  in  adults,  reaching  1015-1020  in  boys  at  14  years. 

Reaction. — In  the  newborn  it  is  acid,  high  coloured,  turbid,  contains 
mucus  and  often  deposits  urates  and  epithelial  cells.  Albumin  and  casts 
may  be  present  for  some  days.  After  a  few  days  it  is  very  pale,  almost 
odourless,  and  neutral  or  faintly  alkaline.  In  atrophy  and  sclerema  it  is 
acid.  The  presence  of  free  alkali  is  recognised  by  holding  moist  litmus 
paper  over  the  test  tube  while  heating.  Turbidity  clears  up  on  heating, 
if  due  to  urates  ;  and  on  the  addition  of  acetic  acid,  if  due  to  phosphates. 
If  filtered  urine  is  turbid,  the  cause  is  either  bacteria  or  blood.  Alkaline 
urine  is  due  to  digestion  (the  alkaline  tide),  vegetable  diet,  and  excess  of 
carbonates  and  salt.  Acid  sodium  phosphate  makes  it  acid.  Ammoniacal 
urine  is  turbid  and  offensive,  usually  due  to  excess  of  fatty  food. 

Urobilin  and  urobilinogen  are  derived  from  bilirubin  (p.  273). 
Urobilinogen  is  absent  in  the  breast-fed,  present  in  the  bottle-fed,  increased 
in  intestinal  affections,  haemorrhages  and  paroxysmal  heemoglobinuria, 
.and  absent  in  obstructive  jaundice.  It  forms  a  colourless  compound  in  an 
alkaline  medium. 

Urea. — The  percentage  of  urea  in  the  urine  is  1'5-1*7  in  children,  and 
2-2  in  adults.  More  protein  per  unit  of  weight  is  taken  by  children,  but 
much  nitrogen  is  used  up  in  the  formation  of  new  tissues.  Per  kilo  of 
weight  the  amount  of  urea  excreted  at  3-6  years  of  age  is  1  gm.,  at 
$-11  years  is  0*8  gm.  (Uhle)  or  0-7  gm.  (Sondern),  and  at  13-16  years 
is  0'3-0-5  gm.  (Sondern).  About  the  second  year  there  is  usually  an 
increase  because  more  protein  food  is  given.  The  amount  varies  directly 
as  the  supply  of  protein  and  inversely  as  the  cell-growth.  The  bulk  of 
the  nitrogen  is  excreted  as  urea.  Urea  is  diminished  and  the  ammonia-N 
increased  in  nutritional  disorders  (p.  151).  The  percentage  of  urea  in  the 
urine  is  higher  in  later  childhood,  particularly  in  boys,  because  of  increased 
•exercise,  loss  of  fluid  by  sweating,  and  a  liberal  supply  of  nitrogenous 
foods.    For  lithuria,  vide  p.  148. 

Turin  bodies  include  xanthin,  hypoxanthin,  adenin,  guanin,  theiri, 
•caffein,  theobromin  and  uric  acid.  The  amount  excreted  per  kilo  of  body- 
weight  varies  with  the  amount  ingested  (exogenous  purins)  and  with  the 
extent  of  cleavage  of  nuclein  in  the  body  (endogenous  purin).  Idiosyn- 
crasy, hereditary  and  constitutional  tendencies,  cold,  fevers  and  gastric 
disturbance  influence  the  amount.     They  are  precipitated  by  ammoniacal 


548  Chapter  XLV. 

solutions  of  silver  nitrate,  and  by  cuprous  sulphide  in  the  presence  of 
sodium  bisulphide. 

Uric  acid  is  very  variable  in  amount.  It  is  tolerably  constant  during 
the  first  few  days  of  life  and  allantoin,  an  allied  body,  may  be  present. 
Uric  acid  infarcts  or  concretions  are  composed  of  uric  acid,  oxalate  or  urate 
of  ammonia,  and  epithelial  debris.  They  were  present  in  the  tubuli 
uriniferi  of  64  out  of  199  infants  dead  under  30  days  of  age,  most  of  them  in 
the  first  3  days  of  life  (Schlossberger),  and  are  sometimes  present  in  the 
foetus  and  stillborn.  Henoch  has  noted  them  7-8  weeks  after  birth.  They 
form  yellowish  red,  brownish  yellow  or  light  yellow  striae  in  the  tubuli 
recti  of  the  pyramids,  converging  toward  the  hilum.  Microscopically, 
they  consist  of  angular  or  spherical  bodies  in  the  urine,  and  granular 
masses  or  yellowish  brown  cylinders  in  the  straight  tubules.  The  passage 
of  these  concretions  down  the  ureters  may  cause  tenderness  in  the  loins,, 
renal  colic,  restlessness,  retention  or  suppression  for  many  hours,  screaming^ 
dysuria  and  even  convulsions.  Usually  they  are  not  sufficiently  large  to 
become  impacted  and  cause  pain,  and  they  are  found  as  brick-red  sand 
or  small  mortar-like  masses  on  the  napkins  and  in  the  chamber  pot.  They 
rarely  cause  local  irritation  of  the  foreskin  or  vulva,  and  enuresis. 

Indican  is  not  present  in  the  newborn  or  the  breast-fed,  except  in 
minute  quantities.  It  is  increased  by  intestinal  troubles,  acute  and  chronic,, 
typhoid  fever,  and  constipation  ;  and  is  often  found  in  tuberculosis,  chorea 
and  acute  illnesses.  It  is  of  little  diagnostic  value,  except  as  a  sign  of 
intestinal  derangement  or  the  decomposition  of  albumin  in  various 
cavities,  e.g.,  decomposing  empyema,  gangrene  of  the  lung  and  bronchi- 
ectasis. It  is  formed  from  the  indol  in  the  alimentary  canal  and  appears  in 
the  urine  as  indoxyl-sulphate  of  potassium  and  as  a  saccharate,  but  not  as- 
indican.  Obermeyer's  and  Jafle's  tests  are  the  best.  Indigo-uria  has  been 
reported. 

Inorganic  salts  vary  much  with  the  amount  ingested.  The  quantity 
is  small  in  the  newborn  and  increases  as  age  advances.  The  amount  of 
chlorine  depends  on  the  intake,  if  the  kidneys  are  healthy.  Insoluble 
carbohydrates  form  a  cloud  on  heating  the  urine  of  those  who  eat  many 
vegetables.    It  is  dissolved  by  strong  nitric  acid  with  effervescence. 

Phosphates  are  normally  present  as  acid  phosphates  of  Ka.  and  K., 
and  earthy  phosphates  of  Ca.  and  Mg.  Earthy  phosphates  are  precipitated 
by  the  addition  of  alkali.  They  are  found  in  excess  in  marasmus  and 
rickets  ;  after  much  vegetable  food  ;  after  violent  vomiting  and  conditions 
in  which  HC1  is  deficient;  dilatation  and  motor  inefficiency  of  the  stomach, 
and  neurasthenia.  The  ratio  of  earthy  to  other  phosphates  in  adults  is  as. 
1  :  2,  and  it  may  rise  to  5  :  2.  They  may  be  deposited  in  the  bladder,  and 
excreted  as  milky  fluid  at  the  end  of  micturition  ;  or  as  an  iridescent 
pellicle  on  the  surface  of  the  urine  ;  or  on  boiling  unacidified  urine.  The 
crystals  are  stellate,  rectangular  plates  or  coffin-lid  in  shape  according  as. 


The    Urinary  System.  549 

they  consist  of  phosphates  of  calcium,  magnesium,  or  ammonio-magnesium. 
Phosphaturia  is  a  disturbance  of  phosphoric  acid  excretion,  diminished 
acidity,  or  an  excessive  excretion  of  lime  by  the  kidneys  instead  of  by  the 
intestines,  the  normal  channel.  The  urine  is  alkaline.  Its  acidity  is 
decreased  in  hyperchlorhydria,  for  less  acid  is  available  for  the  urine  ;  in 
cystitis,  because  of  ammoniacal  decomposition  ;  and  in  wasting  diseases, 
because  of  disintegration  of  nucleo-proteins.  Treatment  consists  in  the 
administration  of  inorganic  acids  and  nux  vomica,  attention  to  the  neuras- 
thenic state,  avoidance  of  worry  and  overwork,  mental  and  physical,  and 
liberal  diet,  containing  less  fruit  and  vegetables. 

Sulphur  excretion  is  due  to  transformation  of  protein.  Large  quan- 
tities of  ethyl-sulphuric  acid  and  phenol  in  the  urine  are  a  sign  of  intestinal 
decomposition. 

Abnormal  Constituents. — Acetonuria  has  been  considered  (p.  149). 
Ehrlictis  reaction  01  the  diazo-reaction  is  present  in  late  measles,  typhoid 
fever  (90  per  cent,  in  the  first  week),  and  miliary  tuberculosis  ;  may  be 
found  in  laryngeal  affections,  pneumonia,  pleurisy,  meningitis  of  all  kinds, 
tuberculosis  of  the  lungs  or  peritoneum,  diphtheria,  scarlatina  and 
erysipelas  ;  and  is  absent  in  pertussis,  mumps,  influenza,  sepsis,  rickets 
and  nervous,  digestive,  circulatory  and  genito-urinary  diseases.  Mix 
the  urine  with  an  equal  quantity  of  a  concentrated  solution  of 
sulphanilic  acid  in  weak  HC1,  and  a  few  drops  of  sodium  nitrite  solution. 
It  turns  red  on  adding  ammonia  and  gives  a  ring-shaped  green 
deposit  on   standing. 

Sugar  is  found  as  the  result  of  diabetes  and  alimentary  disturbance 
(p.  162).  Lactosuria  is  occasionally  seen  in  the  breast-fed.  Sugar  occurs  in 
theurineas:  (l)Monoses;  (a)Pentose;  (b) Hexose,  (i)  glucose,  (ii) levulose ; 
(2)  Bioses  ;  lactose.  It  has  been  found  by  Demme  in  pseudo-hypertrophic 
muscular  dystrophy,  by  Binet  in  severe  diphtheria,  and  sometimes  in 
diseases  of  an  asphyxial  character,  e.g.,  pertussis.  The  best  tests  are  fer- 
mentation, the  phenylhydrasin  test,  Fehling's,  Trommer's,  and  Bottger's 
bismuth  test.  Non-fermentable  copper-reducing  bodies  are  :  (1)  Glycuronio 
acid,  perhaps  due  to  camphor,  turpentine  or  fevers  ;  (2)  Pyrocatechin, 
much  increased  by  protein  diet ;  (3)  Alkapton  ;  (4)  Kreatinin  (for  test, 
v.  Acetonuria,  p.  149). 

Pentosuria  is  a  family  anomaly  of  metabolism  discovered  by  Salkowski 
and  Jastrowitz  (1892)  and  described  by  Salkowski  and  Blumenthal  (1895). 
The  youngest  case  up  to  the  present  was  15  years  old.  It  is  apparently 
harmless  but  important  in  that  it  may  lead  to  an  erroneous  diagnosis  of 
diabetes.  It  chiefly  affects  adult  males,  gives  rise  to  no  symptoms,  and  is 
not  improved  by  anti-diabetic  diet.  It  reduces  Fehling's  solution  atypically. 
The  colour  is  unchanged  for  1-2  minutes  and  then  turns  suddenly  greenish 
yellow  or  dirty  orange.  It  does  not  ferment  or  rotate  the  polariscope,  and 
forms  pentazone  crystals  with  the  phenylhydrasin  test. 


550  Chapter   XL  V. 

Cystinuria  is  an  anomaly  of  metabolism  of  protein,  possibly  due  to  the 
action  of  some  organism.  It  may  be  produced  from  diamines  but  these 
bodies  are  by  no  means  always  found  in  the  urine  and  fasces.  Scholberg 
and  Garrod  investigated  the  urine  of  a  boy,  aged  12,  with  cystinuria  and 
found  diamines  on  3  out  of  10  occasions.  Once  putrescin  was  separated 
as  a  pure  product ;  twice  it  was  found  with  a  smaller  portion  of  cadaverin. 
These  compounds  are  dibenzoyl  derivatives.  Garcia  also  found  putrescin 
in  a  case.  The  disease  is  often  hereditary.  Sometimes  the  patient  is  tuber- 
culous or  of  a  tuberculous  stock.  The  cystin  is  in  the  form  of  calculi,  single 
or  multiple,  or  transparent  hexagonal  crystals.  They  are  soluble  in 
ammonia.  These  children  are  difficult  to  diet.  It  was  detected  in  two 
children  of  the  same  family  at  14  and  21  months  of  age  (Abderhalden). 
On  acidulating  the  urine  with  HC1,  crystals  can  be  skimmed  off  in  an  hour. 

Alkaptonuria  is  another  endogenous  metabolic  freak  of  the  same  type. 
It  has  been  thoroughly  investigated  by  A.  E.  Garrod,  who  groups  it  with 
cystinuria,  pentosuria  and  albinism.  These  affections  are  harmless, 
unless  there  are  secondary  ill-effects.  Direct  transmission  is  rare.  Several 
members  of  a  family,  generally  collaterals  of  the  same  generation,  are 
affected.  Consanguineous  marriages  predispose  to  albinism  and  alkap- 
tonuria.   Garrod's  conclusions  (1908)  are  based  on  many  collected  cases  : — 

Albinism.        Alkaptonuria.        Cystinuria.  Pentosuria. 

Males         ....         34  31  63  19 

Females    ....         28  7  30  7 

Osier  and  Orsi  have  noted  direct  transmission  ;  and  Garrod  remarks 
on  the  special  liability  of  first  cousins  (8  out  of  17  families)  to  alkaptonuria. 
It  is  most  common  in  males.  Its  appearance  dates  from  earliest  infancy, 
even  the  second  day  of  life,  and  it  may  persist  throughout  life.  Rarely  it 
develops  later,  or  temporarily  during  illness.  It  may  give  rise  to  dysuria 
and  pollakiuria  ;  and  to  ochronosis  in  later  life.  The  urine  is  normal  when 
passed  but  becomes  deep  brown  or  black  on  exposure  to  air,  staining  diapers 
and  other  garments.  It  is  darkened  by  alkali,  reduces  Fehling's  solution, 
and  gives  negative  results  with  fermentation,  the  polariscope  and  the 
bismuth  sugar  test.  It  contains  homgentisic  acid  and  sometimes  uroleucic 
acid,  as  a  by-product  (Garrod). 

It  probably  arises  from  tyrosin,  a  product  of  the  pancreatic  digestion 
of  protein,  the  change  taking  place  in  the  tissues.  The  process  is  arrested 
at  an  intermediate  stage.  It  is  not  present  until  food  has  been  taken. 
If  tyrosin  is  given  by  mouth  to  these  subjects  the  homgentisic  acid  in  the 
urine  is  increased.    A  meat  diet  has  a  like  effect. 

Coloured  Urine. — Eosin-coloured  sweets,  e.g.,  musk  lozenges,  make 
the  urine  red,  so  much  so  as  to  suggest  hsematuria.  It  has  a  peculiar 
greenish  fluorescence,  and  is  pink  or  green  according  as  it  is  seen  by  trans- 
mitted or  reflected  light.  The  colour  may  be  that  of  a  weak  solution  of 
eosin.  Methylene  blue  passes  into  the  urine  in  15-30  minutes.  Purple  or 
violet  sweets,   coloured   by   aniline   dyes,   produce   blue   or  green  urine. 


The    Urinary  System.  551 

Methylene  blue  is  the  common  cause.  In  small  doses  it  produces  a  greenish 
tint,  perhaps  only  present  in  the  urine  secreted  during  sleep.  The  urine 
quickly  colours  white  blotting  paper  ;  is  decolourised  by  caustic  potash  ; 
and  readily  gives  up  its  pigment  to  chloroform,  which  becomes  blue. 
An  amyl-alcohol  extract  will  show  the  absorption  bands  and  give  the 
chemical  reactions  of  the  dye.  The  urine  is  made  green  by  biliverdin  ; 
olive  green  to  black  by  carbolic  acid,  creosote,  turpentine,  arbutin  (uva 
ursi),  fuchsin  in  small  doses,  and  alkapton,  the  colour  may  only  develop  on 
exposure  to  air  ;  red  or  purplish,  if  alkaline,  after  large  doses  of  fuchsin, 
rhubarb  or  senna,  due  to  the  chrysophanic  acid  in  the  last  two  drugs. 
Chrysophanic  acid  turns  acid  urine  deep  yellow  or  brownish  yellow, 
becoming  dull  red  on  adding  an  alkali.  Logwood  may  make  alkaline  urine 
reddish  or  violet.  The  red  colour  does  not  fade  on  standing  and  is  pre- 
cipitated by  barium  chloride.  The  yellowish  green  colour  of  acid  urine, 
due  tosantonin,  turns  red  on  adding  alkali.  The  red  colour  fades  on  standing 
and  is  not  precipitated  by  barium  chloride.  Purgen  causes  a  crimson  red 
colour  in  alkaline  urine,  decolourised  by  acid.  If  on  adding  ferric  chloride 
solution  the  urine  becomes  reddish  brown  or  reddish  purple,  the  salicyl 
radicle  is  present,  provided  the  colour  persists  on  boiling  and  is  insoluble  in 
ether.  If  due  to  diacetic  acid,  the  colour  is  discharged  by  boiling  and  is 
soluble  in  ether.  Antipyrin  and  similar  drugs  have  the  same  effect  as 
salicylates.  A  very  dark  inky  colour  is  due  to  tannates  or  gallates.  Tincture 
of  guiacum  gives  a  greenish  blue  reaction,  if  iodides  have  been  taken. 
Bile  pigments  turn  the  urine  a  colour  varying  from  bright  yellow  to  reddish 
brown,  like  beer. 

Albumose  is  precipitated  by  acid,  disappears  on  boiling  and  reappears 
on  cooling.  It  has  been  found  in  measles,  scarlatina,  diphtheria,  mumps, 
typhoid  fever,  and  pysemia  ;  during  the  absorption  of  exudates  in  pneu- 
monia and  pleurisy  ;  in  blood  effusions,  leukaemia  and  purpura.  The  Bence 
Jones  albumose  is  present  in  myelopathic  albumosuria.  Peptone  may  be 
present  in  pneumonia,  empyema  and  other  suppurations,  malnutrition, 
diphtheria  and  nephritis.    It  is  almost  always  accompanied  by  albumin. 

Albuminuria  is  a  sign  of  imperfect  health,  but  by  no  means  always  serious. 
There  may  be  no  structural  renal  changes.  If  so,  it  depends  on  mechanical, 
hematogenous  or  functional  causes  ;  e.g.,  cardiac  failure,  anaemia  and  vaso- 
motor disturbance.  In  many  cases  the  nutrition  of  the  renal  epithelium 
is  impaired.  Albuminuria  is  not  uncommon  in  acute  diseases  and,  in 
conjunction  with  casts,  is  a  sign  of  toxaemia  and  to  a  certain  extent  increases 
the  gravity  of  the  prognosis.  The  most  delicate  tests  show  that  urine 
always  contains  albumin.  Only  an  amount  which  responds  to  the  common 
tests  needs  notice.  Add  a  drop  or  two  of  dilute  acetic  acid  to  the  urine 
and  boil  the  upper  half.  If  albumin  is  present,  it  forms  a  cloud  of  varying 
density  which  does  not  disappear  on  adding  nitric  acid.  The  next  best 
test  is  the  cold  nitric  acid  one.    Or  drop  a  1  gr.  tabloid  of  salicyl-sulphonic 


552  Chapter  XLV. 

acid  into  a  pipette  and  draw  urine  up  into  it.  If  albumin  is  present  it 
becomes  cloudy.  It  is  important  to  distinguish,  albumin  from  nucleo- 
protein  or  nucleo-albumin.  Like  albumin  it  gives  a  cloud  with  the  acetic 
acid  test,  but  the  precipitate  clears  up  on  adding  nitric  acid  ;  and  it  gives 
no  white  ring  with  nitric  acid  in  the  cold.  An  excess  of  nucleo-protein  is 
a  sign  of  irritation  of  the  urinary  tract  below  the  tubules.  Thus  it  is  found 
in  pyuria,  and  if  there  are  many  crystals  of  oxalates,  phosphates  or  uric 
acid. 

In  the  'Newborn. — It  is  variously  stated  that  albumin  is  present  in  the 
urine  of  40-100  per  cent,  of  newborns,  and  may  persist  for  2  weeks.  Flens- 
burg  regards  it  as  a  nucleo-protein.  Ssesenowski  points  out  that  mucin  is 
frequently  mistaken  for  albumin.  He  found  mucin  nearly  always  present, 
albumin  in  22  and  uric  acid  in  60  per  cent.  The  albumin  is  due  to  hyper- 
emia from  circulatory  changes  at  birth,  or  to  renal  irritation  by  highly 
uratic  urine  or  renal  infarcts.  Possibly  it  is  connected  with  incomplete 
development  of  the  glomeruli,  a  persistent  fcetal  state,  or  metabolic  changes 
consequent  on  the  food  supply.  Even  if  nucleo-protein  is  differentiated 
from  albumin,  it  is  true  that  albuminuria  is  quite  common  in  the  newborn 
and  may  be  considerable  in  amount.  It  is  of  little  pathological  significance. 
Casts  and  renal  cells  are  found  on  centrifngalisation,  but  even  in  conjunction 
with  albumin  are  no  proof  of  nephritis.  A  few  cases  of  congenital  or  intra- 
uterine nephritis  are  on  record.  The  possibility  of  chill  or  infection,  at  or 
shortly  after  birth,  must  be  carefully  eliminated  before  accepting  such  a 
diagnosis.  Acute  nephritis  is  liable  to  be  overlooked  in  early  life  because  it 
is  unsuspected.  On  the  other  hand  infantile  oedema  is  by  no  means  always 
due  to  nephritis,  and  indeed  is  rarely  of  renal  origin. 

Functional  Albuminuria. — It  is  by  no  means  uncommon'  to  find 
albuminuria  in  apparently  healthy  children.  It  is  constant  or  present  for 
some  part  of  nearly  every  day,  disappears  in  the  horizontal  position,  and  is 
imassociated  with  organic  disease.  This  was  described  by  Moxon  (1878) 
as  "  albuminuria  in  the  apparently  healthy."  It  has  received  numerous 
names  since,  according  to  the  various  theories  of  its  causation  and  the 
conditions  under  which  it  occurs.  Thus  it  has  been  called  "  physiological," 
a  name  best  reserved  for  "  latent "  albuminuria,  always  present  but 
only  discovered  by  special  tests  ;  "  alimentary  "  or  "  dietetic,"  if  due  to 
excess  of  protein  food,  but  the  influence  of  diet  is  extremely  small ; 
"  postural,"  "  orthotic  "  or  "  orthostatic,"  because  it  depends  on  posture 
or  exercise,  the  name  orthotic  implying  that  it  occurs  while  at  rest  and 
orthostatic  that  it  follows  exercise  ;  "  athletic  "  or  the  "  albuminuria  of 
adolescence,"  because  it  follows  excessive  exercise  during  which  blood 
pressure  is  raised  and  the  splanchnic  veins  contract,  while  those  of  the 
muscles  dilate,  a  stage  followed  by  reaction  and  dilatation  of  the  splanchnic 
veins  and  renal  stasis  ;  "  intermittent,"  "  paroxysmal,"  "  cyclic  or  cyclical," 
for  it  is  apt  to  occur  at  certain  periods  of  the  day  only  ;    "  vasomotor," 


The    Urinary  System.  553 

for  it  follows  cold  baths,  bathing  and  exposure  to  cold,  through  the  effects 
on  the  splanchnic  area  and  renal  stasis  ;  "  neurasthenic,"  for  there  is 
frequently  a  marked  nervous  element  in  these  cases  and  it  may  follow 
psychical  shock.  It  is  also  called  early,  benign,  spurious,  transient,  essential, 
anephritic,  and  the  albuminuria  of  puberty,  youth  or  development.  The 
name  "Functional"  is  most  appropriate  for  it  indicates  neither  organic 
disease  nor  a  special  pathology. 

Etiology. — The  nomenclature  gives  a  fair  idea  of  the  chief  factors 
which  may  be  concerned  in  its  production.  Often  there  is  a  neurotic 
ancestry,  and  the  father  may  have  been  similarly  affected.  All  the  children 
of  the  family  may  suffer.  Both  sexes  are  liable,  girls  much  more  than  boys. 
The  common  age  is  9-14  years.  Dukes  found  over  16  per  cent,  of  the  boys 
entering  Rugby  school  at  13  years  of  age  were  affected.  Statistics  of  chil- 
dren from  10-18  years  of  age  vary  from  17-22  per  cent.  Probably  the  per- 
centage would  be  higher,  if  every  specimen  of  the  daily  urine  were  examined. 
Exciting  causes  are  insufficient  sleep,  malnutrition,  the  strain  of  examina- 
tions, backwardness  at  school  and  the  fear  of  superannuation,  and  mastur- 
bation or  sexual  development  by  indirectly  producing  nerve  exhaustion. 

The  Urine. — The  quantity  is  decreased,  and  more  is  secreted  by  night 
than  day.  Polyuria  is  easily  induced  by  extra  fluids.  That  secreted  by 
night  may  contain  a  mere  trace  or  be  entirely  free  from  albumin,  and 
that  secreted  for  a  few  hours  after  rising  may  contain  serum  albumin, 
serum  globulin  and  nucleo-protein.  During  the  day  the  albumin  gets  less, 
and  is  scanty  or  absent  at  bedtime.  The  amount  may  be  increased  by  food, 
cold  bath,  exertion  or  emotion.  The  percentage  varies  from  0-01-0- 1, 
and  may  exceptionally  reach  0-5,  the  urine  going  solid  on  boiling.  It 
depends  on  the  quantity  of  urine,  being  low  in  diuresis.  There  are  no 
renal  cells  or  casts,  except  a  very  few  small  hyaline  ones  at  times.  Urates, 
oxalates  and  phosphates  may  be  in  excess  in  the  diurnal  urine,  and  raise 
the  specific  gravity.  The  albuminuria  may  be  intermittent,  or  continuous 
and  varying  in  amount.  In  one  case  the  morning  urine  was  always  free 
but  the  evening  specimen  contained  at  different  times  phosphates,  nucleo- 
protein,  and  nucleo-protein  and  albumin.  It  is  by  no  means  uncommon  in 
the  evening  specimen  after  over-exertion.  Sometimes  it  is  absent  for  days. 
The  amount  varies  with  the  quality  of  the  pulse,  increasing  as  it  becomes 
small  and  weak. 

Pathology. — There  is  no  doubt  that  the  albuminuria  has  much  to  do 
with  the  assumption  of  the  erect  posture  for  it  may  appear  within  15  minutes. 
It  is  the  result  of  a  functional  disorder  of  the  renal  circulation,  probably 
glomerular,  for  it  is  associated  with  a  diminution  in  quantity,  increased 
acidity  and  decreased  excretion  of  chlorides.  The  change  in  the  renal 
circulation  may  be  hydrostatic  and  of  vasomotor  origin,  of  which  there 
is  frequently  other  evidence.  Blushing  is  common  at  this  age.  It  would 
be  unjustifiable  to  assert  that  all  cases  are  of  the  same  type  and  pathology. 


554  Chapter   XLV. 

An  unstable  nervous  mechanism  is  apparently  absent  in  some  instances. 
We  must  consider  the  effects  of  the  action  of  gravity  ;  diminished  coagu- 
lability or  lessened  viscidity  of  the  blood,  due  to  the  abstraction  of  lime 
salts  during  the  period  of  active  growth  ;  and  the  rapid  changes  in  blood 
pressure  produced  by  cold,  etc.  Blood  accumulates  in  the  splanchnic  area 
on  assuming  the  erect  posture  and  from  constriction  of  the  peripheral 
vessels. 

It  is  not  due  to  dietetic  causes  or  the  ingestion  of  food  at  breakfast. 
There  is  no  increase  after  the  midday  meal,  nor  does  the  omission  of  break- 
fast render  the  urine  less  albuminous.  It  may  disappear  on  a  milk  diet 
although  the  vertical  posture  is  allowed  ;  possibly  because  of  the  calcium 
in  the  milk.  Such  a  diet  may  increase  the  albumin.  If  the  child  is 
kept  recumbent  during  the  day,  the  albumin  will  appear  on  getting  up  at 
night.  Overfeeding  and  massage  do  not  produce  it  when  the  child  is  kept 
in  bed.  Sitting  up  in  bed  is  less  provocative  than  getting  up.  Estimations 
of  blood  pressure  may  show  a  difference  of  mm.  30-40  in  the  recumbent 
and  the  erect  posture.  Sutherland  found  one  or  both  kidneys  movable  in 
15  out  of  40  of  his  cases  ;  in  10  of  which  pain  referable  to  the  kidney  was 
present  and  relieved  by  recumbency.  Tessier  separates  a  group  in  which 
serum  globulin  is  present  and  perhaps  a  dilated  stomach,  enteroptosis, 
movable  kidney,  mental  depression,  fatigue  and  digestive  disorders ; 
all  more  or  less  signs  of  neurasthenia.  On  the  whole  we  must  regard  the 
bulk  of  the  cases  as  due  to  renal  vasomotor  disturbance,  perhaps  dependent 
on  neurasthenia  and  one  of  the  symptoms  of  neurasthenia  at  puberty. 
Yet  all  are  not  of  this  type,  for  it  would  be  hardly  justifiable  to  assume  that 
about  one-fifth  of  all  children  are  neurasthenic.  It  is  quite  sufficient  to 
ascribe  the  condition  to  vasomotor  instability  and  to  regard  this  as  of  so- 
common  occurrence  as  to  be  almost  a  normal  peculiarity  of  childhood. 
No  doubt  in  many  cases  it  is  partly  hematogenous. 

Symptoms. — Dukes  recognises  three  distinct  types.  The  first  and 
largest  group  presents  increased  arterial  tension,  unstable  in  character,  and 
varying  from  hour  to  hour  and  from  day  to  day.  He  ascribes  it  to  excess 
of  protein  food,  defective  elimination  and  hereditary  gout.  Deficient 
vasomotor  tone  is  the  feature  of  the  next  group  of  children,  who  show  cold 
and  congested  extremities,  and  frequent  chilblains.  In  a  third  group  he 
places  the  spare,  highly  strung,  over-sensitive  neurotics.  The  symptoms 
of  these  groups  overlap. 

These  children  are  nervous,  and  flush  or  turn  pale  readily.  Some  are 
florid  and  full-blooded  ;  or  pale,  flabby  and  ill-nourished.  Others  present 
a  dull,  heavy  aspect,  dilated  pupils,  and  a  chronic  suffused  condition  of  the 
cheeks,  chin  and  forehead  ;  cold,  dusky  red  fingers,  almost  like  local 
asphyxia,  with  patches  of  bright  red,  even  on  a  hot  day,  but  disappearing 
when  the  arm  is  raised.  The  feet  are  in  the  same  state,  always  cold,  and 
develop  chilblains.     Scattered  erythematous  patches  may  be  present  on 


The    Urinary  System.  555 

the  trunk  and  limbs  and  a  variable  degree  of  pigmentation.  Marie  has 
recorded  unilateral  pigmentation  and  sweating.  (Edema  may  be  so  marked 
about  the  eyelids  as  to  suggest  renal  disease  and  a  trace  may  be  found  about 
the  ankles.  Flatfoot  and  lateral  curvature  result  from  weakness  of  muscles 
and  ligaments. 

The  pulse  rate  is  quickened  and  varies  much  under  examination.  It 
may  be  of  low  tension  and  the  heart  small.  Or  the  blood  pressure  is  high, 
the  heart  large,  dilated  and  hypertrophied,  and  palpitations  present.  The 
impulse  of  the  right  ventricle  is  exaggerated.  The  increased  cardiac  impulse 
against  the  chest  wall  is  generally  due  to  the  right  ventricle,  and  it  is  only 
occasionally  that  the  left  ventricle  is  hypertrophied.  The  signs  of  an 
atonic  heart  are  not  apparent  on  examination  before  rising  in  the  morning. 
Abnormally  visible  and  palpable  pulsation  may  be  present  in  the  larger 
arteries  and  the  abdominal  aorta.  Occasionally  there  is  asthenopia, 
muscular  twitchings  and  rheumatic  pains. 

The  subjective  symptoms  are  debility,  languor,  disinclination  for  games 
and  mental  exertion,  headaches,  irritable  and  variable  temper,  depression 
and  tendency  to  weep  for  trivial  causes,  ansemia,  pallor,  attacks  of  faintness, 
flushings,  palpitations,  restlessness,  night  terrors  and  somnambulism. 
The  child  is  always  tired,  even  on  waking,  and  is  disinclined  to  get  up. 
Epistaxis  is  not  uncommon.  Albuminuria  is  always  present  in  children  who 
faint  during  drill  or  morning  chapel.  The  appetite  is  capricious,  sometimes 
ravenous. 

Diagnosis. — Examine  the  urine  secreted  at  different  times  of  the  day. 
Examine  for  slight  renal  changes,  pus  cells  and  urinary  crystals,  spermatozoa 
in  excess,  vasomotor  symptoms,  and  undue  mobility  of  the  kidneys. 
Remember  that  in  the  convalescent  stage  of  acute  nephritis  and  in  chronic 
interstitial  nephritis  the  albuminuria  may  be  of  the  postural  variety. 
According  to  Wright  and  Ross  the  administration  of  calcium  salts  increases 
the  percentage  of  albumin  if  there  is  nephritis,  but  not  otherwise.  Wright 
maintains  that  it  is  a  serous  exudate,  analogous  to  urticaria,  and  dependent 
on  diminished  coagulability  of  the  blood  ;  and  that  it  can  be  cured  by 
calcium  lactate.  This  is  not  confirmed  by  practical  experience.  The  age 
of  the  child,  the  variable  appearance  of  the  albumin,  and  vasomotor  dis- 
turbances are  the  chief  factors  on  which  a  diagnosis  is  based.  Cases,  in 
which  the  blood  pressure  is  high  and  the  arteries  thickened,  must  be  kept 
under  observation  for  at  least  a  year  before  pronouncing  them  absolutely 
free  from  renal  disease.  The  significance  of  albuminuria  depends  on  its 
causation  and  not  on  the  amount.  Hyaline  casts  cannot  be  regarded  as  of 
much  importance  if  found  on  centrifugalisation,  for  they  are  present  in 
many  nervous  and  febrile  states.  The  other  microscopical  signs  of  organic 
renal  disease  must  be  excluded.  Digestive  disturbances  may  cause  albu- 
minuria by  the  action  of  toxins  on  the  renal  epithelium.  So,  too,  all  toxic 
conditions,   many  drugs,   and   affections   of  the   urinary  and   generative 


556 


Chapter  XLV. 


organs  (post-renal  albuminuria).  Malnutrition  of  the  renal  epithelium, 
permitting  transudation,  altered  states  of  the  blood,  and  organic  diseases 
of  the  circulatory  system  must  be  excluded. 

Prognosis. — Patients  always  recover,  but  no  term  can  be  put  to  the 
duration  beyond  stating  that  it  is  rare  after  25  years  of  age.  It  usually 
disappears  after  puberty.  This  affords  some  support  to  the  view  that  it  is 
partly  dependent  on  incomplete  development  of  the  kidneys  and  that  they 
are  not  perfectly  formed  until  puberty.  There  is  no  post  mortem  evidence 
that  it  causes  future  renal  mischief.  Nor  does  scarlatina  make  it  worse  ; 
it  remains  absent  while  the  patient  is  in  bed.  Clearly  the  prognosis  depends 
on  the  exclusion  of  possible  renal  mischief  as  the  cause  of  the  albuminuria. 
Frequent  microscopical  examination  of  the  urine  is  essential  for  this  purpose. 
The  intermittent  character  and  the  small  amount  present  are  features 
sometimes  of  kidney  disease. 

Treatment. — It  is  essential  that  the  child  should  not  be  brought  up 
as  an  invalid  and  that  the  albuminuria  be  not  allowed  to  interfere  with 
education,  school  life,  games  or  a  liberal  food  supply.  Plenty  of  sleep, 
fresh  air,  and  moderate  mental  work  are  needed.  Exercise  should  be  of 
the  nature  of  recreation,  rather  than  dull  monotonous  walks,  but  it  should 
stop  short  of  fatigue.  Mild  cases  are  treated  on  the  above  principles. 
If  there  is  marked  neurasthenia  and  the  albuminuria  is  merely  one  symptom, 
the  child  must  be  relieved  from  all  worries  and  causes  of  anxiety,  lessons, 
and  the  society  of  other  children  or  anxious  parents.  If  there  is  much 
cardiac  weakness  prescribe  isolation,  liberal  diet,  massage,  and  rest  in  bed 
in  a  nursing  home  for  3-4  weeks  ;  followed  by  residence  in  the  country  or 
a  convalescent  home,  with  recumbency  from  12-2  p.m.,  and  for  12  hours 
at  night.  Highly-seasoned  food  and  alcohol  must  be  prohibited.  Give 
an  extra  pint  or  two  of  milk  daily.  Keep  the  bowels  open.  Put  on  an 
abdominal  belt,  if  the  kidney  is  mobile  and  causes  pain.  Drugs  are  rarely 
needed.  Phenacetin  relieves  the  headaches  of  the  high  tension  cases. 
Bromides  are  useful  for  sleeplessness  ;  digitalis,  if  the  heart  is  weak  ; 
and  calcium  salts  to  increase  the  coagulability  of  the  blood.  Nux  vomica 
and  strychnia  are  the  best  tonics  ;  followed  by  arsenic,  iron  and  ccd- 
liver  oil.  The  treatment  is  that  appropriate  to  neurasthenia  in  one  type  of 
case  ;  and  eliminative  in  the  high  tension  variety,  with  reduction  in  the 
amount  of  protein  food,  meat  extracts  and  stimulants.  Once  the  diagnosis 
is  established,  the  treatment  is  directed  to  the  general  state  of  the  patient's 
health  rather  than  to  the  albuminuria.  The  amount  of  albumin  lost 
cannot  be  regarded  as  a  serious  drain  on  the  system. 

Hematuria  and  allied  conditions. — The  appearance  of  urine  which 
contains  blood  or  blood  pigment  varies  with  the  amount,  site  of  origin  and 
nature  of  the  colouring  matter.  In  young  infants  the  napkins  are  stained. 
The  colour  is  not  a  reliable  sign  for  urine  may  be  "  as  red  as  blood  "  from 
excess  of  lithates,  eosin,  etc.  (p.  550).    A  small  amount  of  blood  from  the 


The    Urinary  System. 


557 


kidneys  is  uniformly  mixed  with  the  urine,  which  is  acid  and  has  a  "smoky  '* 
tint.  The  colour  is  due  to  a  mixture  of  urinary  pigments,  oxy-haemoglobin, 
methaemoglobin  and  perhaps  acid  haematin.  In  considerable  renal 
haemorrhage  the  bloody  urine  may  be  seen  by  the  cystoscope  coming  from 
the  ureteral  orifices  in  jerks,  somewhat  like  puffs  of  smoke.  Dark  porter- 
coloured  urine  is  due  to  haenioglobinuria  or  renal  infarcts.  Blood  from  the 
bladder  is  likely  to  contain  clots.  It  is  generally  uniformly  mixed  with  the 
urine,  but  may  be  passed  only  at  the  end  of  micturition.  Blood  from  the 
urethra  is  bright  red  and  passed  first.  The  colour  is  more  likely  to  be 
dark  in  renal  and  bright  red  in  vesical  bleeding,  but  there  are  many 
exceptions.  Longish  cylindrical  clots  are  probably  ureteral.  Renal  casts 
are  a  sign  of  renal  bleeding,  especially  if  there  are  many  casts  with  adherent 
red  cells.  Microscopical  examination  of  the  sediment  may  reveal  red 
cells.  The  spectroscope  gives  reliable  evidence  of  the  nature  of  the  pigment, 
viz.,  oxy-haemoglobin,  reduced  haemoglobin,  methaemoglobin,  h@em.atin  or 
haematoporphyrin. 

DIAGRAM   OF    BLOOD    SPECTRA. 


Acid  Haematin  . . 
Methaenioglobin 
Alkaline  Haematin 
Reduced  Hb. 
Haematoporphyrin 
Oxy-haemoglobin 
Carbonic  Oxide  Hb. 
Reduced  Haematin 


Four  of  these  spectra  possess  one  and  four  have  two  characteristic 
absorption  bands.  Metheemoglobin  and  acid  haematin  have  accessory 
bands  not  here  represented.  The  bands  of  oxy-haemoglobin  and  CO. 
haemoglobin  are  practically  the  same,  and  carmine  gives  an  almost  identical 
spectrum.  The  addition  of  ammonium  sulphide  converts  oxy-haemoglobin 
into  reduced  haemoglobin.  The  band  of  acid  haematin  is  readily  converted 
into  that  of  reduced  haematin  and  can  thus  be  distinguished  from  that  of 
methaemoglobin,  which  it  closely  resembles. 

The  next  most  reliable  test  is  the  formation  of  haemin  crystals  by  boiling 
a  little  of  the  dry  sediment  on  a  cover  slip  with  salt  and  acetic  acid.  The 
ordinary  clinical  test  with  tr.  guiaci  and  ozonic  ether  produces  a  blue 
colour  but  a  like  reaction  may  be  due  to  other  substances.     On  adding  an 


558  Chapter   XL  V. 

alkali  the  phosphates  are  precipitated  and  carry  down  with  them  the  blood 
pigment. 

Ilcematoporphyrinuria. — The  urine  is  pink,  red,  port  wine,  brownish 
or  black,  and  contains  iron-free  haemoglobin.  It  is  rare  in  children  and 
almost  peculiar  to  women ;  due  to  sulphonyl,  trional  or  tetronal.  It  has  been 
found  in  rheumatic  fever,  peritonitis,  hepatic  cirrhosis  and  Addison's 
disease.  Munro  (1908)  reported  a  paroxysmal  case  with  periodic  vomiting 
and  acetonuria,  in  a  boy,  7  years  old.  The  pigment  is  precipitated  by 
barium  chloride  and  hydrate  and  extracted  by  acidified  alcohol. 

Hemoglobinuria. — The  urine  contains  blood  pigment  and  merely 
a  few  red  cells.  It  varies  in  colour  from  red  to  black.  The  redder  it  is, 
the  more  oxy-haemoglobin  it  contains  ;  the  browner  it  is,  the  more  methse- 
moglobin  and  often  haematin  also.  The  niethaemoglobin  is  due  to  the 
action  of  the  kidney  cells,  rather  than  to  the  acidity  of  the  urine.  There  is 
usually  a  little  albumin  ;  on  boiling,  a  brown  coagulum  of  coagulated 
globin  ;  and  on  microscopical  examination,  crystals  of  oxy-haemoglobin, 
brown  granular  masses,  hyaline  and  granular  casts,  and  often  oxalate 
crystals.     Epidemic  hemoglobinuria  has  been  described  (p.  126). 

Paroxysmal  Hemoglobinuria  is  of  obscure  origin.  It  has  been  ascribed 
to  cold,  congenital  syphilis,  oxaluria,  paludism,  uric  acid  diathesis, 
traumatism,  over-exertion  and  febrile  catarrh.  Some  cases  are  associated 
with  Eaynaud's  disease  (p.  454).  It  is  not  common  in  children  but  may 
begin  in  the  fourth  year.  Usually  the  history  is  one  of  chill  or  slight 
malaise  ;  perhaps  a  feeling  of  chilliness,  vomiting  and  headache,  or  an 
attack  of  abdominal  pain  and  screaming.  In  a  few  hours  the  characteristic 
urine  is  passed  with  pain,  and  persists  for  12  hours  to  3-4  days,  gradually 
getting  less.  Slight  albuminuria  may  continue  for  still  longer.  There  may 
be  considerable  fever,  up  to  104°  F.,  and  icterus  in  severe  cases.  Oxalic 
.acid  crystals  are  usually  found,  possibly  accidental  and  not  causative  ; 
-and  vasomotor  symptoms,  such  as  pallor,  slight  lividity  of  lips  and  ears, 
and  cold  extremities. 

The  duration  is  variable.  Many  recover  after  puberty  but  others 
persist.  In  one  boy  it  followed  a  chill  after  a  hot  bath,  and  continued 
weekly  for  more  than  6  months,  after  which  he  was  lost  sight  of.  The 
attacks  came  on  at  night,  sometimes  preceded  by  shivering,  and  the  urine 
was  clear  by  morning.     "Warmth  is  necessary  during  the  attacks. 

The  symptomatic  variety  is  associated  with  a  definite  cause  ;  usually  a 
Hood  infection  or  a  poison.  The  chief  blood  infections  are  pyaemia,  typhoid, 
erysipelas,  typhus,  scarlatina,  measles  and  malaria.  It  has  occurred  in 
severe  burns,  scurvy,  fat  embolism,  jaundice,  acute  nephritis  and  the 
presence  of  nematoid  worms.  The  poisons  are  chlorate  of  potash,  arsenical 
compounds,  phosphorus,  oxalic  acid,  carbolic  and  pyrogallic  acid,  mineral 
acids,  and  the  poison  of  the  edible  mushroom  (helvella  esculenta).  It  can 
.be  induced  by  the  intravenous  injection  of  glycerine,  bile  salts,  distilled 


The    Urinary  System.  559 

water,  and  the  blood  of  another  animal.     Some  cases  are  due  to  oxaluria, 
or  the  eating  of  rhubarb,  spinach  and  fruits  rich  in  oxalates. 

Pathology. — Possibly  there  is  a  predisposing  cause,  such  as  congenital 
syphilis  which  is  present  in  about  one-third  of  the  paroxysmal  cases.  The 
separation  of  the  colouring  matter  takes  place  outside  the  circulation  by  the 
action  of  the  renal  cells,  or  more  probably  within  the  circulation  by  the 
action  of  an  exogenous  or  endogenous  toxin,  or  the  production  of  an 
autolysin  by  cold.  The  bulk  of  the  disintegrated  cells  is  passed  within  a  few 
hours  of  the  onset.  Probably  there  is  a  haemolysin  in  the  blood  serum  which 
acts,  or  is  formed,  when  the  body  temperature  is  reduced  ;  or  the  serum 
normally  contains  an  anti-haemolysin  which  is  destroyed  by  cold.  Eason's 
researches  (1905)  are  in  favour  of  the  view  that  the  haeruolysin  is  normally 
present  and  that  a  secondary  warm  stage,  following  on  exposure  to  cold,  is 
necessary  to  cause  haemolysis.  Against  this  it  may  be  pointed  out  that  if 
the  blood  is  kept  fluid  by  the  addition  of  potassium  oxalate,  haemolysis 
occurs  on  cooling.  Cold  and  fatigue  induce  paroxysms.  It  is  a  curious  fact 
that  these  patients  actually  feel  colder,  instead  of  warmer,  on  exertion.  Uric 
acid  excretion  and  the  percentage  of  urea-N.  in  relation  to  total  nitrogen  are 
increased  during  an  attack.  Haemolysis  is  a  normal  process,  controlled  by  the 
nervous  system,  and  some  cases  may  be  of  nervous  origin.  In  the  sympto- 
matic varieties  it  can  apparently  be  brought  about  by  different  poisons. 

Oxaluria  is  a  cause  of  haematuria  and  haemoglobinuria.  It  is  present 
in  paroxysmal  haemoglobinuria  and  in  Raynaud's  disease.  Haematuria  is 
due  to  mechanical  irritation  and  hemoglobinuria  to  haemolysis  by  the 
action  of  oxalic  acid.  Noel  Paton  asserts  that  urea  excretion  is  increased 
when  there  is  corpuscular  disintegration  in  the  general  circulation.  As 
the  urea  excretion  is  not  increased  the  haemoglobinuria  is  not  due  to  this 
cause,  and  the  separation  of  the  pigment  must  be  by  the  renal  cells. 

Oxalic  acid  is  endogenous  or  exogenous  in  origin.  It  is  contained  in 
spinach,  rhubarb,  sorrel,  to  a  less  extent  in  tomatoes,  strawberries,  potato, 
cabbage,  and  in  tea,  coffee  and  cocoa.  Baldwin's  oxalate-free  diet  consists 
of  milk,  meat,  eggs,  wheat,  flour,  rice,  biscuits,  sugar  and  butter.  The 
endogenous  acid  is  probably  derived  from  carbohydrates.  It  can  be  formed 
by  nitric  acid  from  sugar,  possibly  from  starches,  and  outside  the  body 
from  many  articles  of  diet.  As  a  metabolic  disorder  it  may  be  neglected, 
for  in  practice  it  is  found  to  depend  on  the  amount  ingested  and  the  acidity 
of  the  stomach  contents,  rendering  the  crystals  soluble.  The  acid  is  present 
in  the  urine  as  calcium  oxalate.  Its  precipitation  depends  on  excess  of 
oxalic  acid  and  perhaps  on  deficiency  of  magnesium.  Meat  diet  encourages 
its  deposition  by  increasing  the  acidity  of  the  urine.  The  crystals  may  be 
deposited  in  neutral,  and  even  alkaline  urine  ;  or  by  the  addition  of 
alcohol.  They  are  octohedral  in  shape.  "  Dumb-bells  "  are  crystals  of 
calcium  carbonate  and  their  deposition  commonly  depends  on  an  excess  of 
oxalic  acid  in  the  urine. 


5G0  Chapter  XLV. 

The  symptoms  are  a  low  state  of  health,  depression,  headache,  pains 
in  the  back,  and  dyspepsia  ;  painful  micturition,  intermittent  albuminuria, 
hematuria  and  crystals  in  the  urine.  Enuresis,  excess  of  nucleo-protein, 
and  calculus  are  sequels. 

Treatment. — Avoid  worry,  over-exertion  and  mental  fatigue.  Give 
a  diet  poor  in  oxalates,  lemons,  plenty  of  fluid,  and  little  sugar.  Prescribe 
pot.  citrat.,  as  a  diuretic  and  to  combine  with  the  calcium,  or  sod.  bicarb. ; 
and  magnesia  or  acid  sodium  phosphate  to  render  the  oxalates  more 
soluble.     Peas  contain  much  magnesia  and  little  oxalate. 

Hematuria. — In  the  newborn  the  blood  may  be  due  to  uric  acid 
infarcts  in  the  kidneys,  congestion  from  asphyxia  during  labour,  acute 
nephritis,  traumatism  at  birth,  or  haemorrhagic  disease  (p.  127).  In  older 
children  it  depends  on  : — I.  General  diseases  :  scurvy,  purpura,  leukaemia, 
haemophilia,  and  malignant  exanthems.  II.  Local  affections  of  the  kidney, 
e.g.,  passive  congestion  from  thrombosis  or  obstructive  heart  disease, 
acute  and  chronic  nephritis,  irritant  drugs,  infarcts,  injury,  new  growths, 
tuberculosis,  calculus  and  bilharzia  ;  of  the  ureter,  as  by  the  passage  of  a 
calculus  ;  of  the  bladder,  as  in  cystitis,  injury  and  foreign  bodies,  new 
growths,  tuberculosis,  calculus  and  bilharzia ;  of  the  prostrate,  from 
inflammation,  ulceration  and  stone  ;  of  the  urethra,  from  inflammation, 
passage  of  calculi  and  foreign  bodies,  injury  and  accidents. 

Idiopathic  Hematuria,  congenital,  hereditary  and  familial,  is  of  rare 
occurrence.  W.  H.  Attlee  reported  three  cases  of  recurrent  haematuria  in 
one  family,  all  females.  The  father  died,  aged  30,  from  uraemia .  Guthrie 
has  recorded  12  cases  in  2  generations  of  a  family  ;  5  males,  7  females.  The 
females  transmitted  the  disease  and  all  the  children  showed  it  shortly  after 
birth.  It  is  not  a  haemoglobinuria.  Red  cells  and  blood  casts  are  found. 
It  is  persistent  for  years,  variable  in  extent,  apt  to  be  recurrent,  paroxysmal, 
or  continuous  with  exacerbations.  In  one  case  it  was  continuous  for  2  years. 
Exacerbations  are  attributed  to  "  catching  cold  "  and  accompanied  by 
slight  fever,  headache,  malaise,  vomiting,  and  pain  in  the  back  and  limbs. 
They  may  depend  on  diet.  The  attacks  last  a  few  days  or  weeks,  occur  at 
varying  intervals,  are  uninfluenced  by  posture,  and  become  less  frequent 
after  the  tenth  year.  No  cedema,  ascites  or  cardio-vascular  changes  are 
present ;  and  no  excess  of  urea,  uric  acid  or  oxalates.  Albumin  may  be 
abundant  and  in  excess  of  the  blood.  The  cause  is  unknown.  Possibly  it 
is  a  renal  epistaxis  or  an  angioneurosis,  a  defect  of  the  vasomotor  system. 

Renal  Epistaxis  is  a  name  given  by  Gull  to  cases  of  haematuria  in  the 
young,  paroxysmal,  recurrent,  and  persistent  for  many  years  without 
symptoms  or  a  discoverable  cause.  They  have  been  ascribed  to  a  weakness 
of  the  renal  capillaries  and  increased  blood  pressure.  Isolated  attacks  in 
infants  are  probably  scorbutic.  Others  may  depend  on  renal  congestion 
occurring  in  the  course  of  rheumatism,  influenza,  glandular  fever  and 
pertussis.     Such  congestion  can  occur  without  nephritis.    Inflammation  is 


The   Urinary  System.  561 

probably  present,  if  the  albumin  persists  after  the  hsematuria  ceases.  In 
rheumatic  heematuria  there  are  no  symptoms,  except  pain  in  the  loins  which 
is  followed  by  copious  bleeding.  It  may  follow  tonsillitis.  The  treatment 
of  these  varieties  of  bleeding  is  by  rest  in  bed,  warmth  and  light  diet. 

Micturition. — Urine  is  not  passed  for  some  hours  after  birth,  perhaps 
not  for  3  days,  although  there  is  no  definite  morbid  cause.  The  delay  is  due 
to  deficient  secretion.  A  renal  insufficiency  has  been  described  in  the 
newborn.  The  amount  varies  in  different  infants.  Nurslings  micturate 
6-10  times  in  24  hours,  usually  after  being  fed  or  on  waking  from  sleep. 
They  may  pass  water  every  hour,  or  more  often  while  awake,  and  retain  it 
for  2-6  hours  during  sleep.  Bottle-fed  infants  may  wet  themselves  half- 
hourly.  The  duration  of  the  intervals  increases  as  age  advances.  Under 
5  years  of  age  the  child  micturates  from  6-7  times  ;  from  5-10  years, 
5-6  times  ;  and  after  that  3-4  times  daily. 

Anuria  occurs  in  uraemia,  fatal  diphtheria,  and  from  congenital 
causes.  Oliguria  is  present  in  febrile  states,  watery  diarrhoea,  some  forms 
of  nephritis,  hysteria,  and  certain  cardiac  affections.  Polyuria  is  found 
in  diabetes  insipidus,  diabetes  mellitus,  chronic  interstitial  nephritis, 
hysteria,  during  the  absorption  of  dropsical  effusions  in  nephritis,  digestive 
troubles,  emotional  disturbance,  pneumonic  crises,  and  as  the  effect  of  cold, 
the  ingestion  of  much  fluid  (polydipsia),  barley  water,  excess  of  sugar 
in  the  diet,  diuretics  and  digitalis,  etc.  Polyuria  may  cause  enuresis  but 
enuresis  does  not  always  indicate  polyuria.  Dysuria  depends  on  high 
acidity  of  the  urine  in  fevers,  sweating,  hot  weather,  insufficient  fluid 
ingesta,  etc.  ;  and  on  local  irritation  about  the  foreskin,  glans  penis,  clitoris, 
nymphse  and  vulva.  It  may  be  due  to  urethritis,  foreign  bodies  in  the 
urethra,  and  vesical  or  renal  affections. 

Incontinence  is  normal  during  the  early  months  of  life.  Reflex  excita- 
bility is  great,  sphincter  resistance  small,  and  cerebral  control  wanting. 
Control  is  acquired  much  earlier  by  some  children  than  by  others,  as  the 
result  of  careful  training  ;  perhaps  as  early  as  the  fourth  month  of  life. 
Control  is  established  after  teething  begins,  and  at  night  by  1J-2  years  of 
age.  Delay  in  acquiring  control  is  due  to  bad  training,  a  persistence  of 
the  infantile  state,  backwardness  or  imbecility.  Incontinence  may  depend 
on  genital  deformities,  urethral  irritation,  threadworms,  and  vesical  affec- 
tions, and  occurs  in  certain  nervous  diseases,  e.g.,  convulsions  and  epilepsy. 

Retention  in  the  newborn  may  be  due  to  inspissated  mucus  ;  in  infancy, 
to  impacted  urethral  calculus.  It  may  depend  on  painful  micturition  or 
congenital  defects,  and  occurs  during  hysteria,  meningitis,  enteritis,  stupor 
and  coma.  Other  causes  are  foreign  bodies  in  the  urethra,  ligature  round 
the  penis,  paraphimosis,  and  even  gonorrhoeal  stricture  (at  2^  years,  Abbe). 
It  must  be  distinguished  from  anuria.  I  have  seen  it  in  influenza.  It  gives  rise 
to  inconvenience  and  uneasiness,  passing  on  into  agony.  Overflow  incontin- 
ence may  ensue.  The  urine  must  be  drawn  off  very  slowly  to  prevent  collapse. 

2  o 


562  Chapter  XL  V. 

Diabetes  Insipidus. — Polyuria  must  be  distinguished  from  excessive 
frequency  of  micturition  and  diabetes  insipidus  from  polyuria.  This  is 
a  rare  disease  in  early  life,  but  it  may  date  from  infancy.  A  marked 
hereditary  tendency  is  present.  In  the  family  of  Peter  Schwartz,  born 
1772,  investigated  by  Weil,  out  of  70  members  21  were  certainly  and  13 
doubtfully  affected.  Cases  have  followed  injury,  e.g.,  a  blow  on  the  left 
temple  and  fracture  of  the  base  of  the  skull,  fright,  sunstroke,  specific  fevers 
and  cerebral  tumour.  In  many  no  cause  can  be  found.  Schiff  produced  it 
by  section  of  the  bulb  or  cerebellar  peduncles.  The  onset  is  usually  abrupt. 
The  amount  of  urine  varies  from  5-20  pints  ;  specific  gravity  1001-1006. 
It  is  pale  in  colour  and  contains  neither  albumin  nor  sugar.  Inosite  has 
been  found  in  a  few  cases. 

The  patient  is  generally  thin  and  neurotic,  with  a  dry  mouth  and 
unduly  red  tongue,  a  harsh,  dry,  pigmented  skin,  thirst,  frequent  mic- 
turition and  enuresis.  The  appetite  is  sometimes  increased,  more  often 
diminished.  Languor,  headache,  irritability  and  lumbar  pains  are  not 
infrequent. 

The  prognosis  depends  on  the  cause,  duration,  and  the  presence  of 
organic  disease.  It  is  best  when  the  polyuria  follows  injury  or  fevers,  and 
worst  when  there  is  a  strong  family  predisposition.  Temporary  improve- 
ment and  periodical  relapses  are  common.  A  few  recover  spontaneously. 
Some  of  the  reported  cases  are  probably  instances  of  chronic  interstitial 
nephritis,  a  disease  which  must  always  be  excluded  before  making  a 
diagnosis.    Death  is  due  to  intercurrent  disease. 

The  pathology  is  uncertain.  Probably  it  depends  on  an  inherited 
functional  defect  in  the  kidneys,  rendering  them  unable  to  excrete  urine 
above  a  certain  degree  of  concentration,  much  below  what  is  normal. 
Consequently  an  excess  of  fluid  must  be  ingested.  An  increase  in  the 
salts  ingested  causes  increased  polyuria,  for  the  specific  gravity  of  the 
urine  remains  the  same.  According  to  Meyers  (1908)  the  amount  of  urine 
varies  directly  as  the  amount  of  sodium  chloride  and  protein  ingested  ; 
and  the  defect  is  one  of  the  mechanism  responsible  for  concentration,  pro- 
bably a  fault  iD  the  floor  of  the  fourth  ventricle. 

Treatment  does  good  in  some  cases  and  seems  absolutely  inert  in  others. 
Undue  restriction  of  fluids  impairs  the  appetite  and  digestion,  increases  the 
irritability  and  malnutrition,  and  causes  symptoms  like  uraemia.  The  diet 
should  be  simple  and  nutritious.  Neither  excess  nor  reduction  of  proteins 
has  in  my  cases  proved  beneficial.  Nor  has  a  salt  free  diet  proved  of  any 
value.  General  hygiene  must  be  attended  to.  Valerianates,  phenazone, 
bromides,  arsenic,  atropine  and  belladonna  are  the  most  useful  drugs. 
Phenazone  reduces  the  excretion  of  urine  and  the  reflex  irritability  of  the 
cord.  Occasionally  ergot,  phosphorus,  opium,  and  nitric  acid  have  been 
followed  by  improvement.  Cold  douching  to  the  spine  and  faradism  of  the 
lumbar  region,  or  galvanism  of  the  spine,  may  be  tried  if  other  measures  fail. 


The   Urinary  System.  563 

Enuresis. — The  involuntary,  uncontrolled  evacuation  of  the  bladder, 
called  "  incontinence,"  is  normal  in  infancy  and  a  common  complaint  in 
infants  and  children  up  to  10  years  of  age.  It  is  an  unpleasant  affection, 
difficult  to  deal  with,  troublesome,  and  interferes  with  school  life  and 
occupations. 

Certain  cases  depend  on  malformations  of  the  bladder  or  urethra. 
In  spina  bifida  occulta  it  may  be  due  to  paralysis  of  the  pudic  nerves 
supplying  the  sphincters  of  the  bladder  and  rectum,  and  associated  with 
faecal  incontinence.  Enuresis  uretica  is  a  rare  variety,  usually  in  girls. 
The  ureter  opens  on  the  outer  surface  of  the  body  and  the  urine  trickles 
away  drop  by  drop.  The  child  is  always  wet,  even  immediately  after 
micturition.  The  urine  comes  from  the  vulva  or  the  urethra,  near  its 
orifice,  and  the  opening  is  detected  with  difficulty. 

A  second  group  of  cases  depends  on  inflammatory  affections.  In 
the  third  group  may  be  placed  those  of  nervous  origin.  The  nerve  supply 
■of  the  bladder  consists  of  a  cerebral  centre,  which  receives  afferent  impulses 
from  all  sources  and  sends  out  efferent  ones,  inhibiting  the  sphincter  or 
•exciting  the  detrusor  ;  a  lumbar  centre  in  the  third  and  fourth  segments 
of  the  lumbar  enlargement,  receiving  afferent  impulses  from  the  bladder  and 
sending  out  efferent  ones  by  the  third  and  fourth  sacral  nerves  to  the  bases 
and  neck  of  the  bladder,  and,  therefore,  to  the  sphincter  ;  a  sacral  centre 
which  receives  afferent  impulses  from  the  bladder  and  distributes  efferent 
■ones  to  the  detrusor  and  sympathetic  nerves. 

Cerebral  control  is  in  abeyance  during  epilepsy,  deep  sleep,  stupor  and 
•coma,  pavor  and  bad  dreams.  It  may  be  defective  on  account  of  heredity, 
imperfect  mental  or  cerebral  development,  or  acquired  as  the  result  of  bad 
training,  anaemia,  hypereemia,  malnutrition,  auto-intoxication,  specific 
fevers  and  various  neuroses.  Lesions  in  the  spinal  centres  and  tracts  cause 
general  incontinence.  Frequently  there  is  another  factor  in  the  shape 
•of  some  form  of  reflex  irritation  : — I.  Penile  and  vulvar  affections  ;  phimosis, 
balanitis,  vulvitis,  caruncle,  onanism,  urethritis,  hypospadias  and  thread- 
worms. II.  Bladder  disorders  ;  cystitis,  tuberculosis,  calculus.  III. 
Urinary  conditions ;  polyuria,  bacteriuria,  phosphaturia,  oxaluria,  excess  of 
uric  acid,  and  hyperacidity.  IV.  Renal  diseases  occasionally.  V.  Perineal 
and  anal  irritation ;  eczema  ani,  fissure,  polypus  and  threadworms. 
VI.  General  reflex  irritation  ;  e.g.  cold  bed.  Not  much  importance  need 
be  attached  to  a  small  bladder,  muscular  weakness,  a  poorly  developed 
sphincter  or  a  congenitally  wide  urethra.  Thus  there  may  be 
nervous  instability,  inherited  or  acquired,  of  the  higher  or  lower  nerve 
centres,  together  with  defective  co-ordination,  reflex  irritation  or 
direct  bladder  irritation.  Sometimes  the  lumbar  centre  is  unduly  excitable 
(spinal  hyperaesthesia).  In  such  cases  and  in  those  dependent  on  reflex 
irritability  the  enuresis  is  associated  with  pollakiuria.  In  atony  of  the 
•sphincter  of  the  bladder  the  enuresis  is  continuous,  the  urine  dripping  away. 


564  Chapter   XLV. 

Enuresis  might  be  reserved  as  the  name  for  incontinence  of  purely 
functional  causation,  reserving  "  incontinence  "  for  those  cases  in  which  a 
local  cause  is  present.  E.  nocturna  is  the  most  frequent  variety,  about  half 
the  cases,  and  is  usually  associated  with  dreaming  of  the  act.  In  E.  diurna 
et  nocturna  there  is  intermittent  incontinence,  asleep  and  awake,  and  the 
desire  to  pass  water  must  be  at  once  gratified.  E.  diurna  alone  is  uncommon. 
E.  continua  or  sine  intermissione  is  a  rare  type,  generally  due  to  some 
pathological  state,  e.g.,  Pott's  disease.  Occasionally  the  enuresis  is 
associated  with  fsecal  incontinence  and  sometimes  is  due  to  vesical  spasm. 

Etiology. — There  is  often  a  neurotic  or  tuberculous  family  history. 
The  affection  is  transmitted  from  one  or  other  parent,  more  commonly  the 
mother,  in  many  cases.  The  child  is  often  of  the  neurasthenic  type.  It  is- 
most  common  among  the  poor  from  neglect  of  proper  training  ;  in  cold 
weather,  from  October  to  March  ;  and  affects  both  sexes  about  equally. 
It  dates  from  birth  in  two-fifths  of  the  cases  and  in  one-tenth  begins  at 
1-2  years  of  age.  Many  cases  are  clearly  a  "  persistence  of  the  infantile 
condition."  There  may  be  a  congenital  weakness  of  the  sphincter  and 
undue  strength  of  the  detrusor  muscles,  undue  excitability  of  the  lumbar- 
centres,  or  a  lack  of  acquirement  of  the  inhibitory  function  by  the  higher 
nerve  centres.  Incontinence  may  occur  during  emotion,  fright  and  uncon- 
trollable laughter,  under  similar  conditions  of  pathogenesis.  A  congenital 
weakness  of  the  posterior  part  of  the  urethra  may  explain  some  cases  which 
show  traces  of  bladder  irritability  after  sexual  development.  These 
patients  are  more  subject  to  nocturnal  emissions,  can  bear  less  sexual 
strain,  have  to  empty  the  bladder  frequently,  and  have  difficulty  in 
retaining  water  when  they  feel  the  desire  to  micturate.  Enuresis  often 
leaves  behind  it  a  liability  to  recurrence  on  sexual  or  alcoholic  excess  in 
later  life.  Oberlander  has  pointed  out  that  in  the  young  male  the  caput 
gallaginis  is  very  prominent.  It  is  engorged  by  onanism,  sexual  excess, 
alcohol  and  highly  spiced  foods,  and  then  reflexly  stimulates  the  lumbar 
centres  and  causes  irritability  of  the  bladder.  An  enuresis  which  has 
ceased  for  years  before  puberty  may  recur' at  the  establishment  of  the 
sexual  function  and  be  induced  by  onanism.  Occasionally  it  is  due  to  late 
meals,  too  much  bed  clothing,  stimulants,  sleeping  on  the  back,  etc.,  causes, 
which  produce  emissions  in  later  life.  The  importance  of  adenoids  is  over- 
rated. They  are  one  cause  of  deep  sleep  and  C02  poisoning,  and  act  as  the 
final  straw.  The  removal  of  adenoids  and  enlarged  tonsils  has  been  followed 
by  recovery,  and  by  the  appearance  of  enuresis  in  a  child  previously 
unaffected.  In  a  few  instances  there  is  a  mental  and  physical  state  which  is 
improved  by  thyroid  extract. 

Symptoms. — The  worst  cases  can  be  recognised  by  a  uriniferous  odour 
about  the  child  from  the  constant  wetting.  Shyness,  timidity  and  reserve 
may  be  present.  Boys  are  sometimes  irritable  and  morose,  especially  if 
onanists.     These  children  may  be  normal  in  health,  mentally  active  and. 


The  Urinary  System.  565 

physically  weak,  ill-nourished,  or  below  the  average  in  mental  capacity. 
They  are  usually  nervous  and  excitable  and  reveal  other  signs  of  nervous 
instability,  such  as  habit  spasm,  stuttering,  headaches,  pavor,  lienteric 
diarrhoea,  or  fsecal  incontinence.  Acquired  cases  are  most  common  in 
strong,  full-blooded,  well  nourished  children,  5-8  years  old,  with  hyperacid 
urine.  This  is  the  acid  type  of  enuresis.  In  the  more  common  type  the 
urine  is  neutral  or  faintly  alkaline,  of  low  specific  gravity,  and  perhaps 
contains  triple  phosphates  or  oxalates,  a  few  pus  cells  and  a  trace  of  albumin. 
The  quantity  is  increased. 

Diagnosis. — Whether  the  affection  is  congenital  or  acquired  is 
ascertained  by  a  few  simple  questions.  Diseases  causing  polyuria  and  polla- 
kiuria  must  be  excluded.  The  enuresis  of  epilepsy  is  nocturnal  and 
spasmodic,  with  prolonged  intervals,  and  there  may  be  other  indications  of 
the  fit.  Local  sources  of  irritation  may  be  found  and  a  history  of  onanism 
obtained.  If  there  is  chronic  irritation  of  the  prostatic  urethra,  the  urine 
shows  a  slight  haze  by  transmitted  light  and  a  deposit  of  mucus  and 
leucocytes  on  standing. 

Prognosis. — The  outlook  is  better  in  boys  than  girls.  The  nocturnal 
variety  is  the  most  curable  and  children  with  diurnal  enuresis  also  do  well. 
The  longer  the  affection  has  persisted,  especially  in  girls,  the  more  difficult 
is  it  to  cure.  If  treatment  is  steadily  persisted  in,  about  75  per  cent,  are 
curable  in  3  months,  and  almost  all  within  2  years.  In  many  instances 
spontaneous  cure  takes  place  at  or  before  puberty,  when  the  genital  system 
is  fully  developed,  and  often  earlier.  After  puberty  it  is  very  intractable. 
It  may  cease  on  marriage.  It  is  less  likely  to  persist  after  puberty  in  boys 
because  of  prostatic  development.  Peyer  asserts  that  enuresis  augurs  ill 
for  future  virility,  and  that  the  patients  usually  have  less  sexual  desire 
and  can  bear  less  sexual  strain.  Probably  he  ascribes  to  the  enuresis  effects 
which  should  be  put  down  to  the  onanism  giving  rise  to  it. 

Treatment. — The  mere  psychical  effect  of  change  of  surroundings  may 
be  sufficient  to  break  the  habit.  Remedy  any  local  affection  which  may  be 
a  source  of  irritation  of  the  general  health,  the  nervous  system,  or  of 
reflex  excitability.  These  affections  are  rarely  the  primary  cause  and 
constantly  exist  without  enuresis.  Carefully  examine  the  urine  for  abnor- 
malities. Bacteriuria  may  exist  without  cystitis  and  is  most  common  in 
girls.  No  barbarous  methods  such  as  corporal  punishment,  dark  cupboards, 
and  bread  and  water  diet,  are  permissible.  They  are  cruel  and  apt  to  make 
a  nervous  child  worse.  Occasionally  they  do  good.  In  the  same  category 
may  be  placed  the  application  of  nitrate  of  silver  to  the  neck  of  the  bladder, 
massage  of  the  prostate  and  neck  of  the  bladder,  electrical  applications, 
blistering,  and  epidural  injections  of  normal  saline  or  1  per  cent,  stovain 
solution,  the  effects,  if  any,  being  psychical.  C.  A.  Ball  (1908)  recommends 
circumcision  ;  the  passage  of  a  large  steel  bougie  ;  and  cauterisation  of  the 
sphincteric  region  with  silver  nitrate  under  anaesthesia,  to  set  up  local 


566     '  Chapter  XLV. 

irritation  and  induce  powerful  contraction  of  the  sphincter  when  urine 
trickles  on  to  it.  Such  measures  may  be  perhaps  permissible  in  intractable 
cases  after  puberty.  So,  too,  gradual  dilatation  of  the  bladder  may  be 
then  tried,  for  in  girls  the  constant  enuresis  may  lead  to  the  bladder 
becoming  unduly  small. 

Cold  bathing  and  a  cold  douche  to  the  lumbar  region  at  bedtime  stimu- 
late the  nervous  system  and  have  a  psychical  effect.  Treat  the  general 
health  and  promote  elimination.  The  child  should  be  taught  to  defalcate  at 
night  rather  than  in  the  morning.  Fluid  ingesta  should  be  limited,  and  not 
allowed  after  4  p.m.,  unless  the  urine  is  highly  acid.  The  bedroom  must  be 
well  ventilated,  the  clothing  light  and  not  too  warm,  the  lower  end  of  the 
bed  raised,  and  a  cotton  reel  fixed  with  tapes  so  that  it  rests  on  the  spine 
and  prevents  the  child  sleeping  on  the  back.  Wake  the  child  to  pass  water 
an  hour  after  going  to  sleep.  The  diet  must  be  simple,  digestible,  and 
suitable  to  the  physiological  needs  and  digestive  capacity  of  the  child.  An 
excess  of  sugars  and  starches  is  often  injurious  by  setting  up  carbohydrate 
dyspepsia.  If  the  urine  is  highly  acid,  reduce  protein  food  and  give  plenty 
of  water  and  citrate  of  potash.  In  other  cases  it  is  generally  advisable  to 
increase  proteins.  Alcohol,  tea,  coffee,  beef  tea,  highly  seasoned,  irritant 
and  diuretic  foods  should  be  omitted. 

In  the  purely  nervous  cases  atropine,  belladonna  and  phenazone  give 
the  best  results.  Bromides  are  useful  if  there  is  irritability  of  the  lumbar 
centre.  Atropine  and  belladonna  must  be  pushed  to  the  limit  of  tolerance, 
if  a  good  result  is  to  be  obtained.  Children  stand  these  drugs  well.  Large 
doses  cause  flushing  of  the  face,  dilatation  of  the  pupils,  dimness  of  vision,. 
dryness  of  the  tongue  and  fauces,  and  occasionally  an  erythematous  rash 
and  delirium.  The  last  two  symptoms  are  signs  that  the  dose  must  be 
reduced.  Belladonna  is  said  to  contain  hyoscyamine  and  to  be  safer  than 
atropine,  but  the  amount  of  the  alkaloid  cannot  be  as  accurately  measured. 
Give  it  after  tea  and  before  going  to  bed.  Begin  with  m.  5  and  increase 
each  dose  by  m.  2|,  every  fifth  day  up  to  a  maximum  of  m.  20.  Continue 
the  maximum  dose  for  two  weeks  and  reduce  it  in  the  same  way  as  it  was 
increased.  One  grain  of  the  sulphate  of  atropine  in  water  oz.  1  forms  a 
solution  of  a  strength  of  about  1  in  500.  Give  it  at  4  and  7  p.m.,  and  increase 
one  of  the  doses  alternately,  every  other  day,  until  the  child  is  taking  two 
doses  of  the  same  number  of  minims  as  it  is  years  of  age.  D.  Macalister 
recommends  liq.  atropinse  m.  90,  liq.  strychninse  m.  45,  syr.  aurantii  ad. 
oz.  1  ;  5  drops  are  given  at  9  p.m.  and  the  dose  increased  by  5  drops  every 
fourth  night  up  to  a  maximum  of  30  drops,  or  even  60  drops.  It  is  then 
reduced  by  10  drops  every  fourth  night.  Seeing  that  1  m.  of  the  liquor 
is  equivalent  to  20  of  tr.  belladonnse,  such  large  closes  must  be  used  with 
caution.  The  tincture  is  sometimes  given  in  doses  up  to  dr.  1,  t.d.s.,  com- 
bined with  citrate  of  potash  and  cold  douching.  The  maximum  dose  is 
given  for  a  month  and  then  gradually  reduced.    Tr.  lycopodii  can  be  added 


The   Urinary  System.  567 

in  similar  quantities.  The  addition  of  nux  vomica  or  bromides  may  render 
it  more  efficacious.  Phenazone  in  large  doses  at  7  and  9  p.m.  for  a  week, 
and  repeated  after  a  week's  intermission,  cures  some  cases.  The  tincture 
and  fluid  extract  of  rhus  aromaticus,  m.  10-30,  is  useful  for  vesical  atony, 
but  not  so  much  so  as  arseniate  of  strychnia.  Alkalies,  oxide  and  valer- 
ianate of  zinc,  and  triple  valerianates  have  also  proved  beneficial.  Thus  the 
nature  of  the  drug  treatment  shows  that  cases  are  by  no  means  always  of 
the  same  pathogenesis,  and  that  the  best  results  will  be  obtained  when  the 
causation  is  ascertained  and  the  remedies  suitable  are  then  selected.  It  is 
futile  to  treat  incontinence  dependent  on  bladder  or  urinary  conditions  by 
atropin,  etc.,  and  to  give  strychnia  when  the  irritability  of  the  lumbar 
centres  is  unduly  high.  Each  case  must  be  treated  on  its  merits.  An  irri- 
table bladder  can  be  educated  by  keeping  the  child  in  bed  and  lengthening 
the  intervals  between  micturition.  The  child  should  not  be  sent  to  a 
boarding  school  because  of  ridicule,  worry  and  mental  strain. 

The  Bladder. — In  infancy  the  bladder  is  an  oblong,  acuminated  organ, 
outside  the  pelvis,  with  its  base  at  the  symphysis  pubes.  It  is  small  and 
consequently  micturition  is  frequent.  Its  anterior  aspect  is  in  contact  with 
the  abdominal  wall  over  a  triangular  area,  not  covered  by  peritoneum. 
It  is  rarely  absent,  duplicated,  or  divided  by  incomplete  septa  into  two  or 
more  compartments.  Umbilical  fistula,  due  to  a  persistent  urachus,  and 
cystic  dilatation  of  the  urachus  have  been  described  (p.  120).  Ectopia 
vesicae  is  most  frequent  in  males  and  associated  with  other  deformities. 
It  is  described  in  surgical  works.  A  dilated  bladder  may  be  found  in  a 
foetus  with  imperforate  urethra.  Congenital  diverticulum  is  rare.  It  has 
been  found  behind  the  trigone  (Tillmann),  arising  from  the  lower  and 
back  part  of  the  bladder  (C.  P.  Johnson),  and  somewhat  similar  in  situation 
but  associated  with  a  third  ureter  (Brach).  Wilkinson  reported  a  case 
in  a  girl,  aged  7  years,  in  whom  a  large  diverticulum  communicated  with  the 
bladder  by  a  round  orifice,  just  external  to  the  opening  of  the  right  ureter. 
It  was  full  of  ammoniacal  pus. 

Inversion  of  the  bladder  is  complete  or  incomplete.  Gross  collected 
7  complete  cases  ;  5  girls  between  14  months  and  4  years,  and  2  adult 
women.  In  the  more  common  type  there  is  only  inversion  of  the  mucous 
membrane.  It  is  seen  almost  entirely  in  females.  Bamberger  has  reported 
a  case  of  partial  prolapse  into  the  dilated  male  urethra.  It  is  due  to  con- 
genital weakness  of  the  neck  of  the  bladder  and  urethra,  and  an  exciting 
cause  such  as  the  strain  of  crying,  cough,  sneezing,  constipation,  diarrhoea 
or  cystitis.  The  urethra  is  almost  invariably  dilated.  The  prolapse  forms 
a  red,  vascular,  soft,  elastic,  reducible  tumour,  about  the  size  of  a  walnut 
and  somewhat  pear-shaped.  It  is  situated  below  the  clitoris  and  between 
the  labia.  It  may  become  larger  and  more  injected  on  crying  and  straining, 
and  causes  more  or  less  dysuria  and  incontinence.  The  prolapse  is  usually 
of  the  base  of  the  bladder,  and  the  orifices  of  the  ureters  may  be  visible  or 


568  Chapter  XLY. 

made  so  by  gentle  traction.  Occasionally  the  anterior  wall  is  affected. 
Having  excluded  the  possibility  of  polypus,  reduce  the  prolapse.  It  is 
dangerous  to  excise  it.  In  Wilkinson's  case  the  prolapse  was  strangu- 
lated, gangrenous,  and  the  slough  almost  black.  It  was  excised  and 
the  girl  recovered.    A  plastic  operation  may  narrow  the  neck  of  the  urethra. 

Cystitis  is  usually  due  to  foreign  bodies,  gonorrhoea  or  B.  coli  infection  ; 
possibly  exposure  to  cold  and  injury  to  the  perineum,  and  less  often  to 
other  organisms.  It  may  occur  in  infants  during  infectious  disease  or 
serious  illness,  probably  the  result  of  retention  of  urine  and  colon  infection. 
Some  attacks  are  very  mild  and  merely  cause  increased  frequency  of 
micturition  ;  the  urine  may  remain  acid.  In  more  severe  ones  there  is 
frequent  painful  micturition,  perhaps  causing  rigors  and  screaming  ;  pain 
above  the  pubes  and  in  the  perineum,  and  tenderness  ;  fever  up  to  103°  F., 
enuresis  and  occasionally  bleeding.  These  cases  are  sometimes  differentiated 
with  difficulty  from  baciiluria  and  pyelitis. 

In  pure  Baciiluria  the  urine  is  cloudy,  acid,  and  the  sediment  only 
contains  organisms,  seldom  round  cells  and  bladder  epithelium.  There 
may  be  pollakiuria.  It  occurs  chiefly  in  girl  babies,  due  to  B.  coli  infection 
via  the  urethra,  renal  circulation  or  adjoining  viscera.  Possibly  the  infec- 
tion is  conveyed  by  soiled  napkins,  stools  or  threadworms.  The  organism 
can  grow  in  acid  media,  does  not  decompose  urea  or  cause  ammoniacal 
fermentation,  and  may  set  up  slight  or  superficial  catarrh.  It  is  probably 
fairly  common,  but  not  diagnosed  through  the  urine  not  being  examined 
unless  there  are  symptoms.  If  inflammatory  reaction  ensues,  it  sets  up 
cystitis  or  pyelitis  (q.v.).  Enuresis  is  of  variable  severity  and  may  be  only 
nocturnal.  Cystitis  is  of  two  types.  In  one  there  are  pallor,  debility, 
anorexia,  restlessness  and  fever,  without  local  symptoms.  These  are 
more  probably  cases  of  pyelitis.  In  the  other,  a  true  cystitis,  there  are 
bladder  symptoms  in  addition,  viz.,  increased  frequency  of  micturition, 
dysuria,  pain  in  the  abdominal  region,  bladder  tenderness  on  pressure,  and 
inflammation  of  the  meatus.  The  urine  is  acid  in  colon  infections,  and  not 
acid  if  due  to  staphylococci  or  streptococci.  Other  organisms  are  sometimes 
the  cause. 

Treatment. — Give  uro tropin,  methylene  blue,  benzoate  of  ammonia, 
or  salol  by  mouth  in  order  to  inhibit  the  growth  of  micro-organisms.  In 
severe  cystitis  lavage  of  the  bladder  may  be  needed.  Use  boric  acid,  3  per 
cent,  solution  for  3  days  ;  and  then  silver  nitrate  1  in  1000,  followed  by 
salt  solution,  for  3  days.  The  diet  must  be  simple  and  contain  much  fluid. 
Alkalies  are  beneficial  in  colon  infections.    Possibly  vaccine  may  do  good. 

Tuberculosis  of  the  Bladder  is  said  to  be  extremely  rare  under  8  years. 
It  is  probably  more  common  and  more  curable  than  supposed.  There 
is  increasing  evidence  that  it  may  get  well  by  itself.  It  is  rare  as  a  primary 
disease  ;  more  common  in  boys,  and  due  to  extension  from  the  kidneys 
or  generative  organs.     Perhaps  some  primary  congestion  or  abrasion  is 


The   Urinary  System.  569 

necessary  to  permit  infection,  for  the  disease  can  exist  in  the  kidneys  for 
years  without  infecting  the  bladder.  Small  greyish  nodules  appear  in  the 
congested  mucosa  and  undergo  caseation,  setting  up  necrosis  of  the 
superficial  layers  and  forming  shallow  ulcers  which  may  perforate. 

The  classical  symptoms  are  late  ones.  Early  signs  are  frequent 
micturition,  without  increase  in  quantity,  hsematuria,  pain  and  pyuria  ; 
symptoms  like  those  of  stone.  Heematuria  may  be  the  first  sign,  in  the 
form  of  a  few  drops  of  bright  red  blood  at  the  end  of  micturition,  occurring 
intermittently  for  a  few  days  at  a  time.  It  may  exist  for  months  without 
pain  or  frequent  micturition,  usually  the  two  earliest  signs  and  signs  which 
are  not  influenced  by  exercise  as  in  calculus.  Hematuria  is  sometimes 
profuse,  large  clots  being  passed  although  the  lesion  is  trivial ;  more 
often  it  is  slight  and  infrequent.  Pain  is  burning,  scalding  and  often 
paroxysmal.  At  first  it  is  only  present  on  micturition,  or  if  the  bladder 
is  distended.  It  extends  along  the  urethra,  not  being  confined  to  the 
glans  as  in  stone,  but  may  be  referred  to  the  base  or  tip  of  the  penis  or 
the  perineum.  It  is  most  severe  if  the  trigone  is  involved.  With  extensive 
ulceration,  in  late  stages,  it  becomes  constant  in  the  hypogastrium.  Incon- 
tinence is  more  common  in  boys  than  girls,  and  indicates  that  the  neck 
of  the  bladder  is  affected. 

The  general  symptoms  are  those  of  cystitis  with  loss  of  weight,  fever, 
and  bacilli  in  the  urine. 

Diagnosis. — Stain  the  centrifugalised  urinary  sediment  for  tubercle 
bacilli,  taking  care  to  exclude  the  smegma  bacillus  which  is  present  in 
both  sexes  and  is  not  limited  to  the  genitals  ;  determine  the  tuberculo- 
opsonic  index,  if  thought  advantageous  ;  and  examine  with  the  sound 
and  cystoscope.  A  sound  may  give  a  grating  feel  as  it  passes  over  phos- 
phatic  deposit  on  the  ulcers.  The  'prognosis  is  bad  if  there  is  secondary 
cystitis,  but  some  get  well.  It  is  unduly  gloomy,  because  the  milder  cases 
may  remain  undiagnosed. 

Treatment  is  mainly  general.  Wash  out  the  bladder  with  sublimate 
solution,  1  in  10,000.  Silver  nitrate  is  injurious.  Suppositories  of  opium 
and  belladonna  relieve  pain.    Suprapubic  cystotomy  may  be  needed. 

Vesical  Calculus. — Stone  is  more  common  in  boys  than  girls,  and 
among  the  poor.  It  may  be  composed  of  oxalates,  uric  acid,  urates, 
phosphates  or  cystin.  Many  stones  are  made  of  calcium  oxalate  and 
primarily  renal.  The  symptoms  are  frequent  micturition  with  pain, 
referred  to  the  glans  penis,  and  the  passage  of  blood  at  the  end  of  micturi- 
tion ;  sometimes  pruritus  at  the  meatus,  retention,  sudden  cessation  of  the 
flow,  or  incontinence.  Cystitis  is  often  set  up  and  a  variable  amount  of 
pus  is  found,  the  urine  becoming  alkaline.  This  simulates  tuberculosis 
of  the  bladder.  Prolapse  of  the  rectum,  ulceration  of  the  bladder  and 
pelvic  abscess  are  occasional  sequels.  The  child  should  be  examined  with 
a  sound,  cystoscope  and  per  rectum.     Very  highly  acid  urine  may  give 


570  Chapter  XLV. 

rise  to  the  symptoms  of  stone,  and  on  exploring  the  bladder  with  a  sound 
the  surface  is  felt  rough  or  even  gritty.  It  is  due  to  the  mucous  membrane 
being  thrown  into  rugae  and  may  lead  to  an  erroneous  diagnosis,  but  it 
disappears  on  the  free  administration  of  water  and  alkalies.  A  ureteral 
calculus  impacted  at  the  entrance  into  the  bladder  may  cause  symptoms 
of  vesical  calculus.    It  can  be  removed  by  suprapubic  lithotomy. 

Stones  of  moderate  size  and  not  too  hard  should  be  removed  by 
litholopaxy.  The  meatus  may  require  enlargement.  If  the  child  is  under 
3  years  of  age,  or  the  stone  large  or  composed  of  oxalates,  it  must  be 
removed  by  suprapubic  lithotomy,  an  operation  as  safe  as  lateral  lithotomy 
and  not  likely  to  be  followed  by  the  serious  sequels  sometimes  seen  after  the 
latter  operation.  The  urine  should  be  sterilised  previously  by  the  adminis- 
tration of  urotropin  or  salol  and  the  bladder  washed  out  thoroughly  with 
an  antiseptic  solution. 

Tumour  of  the  bladder  is  rare  and  usually  a  sarcoma.  The  urine  may 
contain  pus,  blood  and  particles  of  tumour.  The  growth  can  be  felt  per 
rectum.  It  may  give  rise  to  secondary  cystitis,  pyelonephritis,  hydro- 
nephrosis and  peritonitis.     Operative  results  are  bad. 


CHAPTER    XLVI. 

DISEASES    OF    THE    KIDNEYS. 

Malformations  —  Movable  Kidney  —  Cystic  Disease  —  Hydronephrosis  — 
Nephritis,  acute  and  chronic — Acute  Pyelitis— Calculus — Tuberculous 
Kidney —  New  Growths. 

The  kidneys  are  relatively  larger  in  the  newborn  than  the  adult, 
weighing  from  12-30  gins.,  and  for  about  the  first  4  years  are  somewhat 
lobulated.  The  medullary  portion  preponderates  over  the  cortical.  The 
hilum  is  on  a  level  with  the  second  lumbar  vertebra.  The  right  kidney  is 
1-2  cm.  lower  than  the  left.  The  index  finger  in  the  rectum  easily  reaches 
the  lower  pole.  The  state  of  the  renal  organs  is  ascertained  by  palpation, 
percussion,  inspection  of  the  dorsum,  X-rays,  and  the  examination  of  the 
urine.  Cystoscopic  examination  may  reveal  blockage  of  one  ureter,  ureteral 
calculus,  and  blood  or  pus  issuing  from  the  ureter.  The  state  of  the  cardio- 
vascular system  and  the  fundus  of  the  eye  are  also  of  assistance. 

Malformations. — The  whole  urinary  system  may  be  absent  or  one 
kidney  alone  wanting.  Complete  Absence  of  a  kidney  is  rare,  1  in  4000 
autopsies.  No  trace  was  found  in  a  5-year  old  boy  who  died  from  spinal 
caries.  Absence  is  4  times  as  common  in  males  as  females.  The  left 
kidney  is  more  often  absent  than  the  right.  The  ureter  and  renal  vessels 
are  absent  or  represented  by  a  fibrous  cord.  The  other  kidney  is  increased 
in  size  sufficiently  to  carry  on  the  renal  functions  adequately,  except  in 
serious  illness.  Atrophy  is  more  common  and  may  be  due  to  thrombosis  of 
the  renal  vein.  The  kidney  is  simply  small  and  f  unctionless,  a  mass  of  fibrous 
tissue,  a  collection  of  cysts  or  a  mere  nodule  of  fat.  Calculi  seem  to  me  to 
develop  with  undue  frequency  in  single  kidneys,  and  uraemia  may  follow 
obstruction  of  the  ureter.  Some  cases  live  to  old  age.  Fused  kidneys  are 
"  horseshoe,"  "  sigmoid,"  or  "  disc  shaped."  Their  frequency  is  given  as 
3  in  2594  autopsies.  W.  G.  Nash  (1908)  recorded  a  case  in  a  girl,  16  months 
old,  with  hydronephrosis  of  the  left  half.  A  supernumerary  kidney  is  also 
rare.  It  is  usually  the  result  of  extreme  segmentation  on  one  side  and  may 
be  entirely  separate.  Occasionally  one  kidney  has  two  pelves,  but  the  ureters 
are  generally  fused.  In  Watson  Cheyne's  case  (1899)  the  third  kidney  was 
movable  and  was  removed.  In  Barlet's  case  (1904)  two  left  kidneys  were 
fused  together,  with  separate  pelves,  ureters  and  openings  into  the  bladder. 


572  Chapter  XL  VI. 

A  displaced  kidney  is  found  in  24  out  of  1000  autopsies  (Newman, 
1898).  The  left  kidney  is  the  one  usually  affected.  It  may  lie  obliquely 
on  the  sacro-iliac  synchondrosis,  transversely  across  the  prominence  of  the 
sacrum  or  between  the  rectum  and  bladder,  or  fixed  beside  the  uterus. 
It  is  generally  much  lobulated,  and  associated  with  abnormalities  of  the 
nreters  and  blood  vessels,  and  alterations  in  position  of  the  large  intestine 
and  peritoneum.  Sometimes  fusion  is  present  and  the  fused  organ  is 
unilateral,  the  adrenals  not  being  displaced.  It  may  be  mistaken  for 
enlarged  glands,  faecal  concretions,  undescended  testis,  tumours,  etc. 
Anomalies  in  the  vascular  supply  are  common.  Occasionally  there  is 
no  renal  pelvis,  the  calyces  entering  separate  tubules  which  unite  to  form 
the  ureter. 

The  Ureters. — The  ureter  may  be  duplicated,  constricted,  impervious 
or  contain  valve-like  folds  of  mucous  membrane.  About  40  cases  of  pro- 
lapse of  the  blind  end  of  the  ureter  into  the  bladder,  and  even  through  the 
urethra,  are  on  record.  C4.  F.  D.  and  A.  L.  H.  Smith  reported  (1906)  a  case 
•of  accessory  left  ureter,  ballooned  at  the  lower  end  or  ending  in  a  cystic 
swelling  in  the  bladder  wall.  It  protruded  as  a  dark  red,  globular  swelling 
from  the  urethra  of  a  girl,  aged  5  days.  The  accessory  ureter  was  much 
dilated  and  opened  into  a  dilated  cyst  of  the  upper  half  of  the  kidney,  the 
lower  half  of  which  was  normal.  Idiopathic  dilatation,  i.e.,  no  obvious 
obstruction,  is  almost  always  associated  with  dilatation  of  the  pelvis. 
Both  may  occur  without  dilatation  or  hypertrophy  of  the  bladder.  It 
may  be  unilateral.  Box  (1909)  found  unilateral  ureteritis  in  one  case. 
This  might  cause  temporary  obstruction  of  the  vesical  orifice.  Dilatation 
secondary  to  urethral  obstruction  can  be  excluded  for  the  bladder  is  normal. 

Movable  Kidney. — Mobility  of  the  kidney  is  not  uncommon  in  children. 
Sutherland  found  it  in  15  out  of  40  cases  of  orthostatic  albuminuria.  It 
may  be  so  mobile  as  to  be  "  floating,"  of  congenital  origin  due  to  a  mesone- 
phron.  It  is  usually  on  the  right  side  and  more  common  in  girls.  Symptoms 
are  absent ;  or  there  may  be  dull,  aching  or  dragging  pain  in  the  loin, 
shooting  down  the  thigh  and  toward  the  umbilicus.  The  pain  is  relieved  by 
recumbency,  and  increased  by  exercise  or  constipation.  Complications 
arise  directly  or  indirectly  from  the  displacement,  and  kinking  or  twisting 
of  the  blood  vessels  or  ureters.  Acute  renal  congestion  and  intense  pain, 
leading  to  collapse,  are  due  to  torsion  of  the  vessels.  Frequent  micturition, 
tenesmus,  and  renal  colic  or  suppression  may  ensue  on  kinking  of  the 
ureter  and  transitory  hydronephrosis.  Pyelitis  and  calculus  may  develop  ; 
constipation,  from  dragging  on  the  colon  ;  headache,  furred  tongue, 
vomiting  and  jaundice,  from  dragging  on  the  duodenum.  The  urine  is 
normal  or  merely  varies  in  quantity.  It  is  treated  by  general  tonics, 
bandages,  belts  and  operation.    In  the  majority  of  cases  it  may  be  ignored. 

Cystic  Kidneys.— Congenitally  cystic  kidney,  unilateral  or  bilateral, 
is  due  to  error  of  development.     There  is  no  evidence  of  intra-uterine 


Diseases  of  the  Kidneys.  573 

inflammation  or  tumour  formation.  Probably  the  renal  changes  are  the 
same  in  adults,  entirely  developmental  and  differing  only  in  degree.  The 
secondary  fibrosis  is  due  to  the  tendency  of  malformed  organs  to  disease. 
The  kidney  is  developed  from  the  metanephros,  which  forms  the  glomeruli 
and  convoluted  tubules  ;  and  from  the  upper  end  of  the  ureter,  which  gives 
origin  to  the  straight  and  collecting  tubules.  If  the  two  fail  to  unite,  the 
parts  arising  from  the  metanephros  become  cystic.  They  are  not  retention 
cysts  arising  in  the  uriniferous  tubules  from  uric  acid  obstruction  or 
embryonic  nephritis.  More  than  one  member  of  a  family  may  be  affected. 
The  surface  may  be  entirely  composed  of  smooth,  translucent  cysts,. 
not  communicating  with  each  other.  The  capsule  is  adherent.  On  section 
there  are  found  smaller  cysts,  irregular  cavities  separated  by  fibrous  tissue, 
very  little  differentiation  between  cortex  and  medulla,  and  no  traces  of 
calyces  or  papilla?.  The  ureter  may  be  impervious.  If  the  urethra  is  imper- 
vious, the  bladder  is  much  dilated.  The  liver  is  cystic  in  20  per  cent, 
of  these  cases  (p.  363). 

The  urine  resembles  that  of  hydronephrosis.  Occasionally  it  is  acid, 
of  high  specific  gravity,  and  contains  blood.  The  amount  of  urea  varies 
and  there  may  be  a  variable  quantity  of  albumin.  The  disease  may  be  so 
advanced  as  to  impede  delivery.  Symptoms  are  absent  in  early  life  or  are 
those  of  a  renal  tumour  : — bulging  of  the  abdomen  in  the  flanks,  dilated 
superficial  veins,  and  a  palpable  tumour  (in  18  out  of  62  cases,  Lejars). 

The  prognosis  is  bad  for  gradual  fibrosis  ensues  and  destroys  the  little 
renal  tissue  remaining.  Some  of  the  later  cysts  may  be  of  similar  origin  to 
those  of  chronic  interstitial  nephritis.  Calculi  may  form.  Death  is  due  to 
convulsions  or  uraemia.  (Edema,  purpuric  rash  and  symptoms  of  chronic 
interstitial  nephritis  may  arise,  and  occasionally  pyuria. 

Nephrectomy  is  not  justifiable  for  an  apparently  complete  cystic  kidney 
often  contains  areas  of  healthy  and  partially  healthy  renal  tissue,  not 
visible  to  the  naked  eye.  The  removal  of  one  kidney  may  be  followed  by 
rapid  enlargement  of  the  opposite  one,  though  previously  small.  Though 
small  it  is  cystic.  Unilateral  enlargement  may  be  caused  by  calculous 
obstruction.    Patients  have  lived  to  over  40  years  of  age. 

Congenital  Hydronephrosis. — This  is  usually  bilateral,  but  may  be 
unilateral.  Often  no  obstruction  is  found.  The  chief  causes  are  imper- 
forate urethra,  membranous  septa,  valves  or  cysts  in  the  urethra  ;  develop- 
mental defects  of  the  ureters  ;  or  torsion  of  the  ureter  due  to  floating 
kidney.  It  is  not  necessary  for  the  obstruction  to  be  absolute.  A  valvular 
urethral  obstruction  may  interfere  with  micturition  but  not  with  cathe- 
terisation.  In  a  boy,  4  years  old,  with  unilateral  hydronephrosis  the 
pelvis  of  the  kidney  was  dilated  and  ended  in  a  small  conical  apex,  separated 
from  the  end  of  the  ureter  by  a  minute  interval.  Anatomically  the  effects 
vary  with  the  causation.  In  bilateral  cases  the  ureters  are  dilated  and 
tortuous.     The  kidneys  show  a  variable  degree  of  cirrhosis  and  dilatation. 


574  Chapter  XLVI. 

Sometimes  one  kidney  is  cystic  and  the  other  hydronephrotic.     Hare-lip, 
club-foot  and  other  deformities  may  be  present. 

The  condition  may  interfere  with  labour.  The  child  may  be  stillborn, 
or  live  for  weeks  to  years.  Most  of  them  die  in  early  infancy.  Out  of  10  cases 
6  died  under  6  months  and  only  2  lived  2  years  (Holt).  It  gives  rise  to  a 
globular,  more  or  less  cystic  swelling  extending  into  the  loin  ;  perhaps  so 
large  as  to  pass  the  middle  line  and  yield  a  thrill.  It  is  often  not  diagnosed 
during  life  for  genito-urinary  symptoms  are  usually  absent.  The  urine 
from  some  cases  has  contained  little  or  no  urea.  If  unilateral  and  increasing 
in  size,  sufficiently  to  cause  symptoms,  it  should  be  removed. 

Acquired  Hydronephrosis  is  usually  the  result  of  calculous  or  other 
obstruction,  external  pressure  on  the  ureter  and,  rarely,  ureteral  stricture 
such  as  may  follow  septic  infection  and  surgical  kidney.  If  the  obstruction 
is  variable  in  degree  it  is  apt  to  give  rise  to  attacks  of  pain  in  the  abdomen 
and  renal  region  ;  tenderness,  rigidity  and  fulness  ;  and  scanty  micturition. 
Such  an  attack  may  end  with  the  passage  of  a  large  quantity  of  urine  of 
low  specific  gravity.  Hydronephrosis  must  be  diagnosed  from  simple  cyst, 
cystic  disease,  tumour,  pyonephrosis  and  tuberculous  kidney. 

Nephritis. — The  urine  should  be  examined  in  fever  and  acute  disease 
lor  nephritis  is  a  common  complication  and  albuminuria  still  more  frequent. 
Albuminuria,  even  with  oedema,  is  not  proof  of  nephritis.  Both  these 
signs,  and  possibly  hsematuria  also,  may  be  present  apart  from  actual 
inflammation  of  the  kidney.  On  the  other  hand  nephritis  may  be  found 
post  mortem  although  no  albuminuria  was  present  during  life.  In  nephritis 
the  diagnosis  is  based  on  the  urinary  analysis  and  associated  symptoms, 
as  in  adults  :  viz.,  blood,  albumin,  casts,  alterations  in  the  quantity, 
colour  and  specific  gravity ;  cardio-vascular  changes,  retinal  changes, 
oedema,  and  complications  affecting  the  serous  membranes.  It  is  almost 
impossible  to  make  an  exact  diagnosis  of  the  special  variety  of  renal 
disease  by  urinalysis.  The  want  of  correspondence  between  clinical 
symptoms  and  renal  changes  is  a  frequent  and  striking  characteristic. 
The  causes  of  albuminuria  without  nephritis  have  been  already  mentioned 
and  discussed  (pp.  551-556). 

Infantile  oedema  is  by  no  means  always  due  to  nephritis,  e.g.,  oedema 
neonatorum  (p.  146),  which  develops  within  a  few  days  of  birth  and  is 
-analogous  to  phlegmasia  alba  dolens  in  some  instances,  due  to  thrombosis 
of  the  vena  cava  inferior.  Idiopathic  or  essential  oedema  (L.  F.  Meyer, 
1905)  is  a  type  in  which  neither  albumin  nor  casts  are  found  in  the  urine, 
.and  the  kidneys  in  fatal  cases  appear  unaffected.  It  is  increased  by  adding 
common  salt,  gm.  1-2  daily,  or  sodium  phosphate  to  the  diet.  Meyer 
ascribes  it  to  a  functional  derangement  of  the  renal  epithelium,  whereby 
the  salts  are  imperfectly  excreted  and,  accumulating  in  the  tissues,  cause 
retention  of  water  (Hutinel's  theory).  Some  cases  can  be  cured  by  increasing 
the  percentage  of  protein  in  the  food.    To  a  similar  condition  S.  West  gives 


Diseases  of  the  Kidneys.  575 

the  name  of  pseudo-renal  dropsy.  It  occurs  in  infants  and  young  children 
with  marasmus  or  malnutrition,  anaemia,  and  often  prolonged  diarrhoea. 
It  may  become  extreme  in  a  few  days  and  even  cause  serous  effusions. 
No  nephritis  is  found  after  death.  Digitalis  is  useful.  An  acute  general 
azdema  is  occasionally  seen  in  infants  and  children,  for  which  no  cause  can 
be  ascertained  and  one  is  reduced  to  a  diagnosis  of  some  kind  of  toxsemia 
affecting  the  blood  and  possibly  the  renal  epithelium.  I  have  noted  in  a 
few  cases  of  this  type  that  the  secretion  of  urine  was  scanty  at  the  onset 
and  that  a  trace  of  albumin  and  a  few  red  cells  were  present ;  but  the 
child  recovered  in  a  few  days.  Perhaps  these  are  instances  of  renal  urticaria. 
Generally  speaking  we  must  regard  oedema  in  the  above  instances  as 
dependent  on  altered  states  of  the  blood  or  on  malnutrition  of  the  renal 
cells,  causing  a  renal  inadequacy.  These  remarks  must  be  read  in  con- 
junction with  those  on  oedema  as  a  symptom  (p.  457).  (Edema,  albumin 
and  hyaline  casts  can  occur  in  the  newborn  without  nephritis.  The  amount 
of  oedema  depends  on  the  scantiness  of  the  urine.  The  prognosis  is  that 
of  the  cachexia. 

Nephritis  in  Infancy. — It  may  occur  in  the  newborn  and  be  even  intra- 
uterine in  origin.  Ashby  reported  the  case  of  an  infant  who  developed 
oedema  of  the  face  on  the  second  day  of  life,  followed  by  general  oedema, 
diarrhoea,  vomiting,  oliguria,  and  death  from  convulsions  at  4  weeks  of  age. 
Nephritis  of  the  type  of  scarlatinal  nephritis  was  found  after  death. 
G.  Carpenter  and  Henoch  have  recorded  cases  in  infants  5  weeks  old,  and 
Jacobi  mentions  5  cases  seen  within  the  first  5  weeks  of  life,  for  which  no 
cause  could  be  discovered  except  prolonged  asphyxia  at  birth.  One  of 
Carpenter's  patients  was  syphilitic.  Nephritis  in  infants  may  be  of  gastro- 
intestinal origin  or  due  to  other  infections  and  intoxications.  The  con- 
tracted kidney  is  a  curiosity  at  this  age  and  nephritis  due  to  congenital 
syphilis  very  rare. 

G astro-intestinal  nephritis  may  occur  in  any  acute  attack  of  infective 
diarrhoea,  possibly  in  toxsemic  diarrhoea.  It  is  degenerative,  if  of  toxic 
origin,  or  hemorrhagic  in  type.  Albumin,  casts,  renal  epithelium  and 
blood  cells  may  be  found  in  the  urine.  The  chief  symptoms  are  debility, 
sighing,  vomiting,  diarrhoea,  tense  fontanelle,  oedema  and  convulsions  ; 
or  anuria,  oedema,  rapid  pulse,  high  temperature  and  slight  dyspnoea, 
which  may  end  in  vomiting,  restlessness,  screaming,  convulsions  and 
drowsiness  or  coma.  Many  of  the  fatal  nervous  symptoms  and  the 
hydrocephaloid  state  may  be  of  uremic  origin.  The  urine  is  suppressed  or 
scanty.  The  kidneys  recover  in  toxic  cases  as  the  primary  disease  gets 
well.  In  bacterial  infections  the  course  is  more  prolonged  and  the  disease 
may  become  chronic.  Hematuria  and  infarcts  may  be  due  to  thrombosis 
of  veins  ;  and  death  may  ensue  from  ursemia.  Acute  nephritis  in  infants 
from  other  causes  presents  similar  symptoms.  It  may  simulate  encephalitis 
or  meningitis.  The  prognosis  is  grave.  Out  of  23  cases  under  2  years  of 
age  11  died  (Holt). 


576  Chapter  XL  VI. 

The  kidneys  show  fatty  degeneration  of  the  epithelium  of  the  con- 
voluted tubules  and  swelling  of  that  of  the  straight  tubules  ;  areas  of  infil- 
tration of  round  cells  and  erythrocytes  in  the  renal  cortex  ;  and  organisms 
in  the  ATessels  and  exudate.  In  5  of  Holt's  fatal  cases  the  nephritis  was 
interstitial,  and  in  5  parenchymatous. 

Varieties  of  Nephritis. — All  types  are  seen  in  early  life,  running  much 
the  same  course  as  in  adults.  Some  are  primary,  others  secondary  and 
occurring  in  the  course  of  another  disease.  The  inflammation  is  acute, 
subacute  or  chronic.  The  anatomical  changes  are  parenchymatous  (glomer- 
ular or  tubular),  interstitial,  or  diffuse  and  mixed.  Thus  acute  nephritis 
may  be  of  any  of  the  above  pathological  types,  and  primary  or  secondary. 
Many  cases  are  really  chronic  ones  with  sudden  exacerbations.  It  is  a 
bilateral  affection  with  invariably  a  certain  amount  of  interstitial  change. 
It  terminates  in  recovery,  chronic  nephritis  or  death.  The  diffuse  or  mixed 
type  produces  the  diffuse  or  "  large  white  "  kidney  ;  if  there  is  much 
interstitial  change,  it  ends  in  the  "  contracted  white  "  kidney.  The  latter 
variety  may  possibly  depend  on  a  tubular  inflammation  supervening  on  a 
primary  interstitial  nephritis. 

Acute  Nephritis. — This  is  glomerular  or  tubular,  according  to  the 
main  distribution  of  the  inflammation.  The  type  is  only  distinguishable 
after  death.  The  glomerular  variety  is  the  one  so  often  seen  in  scarlatina 
and  other  infections. 

Etiology. — Primary  and  secondary  nephritis  are  quite  frequent  in 
children,  especially  at  the  age  of  3-9  years.  The  sex-incidence  is  3  males 
to  2  females.  They  are  most  common  in  temperate  climates.  Primary 
nephritis  may  be  due  to  mechanical  injury  during  or  after  birth,  renal 
infarcts  and  calculi ;  circulatory  disturbances  such  as  chills  and  cold  baths, 
extreme  heat,  too  hot  baths,  asphyxia  neonatorum,  embolism,  infarcts, 
and  hemorrhagic  effusions  in  purpura  and  scurvy  ;  toxic  causes,  e.g., 
turpentine,  cantharides,  mercury,  storax,  balsam  of  Peru  ;  toxins  derived 
from  the  throat,  intestines,  etc.    A  history  of  sore-throat  is  common. 

Secondary  nephritis  occurs  in  the  course  of  any  specific  infection, 
especially  scarlatina,  measles,  influenza,  variola,  diphtheria  and,  less  often, 
typhoid,  varicella,  mumps,  glandular  fever,  pneumonia,  pertussis,  acute 
rheumatism,  erysipelas,  general  sepsis,  and  syphilis.  Diphtheria  is  more 
likely  to  give  rise  to  albuminuria  from  toxic  degeneration  of  the  tubular 
epithelium  or  cloudy  swelling,  similar  to  what  happens  in  high  fever.  The 
differentiation  between  the  albuminuria  of  fever  or  toxaemia  from  that  of 
nephritis  is  not  always  easy. 

Scarlatinal  Nephritis  is  the  type  of  acute  nephritis  in  early  life.  It 
must  be  distinguished  from  the  febrile  albuminuria  with  casts  in  scarlet 
fever,  and  from  the  septic  nephritis  which  occurs  in  septic  scarlatina  and 
other  septic  states.  Its  frequency  varies  in  different  epidemics.  Ashby 
found  it  in  6-7  per  cent,    of  over  3000  cases.      Caiger  states  that  it  was 


Diseases  of  the  Kidneys.  577 

present  in  2.8  per  cent,  of  over  67,000  cases  ;  but  he  found  it  in  77  out  of 
2148  cases  in  hospital.    A  family  predisposition  has  been  noted. 

It  begins  at  the  end  of  the  second  or  during  the  third  week,  that  is 
at  a  time  when  the  scarlet  fever  is  over.  The  initial  albuminuria  may  have 
been  absent  for  some  days.  About  half  the  fatal  cases  begin  in  the  first 
week.  Sometimes  the  onset  is  delayed  until  the  fourth  week.  The  onset 
may  be  preceded  by  a  fall  in  specific  gravity  of  the  urine  ;  an  increase  in 
quantity  and  frequency  of  micturition  ;  a  slight  rise  of  temperature  and 
excess  of  urates  ;  or  commencing  oedema  and  increased  arterial  tension. 
It  may  be  ushered  in  with  fever  ;  hematuria,  or  albuminuria  at  first  and 
hematuria  in  2-3  days  ;  or  with  vomiting,  fever,  anorexia,  pallor  and  puffy 
eyelids.  The  vomiting  is  a  bad  sign,  if  it  is  persistent.  The  severity  of  the 
onset  varies  from  scarcely  any  disturbance  to  a  severe  illness  with  nausea, 
vomiting,  anorexia,  headache,  restless  sleep,  rapid  pulse,  a  temperature  of 
104-106°  F.,  rigor  and  sweating.  Sometimes  the  pulse  is  infrequent  though 
the  temperature  is  high.  Pallor,  swelling  of  the  face  and  oedema  over  the 
tibiae  are  early  signs. 

The  urine  is  turbid,  high-coloured,  of  high  specific  gravity,  1025-1040, 
and  later  falls  to  1015.  At  first  it  may  be  clear  though  containing  albumin, 
casts,  red  and  white  cells,  and  renal  epithelium.  Casts  may  be  present 
without  albumin.  The  colour  depends  on  the  quantity  of  urine  and  the 
amount  of  blood.  It  may  be  solid  with  albumin  on  boiling  and  the  coagulum 
a  dirty  brown.  The  deposit  contains  many  red  cells,  microcytes,  hyaline 
casts  of  all  sizes,  granular,  epithelial  and  blood  casts,  renal  epithelium, 
leucocytes  and  fatty  cells. 

Morbid  Anatomy. — Sometimes  the  kidneys  are  large,  red  and  vascular. 
Usually  they  are  pale,  mottled  and  streaked  with  dark  red.  The  capsule 
peels  off  easily  and  leaves  a  smooth  surface.  The  cortex  is  wide  and  ill- 
defined,  and  the  arteries  are  not  thickened.  The  whole  organ  is  involved, 
some  parts  more  than  others,  in  an  inflammatory  engorgement  or  hyper- 
emia. It  is  an  acute  interstitial  nephritis,  hsemorrhagic  in  character,  which 
may  extend  only  to  the  glomeruli  (glomcrulo-nephritis  or  hgeniorrhagic 
glomerulitis)  or  be  uniformly  distributed.  The  glomeruli  are  swollen  and 
crammed  with  red  cells,  with  some  small  celled  exudation  between  the 
capillaries.  Similar  exudation  is  found  between  the  tubules  and  the 
vessels  are  engorged.  Exudation  takes  place  into  the  tubules,  which 
become  blocked  with  coagulated  blood  and  fibrin,  causing  oliguria.  The 
epithelium  of  the  glomeruli  is  cloudy,  swollen  and  finely  granular.  Later, 
the  cells  undergo  fatty  degeneration,  and  granular  and  fatty  epithelial 
casts  are  found  in  the  urine.  Sometimes  the  streptococcus  pyogenes  can  be 
cultivated  from  the  kidney.  If  recovery  is  imperfect,  fibroid  interstitial 
changes  occur  about  the  glomeruli  and  throughout  the  kidney. 

In  primary  nephritis  the  main  change  is  round  and  in  the  tubules, 
the  glomeruli  not  being  affected  more  than  the  other  parts.     The  changes 

2p 


578  Chapter  XL  VI. 

are  primarily  vascular  and  are  followed  by  degeneration  of  the  renal 
epithelium,  regeneration,  and  the  formation  of  new  fibrous  tissue. 

Course  and  Complications. — The  attack  may  be  mild,  severe  or  very 
severe.  In  mild  cases  there  is  a  little  fever,  with  slightly  smoky  urine,  and 
the  attack  clears  up  in  a  week  or  two.  In  a  more  severe  one  there  is  scanty 
urine,  much  albumin  and  cedema.  The  attack  ends  rather  abruptly  in 
1-3  weeks,  but  slight  albuminuria  may  reappear  during  convalescence,  when 
the  patient  gets  up,  or  may  persist  for  weeks  and  months  ;  usually  running 
a  fairly  definite  course  and  ending  in  1-3  months.  In  the  worst  cases  the 
temperature  is  continuously  raised,  the  urine  very  scanty,  the  amount  of 
albumin  up  to  one-third  or  more,  and  the  cedema  is  extreme  and  may 
affect  the  mucous  membranes,  e.g.,  the  glottis.  Dropsical  effusions  into  all 
the  serous  cavities  and  uraemia  may  develop,  with  epistaxis,  twitchings, 
convulsions  and  coma.  These  attacks  are  associated  with  complications, 
such  as  pericarditis,  myocarditis,  cardiac  dilatation,  peritonitis,  pleurisy, 
pneumonia  and  even  gangrene  of  the  lung.  All  the  tissues  of  the  body 
are  water-logged.  The  dropsy  is  due  to  impaired  nutrition  of  the  arterioles 
or  to  cardiac  failure.  Death  is  caused  by  suppression  of  urine,  uraemia 
or  complications. 

The  heart  is  often  involved  quite  early  ;  generally  the  left  ventricle 
is  dilated  and  there  is  a  small  frequent  pulse,  precordial  pain  and  dyspnoea. 
The  dyspnoea  may  come  on  quite  suddenly,  when  due  to  cardiac  failure. 
It  is  called  ursemic  asthma  or  cardiac  dyspnoea.  It  may  depend  on  the 
uraemia  or  on  pulmonary  cedema,  occurring  in  dropsical  cases  or  in  uraemia 
without  dropsy.    Progressive  anaemia  is  often  present. 

Diagnosis. — In  one  type  of  case  there  is  marked  dropsy  ;  in  another 
it  is  absent.  In  the  latter  variety  the  nephritis  is  apt  to  be  overlooked 
and  the  albuminuria  regarded  as  simple.  Microscopical  examination  of  the 
urine  is  essential.  Scanty  blood-stained  urine  is  due  to  acute  nephritis, 
extreme  passive  congestion  or  infarction.  In  cases  of  infarction  the  onset 
is  sudden,  with  perhaps  copious  albuminuria  and  no  blood,  no  dropsy, 
evidence  of  a  source  of  embolism  or  thrombosis,  and  sudden  subsidence. 
(Edema  may  be  secondary  to  heart  or  lung  complications.  It  can  occur 
in  oliguria  without  albuminuria,  although  there  is  scarlatinal  nephritis,  as 
shown  by  peeling  and  subsequent  urinary  changes.  (Edema  is  most 
frequent  in  glomerular  nephritis  and  may  be  associated  with  effusion  into 
serous  cavities,  uraemia  and  convulsions,  and  yet  end  in  recovery.  A  past 
history  of  scarlatina,  a  history  of  other  cases  in  the  house  or  neighbourhood, 
and  peeling  are  important  aids  in  the  diagnosis  of  scarlatinal  nephritis 
from  other  varieties. 

Prognosis. — Few  cases  are  fatal  and  uraemia  is  rare.  Most  patients 
recover  in  1-3  weeks,  if  there  is  no  dropsy  or  uraemia.  The  urine  becomes 
clearer  and  more  plentiful,  and  albumin  disappears  ;  sediment  on  standing 
persists  longer.     In  worse  cases  the  dropsy  spreads  and  becomes  general ; 


Diseases  of  the   Kidneys.  5791 

and  the  kidneys  are  enlarged  and  painful  on  pressure.  Even  serious  cases 
of  dropsy  and  uraemia  recover.  The  outlook  depends  on  the  general  con- 
dition. It  is  bad  if  the  heart  is  involved  ;  and  the  gravity  is  increased  by 
high  fever,  anuria,  alimentary  troubles,  and  tachycardia  or  bradycardia. 
Inflammation  of  the  lungs  or  pleura  and  uraemia  are  the  chief  causes  of 
death.  There  is  considerable  liability  to  exacerbations  and  relapses.  Some 
cases  become  chronic,  but  it  is  rare  for  an  acute  attack  to  pass  at  once  into 
the  chronic  variety.  The  prognosis  is  influenced  by  the  age  of  the  child 
and  the  period  of  the  fever  at  which  it  begins.  If  the  fever  has  subsided 
for  some  time  before  the  onset,  the  outlook  is  favourable.  Death  is  rare 
under  10  years  of  age.  There  is  hope  for  cure  as  long  as  red  cells  are  still 
present.    The  night  urine  first  becomes  free  from  albumin. 

Septic  Nephritis  may  be  primary,  without  any  evident  source  of  infec- 
tion, but  is  generally  due  to  the  septic  complications  of  scarlatina.  The 
inflammation  is  local  rather  than  general ;  great  exudation  of  leucocytes 
from  the  vessels,  coagula  crowded  with  cocci  in  the  tubules,  much  epithelial 
•degeneration,  mmute  haemorrhages  and  small  points  of  suppuration  at  the 
bases  of  the  pyramids.  Albuminuria  without  haematuria  is  found  ;  some- 
times casts  and  pus.  There  is  no  oedema  and  rarely  uraemia.  Vomiting, 
•occasionally  diarrhoea,  anaemia,  bronchial  catarrh  and  irregular  fever  are 
•often  present.  A  septic  nephritis,  due  to  ascending  urinary  infections,  is 
indistinguishable  from  pyelonephritis.  Sometimes  during  the  first  month 
■of  scarlatina  a  virulent  haemorrhagic  nephritis  occurs.  It  runs  a  rapid 
course  and  is  very  fatal.  The  urine  may  be  normal  until  within  a  day 
or  two  of  death. 

Influenzal  Nephritis  is  sometimes  of  the  ordinary  glomerular  type, 
more  often  haemorrhagic.  It  is  usually  an  early  complication  but  may 
•appear  at  any  stage.  (Edema,  not  often  marked,  is  present  in  about  half 
the  cases.  The  attack  is  over  within  3  weeks  and  the  prognosis  good. 
It  may  become  chronic.  The  toxaemia  of  severe  influenza  may  cause  albu- 
minuria, or  haematuria  only. 

Diphtheritic  Nephritis  is  a  toxic  nephritis  with  slight  tendency  to 
oedema  and  uraemia,  and  few  general  symptoms.  The  convoluted  tubules 
and  descending  limbs  of  the  loops  of  Henle,  and  next  the  collecting  tubules, 
•■are  chiefly  affected.  The  change  is  a  fatty  epithelial  one,  purely  parenchy- 
matous. Haemorrhages  are  rare.  The  urine  is  of  normal  colour,  high 
.specific  gravity,  and  contains  hyaline  and  epithelial  casts,  leucocytes, 
fat  cells,  and  few  red  cells.  It  is  really  a  toxic  degeneration  which  may  be 
associated  with  a  mild  degree  of  haemorrhagic  nephritis.  Recovery  takes 
place  in  1-2  weeks. 

Primary  Nephritis  is  insidious  in  its  onset,  but  may  be  acute  and 
■ushered  in  by  vomiting,  headache,  general  malaise,  a  rise  of  2-3°  F.  in 
temperature  for  a  few  days,  and  urinary  changes.  Puffiness  of  the  eyes, 
.swelling  of  the  face  and  oedema  are  often  the  first  signs.    The  symptoms  are 


580  Chapter   XL  VI. 

less  severe  than  in  adults,  headache  less  common  and  backache  rare* 
Blood  pressure  rises  from  60-120  mm.  of  mercury.  Dropsy  may  be  slight. 
Some  attacks  are  very  short.  Others  run  a  long  subacute  course,  and  the- 
prognosis  is  not  as  good  as  in  the  scarlatinal  type.  An  average  duration  is- 
1-3  months.  Convalescence  is  often  prolonged  and  albumin  may  appear 
from  time  to  time  for  2  years.  Few  chronic  cases  are  seen  and  recurrence  is 
rare.  Death  may  ensue  from  high  fever,  complications,  uraemia,  convulsions 
and  coma.  The  chief  complications  are  serous  effusions  and  inflammations,, 
pneumonia,  toxic  gastro-enteritis,  and  rarely  oedema  of  the  glottis  and 
lungs,  amaurosis,  oedema  of  the  discs  and  optic  neuritis.  Many  of  these- 
attacks  are  no  doubt  of  infectious  origin,  although  the  course  of  infection 
is  not  found,  and  are  haemorrhagic  in  type. 

Chronic  Parenchymatous  Nephritis  is  the  sequel  of  an  acute  or  subacute- 
attack  of  primary  or  secondary  acute  nephritis.  It  affects  3  boys  to  2  girls. 
Possibly  there  is  an  hereditary  tendency  to  renal  weakness,  for  Heubner 
has  met  with  it  in  several  members  of  the  same  family  and  I  know  of  a 
family  in  which  4  children  were  affected  after  scarlatina.  The  common  age 
is  6-14  years,  but  it  may  occur  earlier  and  even  in  infancy.  The  usual 
variety  is  the  large  white  kidney.  Some  cases  are  insidious  in  onset,  with 
nothing  to  suggest  an  acute  attack.  Probably  some  of  these  result  from, 
mild  unsuspected  scarlatina.  The  symptoms  and  course  are  the  same  as  in 
adults.  The  urine  is  scanty,  highly  albuminous,  and  contains  hyaline, 
granular,  fatty  and  epithelial  casts.  The  main  symptoms  are  pallor,, 
pufnness,  extensive  oedema,  vomiting  and  general  malaise.  There  is  much 
liability  to  bronchitis  and  pulmonary  affections,  and  to  serous  inflammations, 
and  exudations,  occasionally  retinitis.  The  urine  may  clear  up  on  milk 
diet  and  rest  in  bed,  but  almost  invariably  relapses  on  getting  up. 

No  case  is  hopeless.  A  few  are  cured  although  they  have  gone  on  for 
years.  Eecovery  is  rare  if  albuminuria  has  persisted  for  one  year.  The 
disease  is  essentially  chronic  and  may  last  for  20  years.  These  prolonged 
cases,  in  which  the  urine  persistently  contains  small  quantities  of  albumin 
and  hyaline  casts,  are  somewhat  different.  The  quantity,  colour,  reaction 
and  specific  gravity  are  normal.  There  are  no  symptoms  and  no  ill  effects, 
beyond  slight  pallor  and  loss  of  tone.  Probably  a  limited  area  of.  renal 
tissue  only  is  damaged.  It  is  impossible  to  give  an  accurate  prognosis  as  the 
amount  of  kidney  permanently  damaged  cannot  be  estimated.  The 
quantity  of  albumin  and  fatty  casts  affords  a  fair  guide  to  the  severity  of  the 
case.  As  long  as  the  child  does  not  become  distinctly  anaemic  the  outlook 
is  not  bad. 

If  the  urine  increases  in  quantity  and  diminishes  in  specific  gravity 
it  is  probable  that  interstitial  changes  are  taking  place,  producing  the 
contracted  white  kidney.  Cardiac  hypertrophy,  raised  blood  pressure 
and  thickening  of  the  arteries,  possibly  other  signs,  will  then  be  found. 
Occasionally  a  chronic    hemorrhagic  variety  is  seen  in  which  there  are 


Diseases  of  the  Kidneys.  581 

acute  exacerbations  with  haeinaturia  and  scanty  urine,  and  no  oedema. 
These  are  less  serious. 

Chronic  Interstitial  Nephritis  or  "  granular  kidney  "  is  seen  at  times 
in  the  young.  The  sex-incidence  is  2  males  to  3  females.  Nettleship  (1901) 
collected  80  cases  under  21  years  of  age.  J.  E.  H.  Sawyer  (1907) 
collected  55  ;  males  22,  females  33.  Of  Sawyer's  cases  23  were  under 
10  years,  21  more  under  15,  and  the  remainder  under  21  years  of  age. 

Its  etiology  is  doubtful.  It  has  been  regarded  as  hereditary  (4  genera- 
tions, Dickinson),  congenital,  due  to  hereditary  syphilis,  or  a  sequel  of 
infective  disease,  notably  scarlatina  and  less  often  measles  and  varicella. 
In  some  instances  there  has  been  a  history  of  alcoholism  and  a  few  have  been 
due  to  renal  calculus.  It  may  be  unilateral  or  much  more  marked  on  one 
side  than  the  other.  Probably  most  cases  are  primary  and  of  insidious 
onset ;   and  others  are  secondary  to  mild  unrecognised  nephritis  in  infancy. 

The  symptoms  and  physical  signs  are  the  same  as  in  adults,  but,  not 
being  suspected,  are  often  overlooked.  The  child  comes  under  observation 
for  wasting,  gastro-intestinal  catarrh  or  cough.  Or  thirst,  polyuria  and 
enuresis  are  the  first  symptoms,  though  not  always  prominent.  A  few 
are  ushered  in  by  convulsions  and  coma.  The  child  is  listless,  small,  stunted, 
wasted  and  anaemic  ;  the  cheeks  may  show  a  dusky  flush.  The  skin  is 
harsh  and  dry,  devoid  of  sweat,  coarse,  inelastic  and  pigmented,  of  a  dirty, 
brownish  yellow  or  brown  colour,  suggestive  of  Addison's  disease.  The 
pigmentation,  if  present,  is  chiefly  on  the  abdomen,  flanks,  axillae  and 
groins.  The  heart  is  hypertrophied,  the  aortic  second  sound  accentuated, 
and  the  arteries  thickened.  Dropsy  is  almost  always  absent ;  a  little  may 
result  from  cardiac  failure.  The  mental  state  is  precocious,  sometimes 
perverse. 

The  cerebral  symptoms  are  headache,  vomiting,  vertigo,  restlessness, 
mental  disturbance,  tremors,  tetany,  convulsions  and  those  of  cerebral 
haemorrhage.  Amaurosis,  diplopia,  retinitis  and  retinal  haemorrhage  maybe 
present.  The  gastro-intestinal  signs  are  thirst,  vomiting,  diarrhoea, 
obstinate  constipation,  and  abdominal  pain  ;  pulmonary  ones  are  bron- 
chitis, dyspnoea,  oedema  and  asthma  ;  cardiac  ones,  precordial  pain  and 
dyspnoea.  Many  of  these  symptoms  may  be  absent.  Severe  bleeding  after 
tooth  extraction  has  been  noted.  Epistaxis  may  occur  early  from  toxaemia. 
The  morning  headache  is  due  to  the  accumulation  of  toxins  during  the 
night,  or  altered  cerebral  circulation,  sudden  tension  after  relaxation  during 
sleep.     The  vomiting  may  be  the  result  of  similar  causes  or  purely  gastric. 

The  urine  is  profuse,  3-5  pints,  pale,  specific  gravity  1004-1020,  and  con- 
tains a  small,  variable  amount  of  albumin,  and  a  few  hyaline  and  granular 
casts.  Haematuria  may  result  from  an  exacerbation  and  even  severe 
bleeding  may  occur. 

Cases  are  mistaken  for  enuresis,  diabetes  insipidus,  functional  albu- 
minuria, the  uric  acid  diathesis,  and  simple  malnutrition.     A  mild  attack 


582  Chapter  XL  VI. 

of  hematuria  may  be  diagnosed  as  acute  nephritis  but  there  is  no 
oedema,  and  the  amount  of  blood  and  albumin  fluctuate  from  day  to  day. 
Death  results  from  uraemia  ;  occasionally  from  cerebral  haemorrhage 
or  some  complication.  The  duration  of  life  depends  on  the  duration  of  the 
disease  previous  to  diagnosis,  and  this  cannot  be  estimated  accurately.  It 
varies  with  the  degree  of  cardio-vascular  changes  and  the  possibility  of 
maintaining  cardiac  hypertrophy. 

Eye  Symptoms  in  Nephritis. — In  acute  nephritis  eye  changes  are 
uncommon.  Optic  neuritis  is  the  most  frequent.  Uraemic  blindness  is 
probably  central  and  toxic.  Retinal  haemorrhage  may  occur.  Albuminuric 
optic  neuritis  is  diagnosed  with  difficulty  from  other  varieties  unless  there 
are  retinal  changes,  such  as  haemorrhages,  old  or  recent,  patchy  atrophy 
of  the  retina,  or  acute  inflammation  and  effusion  of  lymph. 

Albuminuric  retinitis  is  quite  rare  in  children  and  seldom  seen  in  acute 
nephritis.  It  is  a  true  inflammation  and  liable  to  occur  in  the  chronic 
parenchymatous  type  (10-15  per  cent.).  The  retina  is  opaque  and  hazy  ; 
the  optic  discs  swollen  ;  and  there  are  opaque,  white,  non-glistening  patches- 
of  exudation  obliterating  or  obscuring  the  vessels,  and  few  haemorrhages. 
It  may  get  well,  but  the  prognosis  is  probably  as  bad  as  in  adults. 

The  degenerative  type  of  retinal  change  is  seen  in  cases  of  granular 
kidney  (5-10  per  cent.).  It  is  due  to  arterial  disease  and  haemorrhage. 
The  arteries  are  thick  and  look  like  silver  wire.  The  haemorrhages  are 
distributed  along  the  vessels  or  as  flame-shaped  patches  between  the  nerve 
fibre  layers.  Brilliant  glistening  white  patches  of  choroido-retinal  atrophy 
are  scattered  about  the  macula  and  radiating  from  it.  White  patches  in  the 
retina  may  be  due  to  exudation  of  lymph,  old  haemorrhages,  or  atrophy 
of  the  retina  and  choroid.  Optic  neuritis  is  absent  or  slight.  The  retina 
may  become  detached.  Vision  may  remain  good,  if  the  macula  is  little  or 
not  at  all  involved.  The  extent  of  vision  is  variable  and  complete  blindness 
rare.  The  prognosis  is  grave.  Haemorrhage  indicates  advanced  disease  and 
a  short  life.  Death  may  follow  in  a  few  months  or  not  for  3  years,  but  life 
is  rarely  prolonged  beyond  a  year. 

Uraemia  is  latent,  acute  or  chronic.  It  is  due  to  the  accumulation 
of  products  of  metabolism,  which  should  be  excreted  by  the  kidneys,  or 
to  the  failure  of  an  internal  renal  secretion,  or  to  cytotoxins  formed  from 
degenerated  or  diseased  renal  cells.  It  is  noteworthy  that  symptoms  are 
absent  in  hysterical  anuria,  lasting  for  days  or  wTeeks,  and  in  anuria  from 
calculous  obstruction  unless  there  are  secondary  renal  changes.  Ammonia, 
urea,  creatinin  potassium,  chlorides  and  acids  have  all  been  excluded  as 
causes.  Uiea  is  excreted  by  the  intestines  when  the  kidneys  fail.  In  uraemic 
diarrhoea  the  faeces  contain  much  ammonia ;  and  in  renal  disease,  an  excess 
of  nitrogen  over  that  in  the  food.     Ammonia  is  also  found  in  the  stomach. 

Acute  uraemia  is  most  frequent  in  scarlatinal  nephritis,  but  may  occur 
in  granular  kidney.     The  chronic  form  occurs  with  the  granular  and  the 


Diseases  of  the  Kidneys.  583 

large  white  kidney.  The  latent  type  is  that  of  calculous  anuria,  obstructive 
suppression  from  blockage  of  the  ureter,  reflex  arrest  of  the  functions  of 
the  kidneys,  or  destruction  of  the  cortex  in  cystic  disease  and  hydro- 
nephrosis. It  is  the  same  as  that  produced  experimentally  in  the  laboratory. 
Penrose  (1904)  reported  a  case  of  ureemic  fits  in  a  boy,  1  month  old,  causing 
tonic  spasm  of  the  fingers  and  hands,  fixation  of  the  eyes,  occasional  rigidity 
of  the  head  and  neck,  cyanosis,  slow  and  laboured  breathing,  but  no  general 
convulsions.  Death  occurred  next  day.  The  foreskin  showed  a  pin-point 
phimosis.  The  ureters  were  enormously  dilated  and  filled  with  greenish 
purulent  urine  ;  the  bladder  a  little  dilated  and  contained  similar  urine  ; 
and  there  was  advanced  pyelitis,  and  multiple  abscesses  in  the  renal  cortex. 

Latent  Urcemia. — The  urine  may  not  be  notably  reduced  in  quantity  ; 
perhaps  it  cannot  be  estimated,  through  being  passed  in  bed.  The  tem- 
perature is  subnormal,  pupils  small,  vomiting  occasional,  and  the  child 
conscious,  sometimes  irritable  and  restless.  Dyspnoea,  convulsions  and 
coma  are  absent.  Ursemic  dyspnoea  may  occur  in  calculous  anuria  with 
pyelo-nephritis.  Toward  the  end  there  may  be  slight  muscular  twitches 
and  some  drowsiness.    The  duration  is  from  5-9  days. 

Acute  Urcemia  exhibits  nervous  symptoms,  with  or  without  those 
of  alimentary  disturbance.  Convulsions  and  coma  may  come  on  suddenly, 
simulating  epilepsy.  The  pupils  are  contracted.  More  commonly  the 
signs  are  anorexia,  ammoniacal  breath,  thickly  furred  tongue,  vomiting, 
headache,  dyspnoea,  restlessness,  anxiety  and  nervousness,  dilated  pupils, 
frequent  pulse,  subnormal  temperature,  muscular  twitches  and  scanty 
urine.  These  symptoms  are  followed  by  drowsiness  and  convulsions. 
Between  the  fits  the  child  may  be  comatose,  or  violently  excited 
and  restless.  Gradually  the  drowsiness  increases ;  the  deep,  jerky 
respirations  assume  the  Cheyne-Stokes  type;  the  pulse  becomes  more 
frequent ;  and  twitchings,  convulsions  and  coma  end  the  scene,  or  death 
may  occur  suddenly.  Sometimes  there  is  great  weakness,  epigastric  dis- 
comfort and  inability  to  swallow.  Ursemic  blindness  may  come  on  quite 
suddenly,  without  any  fundus  change. 

The  features  of  uraemia  vary  according  to  the  predominance  of  cerebral 
or  motor  symptoms.  The  respiratory  peculiarities  are  due  to  the  action  of 
the  poison  on  the  respiratory  centre,  for  even  in  severe  dyspnoea  the  lungs 
may  show  nothing  abnormal.    Vomiting  is  partly  cerebral,  partly  gastric. 

Acute  uraemia  can  occur  although  large  quantities  of  urine  and  urea 
are  evacuated,  and  in  the  absence  of  albuminuria.  The  prognosis  depends 
on  the  stage  of  the  renal  disease  and  the  absence  of  complications.  It  is 
fairly  good  in  scarlatinal  and  other  forms  of  acute  nephritis,  except  when 
grafted  on  chronic  renal  mischief.  After  a  few  convulsions  recovery  may 
ensue.  The  fits  may  be  accompanied  or  followed  by  amblyopia,  amaurosis, 
aphasia,  local  palsies,  or  various  psychoses. 


584  Chapter  XL  VI. 

Chronic  Urcemia  is  indicated  by  some  of  the  following  signs  : — languor 
and  torpidity,  restlessness,  sleeplessness,  nervousness,  vertigo,  headache  ; 
dirty  tongue,  attacks  of  vomiting,  perhaps  diarrhoea,  hiccough  ;  dyspnoea 
or  ursemic  asthma  ;  slight  twitchings,  first  noticed  in  the  muscles  of  the 
thumb  ;  and,  less  often,  itching  of  the  skin,  drooping  of  the  eyelid  or  some 
other  paresis,  noisy  or  muttering  delirium,  delusions,  gradual  unconscious- 
ness, coma  and  even  convulsions.  The  duration  is  about  10  days.  It  is 
rarely  recovered  from. 

Treatment  of  Renal  Disease. — Reduce  the  work  the  kidneys  have  to  do, 
by  limiting  the  diet,  especially  protein  foods  ;  and  replace  their  activities 
by  increased  action  of  the  skin  and  bowels.  In  acute  nephritis  bed  is 
essential,  flannels  and  blankets  for  clothing,  and  the  horizontal  posture  to 
limit  the  strain  on  the  heart.  A  diet  of  sugar  (5-7  oz.  for  adidts)  and  water 
only  is  recommended  by  v.  Noorden.  Generally  it  is  permissible  to  give 
hot  tea,  mineral  waters,  milk,  fruit,  and  carbohydrates,  or  diluted  milk 
alone  in  the  acute  stage.  Prohibit  meat  extracts.  Warm  baths,  and 
counter-irritation  in  the  lumbar  region  by  mustard  leaves,  poultices  or 
dry  cupping,  will  relieve  the  renal  congestion.  Keep  the  bowels  freely  open, 
without  excessive  purgation,  by  mag.  sulph.,  sod.  sulph.,  or  pulv.  jalapaj  co. 
Do  not  give  mercurials.  Internally,  let  the  child  have  plenty  of  water, 
imperial  drink,  and  drugs  such  as  effervescing  citrate  of  potash,  acetate  of 
ammonia,  and  the  tartrate,  phosphate  and  benzoate  of  soda.  The  addition 
of  sod.  bicarb,  and  pot.  citrat.,  aa  grs.  2-5,  to  each  milk  feed  is  beneficial. 

When  the  acute  sbage  has  subsided  and  there  is  no  longer  blood  in  the 
urine,  give  more  active  diuretics,  viz.,  tincture  and  liquid  extract  of 
jaborandi,  digitalis,  strophanthus  and  sal  volatile,  and  caffeine.  Fish  and 
eggs  can  be  added  to  the  diet,  and  subsequently  chicken,  calves  head  and 
other  proteins,  if  the  albumin  does  not  increase.  A  much  restricted  diet, 
too  long  continued,  impairs  the  general  health  and  retards  recovery. 

Subsequently,  and  in  all  cases  of  large  white  kidney,  rely  on  iron.  It 
may  be  tried  tentatively,  in  conjunction  with  digitalis,  in  prolonged  cases 
before  the  hematuria  has  entirely  ceased,  provided  it  is  at  once  omitted 
if  the  blood  increases.  The  best  results  are  obtained  with  tr.  ferri  perchlor. 
In  one  case  it  was  given  for  over  3  years  and  the  patient  recovered.  The 
chief  drawbacks  to  its  use  are  the  discoloration  of  the  teeth  and  the 
liability  to  upset  the  digestion.  Iron  must  be  used  with  caution,  if  there 
is  any  cardio-vascular  change,  and  given  in  milder  forms. 

For  ce&ema  give  hot  air  or  vapour  baths,  diuretics  and  purgatives. 
Care  must  be  taken  to  avoid  scalding.  The  fluid  intake  and  the  amount 
of  salt  should  be  reduced,  or  a  salt-free  diet  tried.  After  the  first  year  of 
life,  diuretin  grs.  2-10,  q.i.d.,  is  a  useful  diuretic,  if  the  oedema  is  due  to 
cardiac  failure.  It  apparently  does  not  injure  the  renal  epithelium.  In 
infants  it  may  cause,  gastro-intestinal  derangement.  Other  diuretics  are 
available.      Pilocarpin   and   jaborandi   induce   profuse   sweating  and  are 


Diseases  of  the  Kidneys.  585 

rarely  advisable.  If  there  is  excessive  effusion,  it  may  be  necessary  to 
tap  the  legs  with  Southey's  trocars,  taking  the  utmost  care  to  prevent 
secondary  sepsis.    As  the  oedema  diminishes  the  kidneys  improve. 

Uraemia,  if  acute,  must  be  actively  treated  by  hydragogue  cathartics, 
vapour  baths  and  pilocarpin,  provided  it  is  associated  with  oedema.  Other- 
wise the  treatment  is  apt  to  make  the  patient  worse  by  concentrating  the 
blood  and  the  poison  therein.  For  twitchings  and  convulsions  give  chloral 
per  rectum,  bromides,  chloroform  inhalations,  or  minute  doses  of  morphia. 
Venesection  may  induce  the  cessation  of  the  fits  and  abundant  urination. 
It  is  indicated  in  early  stages  showing  brain  irritation,  whether  the  child 
is  robust  or  weakly.  It  does  most  good  in  first  attacks  during  scarlatinal 
nephritis.  Saline  injections  are  also  useful.  Decapsulation  has  been  used 
in  acute  and  subacute  cases  which  do  not  yield  to  treatment,  especially  in 
commencing  uraemia.  It  is  applied  to  both  kidneys.  It  reduces  tension 
and  drains  the  ©edematous  tissues.  Possibly  the  benefit  is  due  to  the  latter 
result.  A  new  capsule  forms  in  3-4  months.  It  is  extremely  difficult  to 
estimate  the  value  of  treatment  in  acute  nephritis  for  many  cases  are  mild 
and  recover  under  the  simplest  measures.  I  am  strongly  opposed  to  the 
nse  of  an  icebag  locally  and  even  dry  cupping  is  unnecessary,  unless  there 
is  anuria. 

Granular  Kidney. — Rely  on  general  and  symptomatic  treatment  : — 
hot  or  Turkish  baths,  suitable  exercise,  avoidance  of  chill,  warm  clothing, 
and  the  moderate  use  of  purgatives,  diuretics  and  diaphoretics  ;  a  limited 
nutritious  diet,  with  little  protein  food ;  strophanthus  and  ammonia, 
•digitalis  and  tonics  for  cardiac  failure  ;  pot.  iod.,  nitrites  or  trinitrin  for 
high  tension,  headaches,  insomnia  and  irritability.  These  patients  must  live 
in  a  warm  equable  climate. 

Acute  Pyelitis  or  Pyelonephritis  is  primary  in  infants  and  secondary 
at  all  ages.  The  rarity  of  the  disease  in  infants  varies  inversely  as  the 
frequency  of  urinalysis  and  the  difficulty  of  obtaining  the  urine.  Pyelitis, 
pyelonephritis  and  pyonephrosis  are  progressive  stages.  Pyelitis  may  be 
limited  to  the  pelvis  of  the  kidney,  or  may  be  secondary  to  and  associated 
with  cystitis. 

Etiology. — The  common  causes  are  calculous  irritation  ;  drugs  such  as 
turpentine,  cantharides,  carbolic  and  salicylic  acid  ;  B.  coli  infection  of 
retained  urine  ;  gonococcal  and  other  infections  extending  upward  ; 
pyaemia  and  acute  infectious  diseases.  Infantile  cases  are  generally  seen 
in  girl  babies,  usually  bottle-fed,  under  2  years  of  age.  They  are  due  to 
microbial  infection  per  urethram  or  from  the  alimentary  tract,  secondary 
to  an  acute  gastro-enteric  infection,  via  the  blood  or  lymphatics.  Often 
there  is  a  history  of  constipation.  Excoriation  or  fissure  of  the  anus  was  found 
by  John  Thomson  in  5,  and  some  soreness  of  the  vulva  in  2,  out  of  8  cases. 

Symptoms. — The  onset  is  sudden   with  fever,  shivering,  blueness  of 

*~-™--— — — 


586  Chapter  XL  VI. 

colicky  pains.  Sometimes  there  is  headache,  drowsiness,  and  delirium  ; 
occasionally  vomiting  and  diarrhoea.  The  fever  is  high,  perhaps  104-106°  F., 
and  runs  a  course  very  suggestive  of  typhoid  fever,  or  more  like  pneumonia, 
and  at  times  with  intervals  of  apyrexia.  Its  duration  is  variable  ;  it  may 
last  for  2-4  weeks.  Rigors  are  rather  characteristic,  if  they  occur,  for 
they  are  rare  in  infancy.  The  pain  is  variable  in  character,  severity  and 
distribution.  It  is  usually  in  the  loins  or  subcostal,  and  often  unilateral. 
It  may  induce  screaming  attacks,  frequent  micturition  and  defaecation. 
Tenderness  may  be  found  over  one  kidney,  generally  the  right.  There 
may  be  anorexia  or  an  unimpaired  appetite,  regular  action  of  the  bowels, 
and  no  marked  wasting  unless  the  attack  is  prolonged.  The  child  becomes 
very  pale.  Anorexia,  irritability,  extreme  pallor  and  occasional  fever  may 
be  the  only  symptoms.  Rarely  there  are  convulsions,  opisthotonos,  coma, 
high  fever,  urinary  intoxication,  septic  infection  and  a  fatal  issue. 

The  urine  is  increased  in  quantity,  slightly  turbid  or  opalescent,  not 
clearing  on  heating,  and  acid.  It  contains  a  variable  amount  of  pus,  rarely 
much,  and  a  little  albumin  or  nucleo-protein  which  is  due  to  the  pus, 
some  epithelial  cells  from  the  pelvis  and  ureters,  distorted  white  and 
crenated  red  cells,  and  crowds  of  motile  bacilli  which  prove  to  be  B.  coli 
in  90  per  cent.  The  urine  is  turbid,  even  after  nitration  through  filter 
paper,  for  the  organisms  pass  through  though  the  pus  cells  are  retained. 
There  may  be  partial  suppression  at  the  onset.  Some  cases  show  crystals 
of  uric  acid  or  oxalates.    There  are  no  casts. 

The  attack  lasts  for  2-6  weeks  ;  pyuria  perhaps  for  months.  Sweating 
is  marked  in  some  cases  and  splenic  hyperplasia  is  not  uncommon.  It  is 
rarely  fatal.    Convalescence  is  tedious. 

Diagnosis. — The  illness  closely  resembles  typhoid  fever  clinically. 
Possibly  some  cases  are  really  due  to  paratyphoid  or  paracolon  infection. 
Cystitis  is  indicated  by  frequent  and  painful  micturition.  In  ordinary 
pyelonephritis  the  urine  is  acid  and  contains  much  pus,  albumin  and  many 
organisms.  In  nephritis  there  are  casts,  renal  cells,  much  albumin,  and 
scanty  urine.  Pyuria  is  not  infrequent  in  convalescence  from  pneumonia, 
typhoid  fever,  measles  and  diphtheria  ;  and  in  delicate  and  anaemic  children. 
In  small  amounts  it  does  not  mean  pyelitis.  It  is  necessary  to  exclude  pus  from 
the  urethra,  bladder,  vulva,  vagina,  or  an  abscess  opening  into  the  urinary 
tract;  renal  calculus  and  tuberculosis.  The  acute  onset  suggests  influenza 
and  the  illness  is  alarming  and  undiagnosed  unless  the  urine  is  examined. 

Pyelonephritis  in  children  may  be  of  three  types  : — (1)  Acute  ;  with 
rigors,  fever,  lumbar  pain,  abdominal  pains  and  sweating.  The  urine  is 
unaffected  for  2-3  days  and  then  shows  pus  and  organisms.  Sometimes 
there  is  retention,  occasionally  blood.  (2)  Subacute  ;  with  unexplained 
fever,  anorexia,  malaise,  anaemia  and  wasting.  (3)  Chronic  and  relapsing  ; — 
recurrent  attacks  with  fever,  headache  and  vomiting,  malaise,  painful 
micturition,  and  perhaps  lumbar  pain,  suggestive  of  stone. 


Diseases  of  the  Kidneys.  587 

Treatment. — Potassium  citrate,  grs.  24-48  daily,  is  useful  for  the 
infantile  disease.  It  renders  the  urine  alkaline  and  thus  hinders  the  growth 
of  the  organisms,  for  B.  coli  will  not  grow  in  an  alkaline  medium.  Unfor- 
tunately it  causes  nausea,  depression,  flabbiness  and  low  temperature. 
Urotropin,  excreted  as  formalin  in  the  urine,  and  its  allies  are  chiefly  of 
value  in  the  bacteriuria  of  typhoid  fever  and  in  pyelonephritis,  and  much 
less  efficacious  in  infantile  pyelitis.  It  must  be  given  in  a  large  quantity  of 
water,  e.g.,  grs.  5-10  in  water  oz.  4.  Methylene  blue,  creosote  and  salol, 
excreted  as  a  phenyl  compound,  are  sometimes  beneficial. 

Renal  Calculus. — Calculous  concretions  may  be  found  at  any  age  in  the 
kidney,  ureter,  bladder  or  impacted  in  the  urethra.  Uric  acid  concretions 
in  the  kidneys  in  the  first  few  days  of  life  have  been  already  described 
(p.  548).  At  a  later  age  an  excess  of  uric  acid  crystals  in  the  urine  is  due 
to  a  gouty  heredity,  cold,  unsuitable  diet,  digestive  and  hepatic  disturbance, 
and  scurvy.  It  is  aided  by  deficient  cutaneous  excretion,  the  result  of  dirt 
or  unsuitable  clothing,  hot  days  and  chilly  nights,  and  deficient  supply  of 
fluids.  Most  renal  calculi  are  composed  of  urates  or  uric  acid  ;  a  few  of 
oxalate  of  lime,  and,  still  more  rarely,  cystin.  They  are  comparatively 
rare  ;  vary  in  frequency  in  different  localities  ;  more  common  in  boys  than 
girls,  and  at  2-6  years  old  ;   and  may  be  present  in  large  numbers. 

The  passage  of  gravel  (uric  acid)  or  oxalates  may  cause  symptoms  of 
stone ;  viz.,  pain  and  tenderness  in  the  lumbar  region,  dysuria,  pain  referred 
to  the  end  of  the  penis,  and  attacks  of  colic  which  are  generally  mistaken 
for  intestinal  colic  ;  sometimes  irritable  bladder  and  enuresis  ;  hsematuria, 
albuminuria  and  crystals.  The  urine  may  be  very  pale,  of  low  specific 
gravity,  and  contain  very  little  urea.  The  pain  of  lithiasis  and  oxaluria 
is  usually  bilateral,  that  of  stone  is  unilateral. 

The  passage  of  crystals  may  give  rise  to  renal  colic  in  quite  young 
infants  ;  with  paroxysms  of  pain,  vomiting,  drawing  up  the  legs,  tenderness 
in  one  or  both  lumbar  regions,  anuria  or  retention,  or  the  frequent  passage 
of  urine  containing  crystals,  mucus  and  blood.  Shrieking  attacks  may  be 
the  only  symptom.  Sometimes  there  is  violent  spasmodic  pain,  with 
dysuria,  priapism  and  even  convulsions  ;  the  attack  ending  suddenly  with 
polyuria. 

Symptoms  of  stone  may  be  absent  if  it  is  in  the  substance  of  the  kidney, 
and  even  when  the  pelvis  and  calyces  are  full  of  stones.  The  pain  depends 
on  their  position  and  mobility.  The  pelvis  and  its  branches  are  very 
sensitive,  the  renal  substance  insensitive.  It  is  unilateral,  variable  in 
character,  increased  by  exercise,  and  may  be  renal  colic.  The  pain  comes  on 
suddenly  in  the  lumbar  region  or  hypochondrium,  and  runs  down  the  ureter 
to  groin,  bladder  and  penis.  Retraction  of  the  testis  is  more  common  in 
boys  than  men.  The  colic  is  due  to  temporary  obstruction  at  the  mouth  of 
the  ureter  and  backward  renal  distension,  clots  of  blood  in  the  pelvis  and 
passing  down  the  ureter,  or  the  passage  of  a  stone. 


588  Chapter  XL  VI. 

Tenderness  is  found  over  the  kidne)r,  and  perhaps  blood  in  the  urine 
after  the  manipulation.  Heematuria  is  often  absent ;  sometimes  the  only 
symptom  and  may  be  profuse  ;  is  excited  or  increased  by  exercise,  and  is 
apt  to  follow  renal  colic.  Micturition  is  often  frequent,  sudden  and  uncon- 
trollable, but  by  no  means  always  so.  It  may  be  reflex  in  origin,  or  due  to 
the  blood  or  pus.  Keflex  distension  of  the  bladder  may  occur  ;  so,  too, 
retention  or  anuria.  Many  of  the  symptoms  are  those  of  pyelitis  or  pyelo- 
nephritis.   There  is  rarely  fever.    Gravel  may  be  found  in  the  urine. 

Diagnosis.— Examination  with  X-rays  generally  enables  the  stone, 
if  present,  to  be  localised  in  the  kidney  or  ureter.  It  is  much  more  often 
in  the  ureter  than  formerly  supposed.  Oxalate  stones  give  the  best,  and 
uric  acid  ones  the  worst  shadows.  It  has  to  be  diagnosed  from  simple 
lithiasis  and  oxaluria,  intestinal  and  appendicular  colic,  caries  of  the  lumbar 
spine,  movable  and  tuberculous  kidney.  The  chief  sequels  are  hydro- 
nephrosis, pyonephrosis  and  latent  ursemia.  Renal  colic  is  less  severe  than 
in  adults. 

Treatment  is  more  medical  than  surgical.  Nephrolithotomy  is  rarely 
needed.  Give  alkaline  waters,  e.g.,  Vichy  and  Contrexeville  freely,  and  a 
moderate  mixed  diet  free  from  meat  and  meat  extractives  and  containing  a 
minimum  amount  of  protein.  Glycerine  in  doses  of  drs.  1-4  has  been 
recommended. 

Tuberculous  Kidney. — Tuberculosis  produces  3  types  of  renal  disease  : — 
(1)  Caseation  and  the  formation  of  cavities.  (2)  Scattered  nodules  through- 
out the  kidney.    (3)  Primary  ulceration  of  the  apices  of  the  papilla?. 

Hematuria  may  be  the  first  symptom,  and  marked  in  early  stages 
without  much  pain.  It  is  most  at  night.  It  may  only  be  discoverable  by 
microscopical  examination.  In  later  stages  it  is  often  slight  or  absent. 
Micturition  is  frequent,  if  the  bladder  is  involved,  and  vesical  tenesmus 
common.    Incontinence  and  dysuria  occur  in  the  younger  children. 

Pus  is  found  early,  and  the  urine  is  acid  if  the  pus  is  not  excessive. 
Unless  the  ureter  is  occluded  the  urine  contains  much  albumin,  casts,  pus, 
lymphocytes  and  red  cells.  Bacilli  can  be  found  on  examination  of  the 
centrifugalised  deposit,  and  may  be  present  in  the  absence  of  pyuria.  The 
smegma  bacillus  must  not  be  mistaken  for  that  of  tuberculosis.  Inocula- 
tion of  guinea  pigs  affords  confirmation,  but  takes  5  weeks. 

Pain  is  dull,  aching,  continuous,  without  exacerbations  and  not 
increased  by  exercise,  and  chiefly  felt  in  the  loin  or  reflected  therefrom. 
At  the  disease  progresses  the  symptoms  are  anorexia,  furred  tongue, 
sweating,  frequent  pulse,  emaciation  and  hectic  fever.  A  lump  is  felt  in  the 
loin,  and  per  abdomen  if  there  is  much  wasting.  The  disease  spreads  down 
the  ureter  to  the  bladder,  modifying  the  symptoms.  Cystoscopic  examina- 
tion may  show  changes  at  the  ureteric  orifices.  The  second  kidney  is 
affected  late  or  not  at  all.  The  urine  must  be  segregated,  to  ascertain  if  one 
kidney  only  is  diseased. 


Diseases  of  the  Kidneys.  589 

It  must  be  diagnosed  from  calculus,  pyelonephritis,  nephritis  and 
tumours.  "  Pain  in  excess  of  pus  indicates  calculus,  pus  in  excess  of  pain 
tuberculous  pyelitis  "  (Clement  Lucas).  The  treatment  is  that  of  tuber- 
culosis and  removal  of  the  kidney,  if  the  disease  is  unilateral. 

Renal  Tumours. — Most  of  these  are  congenital  in  origin.  Bireh- 
Hirschfeld  (1898)  called  them  "  embryonal  adeno-sarcomata."  They  con- 
tain a  mixture  of  epithelial,  adenomatous  and  connective  tissue  elements  ; 
frequently  striped  and  unstriped  muscle  fibres,  occasionally  cartilage  and 
bone;  and  grow  in  a  markedly  embryonal  way.  Various  structures  may 
preponderate  in  different  parts  of  the  same  tumour.  They  originate,  in  the 
remains  of  the  Wolffian  body  or  from  an  inclusion  of  neighbouring  structures 
in  the  capsule  of  the  embryonic  kidney.  Frequently  they  are  described  as 
sarcoma,  adeno-,  lympho-,  myxo-,  fibro-myxo-,  round  or  spindle  celled 
sarcoma,  and  some  are  hypernephromata.  A  few  are  secondary  growths. 
Papilloma  of  the  kidney  has  been  recorded. 

They  are  more  common  on  the  left  side.  Usually  they  are  extra-renal 
and  intra-capsular.  They  surround  or  displace  rather  than  invade  the 
kidney,  which  becomes  flattened.  Some  of  them  infiltrate  the  kidney.  A 
few  may  arise  from  the  cortex  and  even  from  the  pelvis  ;  a  few  are  retro- 
peritoneal or  commence  in  the  adrenals. 

Both  sexes  are  about  equally  liable,  the  males  a  little  in  excess.  It  is- 
most  frequent  in  the  second  year  of  life  and  most  of  the  patients  are  under 
5  years.  Out  of  Steffen's  219  collected  cases  168  were  under  5  years,  and  of 
these  34  were  under  1  and  55  in  the  second  year.  Of  Senator's  96  cases- 
under  10  years  55  per  cent,  were  under  2  and  85  per  cent,  under  5  years. 
Of  Starr's  54  cases  44  were  under  5  years.  Other  collections  show  a  similar 
preponderance  in  the  early  years  of  life. 

The  tumour  grows  rapidly  but  produces  no  constitutional  symptoms 
during  the  first  half  of  its  course.  Later,  great  and  rapid  constitutional 
disturbance  sets  in.  The  growth  may  become  so  enormous  that  one  might 
speak  of  the  case  as  a  tumour  with  a  baby  attached.  Abbe  removed  a 
7-lb.  tumour  from  a  13-month  old  child  who  only  weighed  15  lbs.  after  the 
operation.  The  child  was  in  perfect  health  3  years  later.  In  the  Middlesex 
Hospital  Museum  is  one  weighing  31  lbs.,  removed  from  an  8-year  old  boy. 

Symptoms. — There  is  rarely  much  pain  or  marked  urinary  symptoms. 
Hematuria  is  the  first  sign  in  about  10  per  cent.,  usually  microscopical  in 
amount.  It  may  occur  early  or  late,  once  or  frequently,  be  scanty  or 
abundant,  and  intermittent.  Occasionally  it  is  profuse,  forms  clots  in  the 
ureter  or  bladder,  and  causes  pain.  Wentworth  states  that  it  was  present 
in  85  out  of  232  cases  (36  per  cent.).  A  tumour  was  noted  in  over  half  his 
cases.  Pseudo-fluctuation  is  often  present,  sometimes  pulsation  and  a 
souffle.  The  presence  of  resonance,  due  to  the  colon,  between  the  upper 
part  of  the  tumour  and  the  liver  or  spleen  is  of  great  diagnostic  value.  The 
outline  is  smooth  and  rounded  ;   and  the  tumour  is  movable,  grows  forward 


590  Chapter  XL  VI. 

and  does  not  bulge  in  the  lumbar  region.  Either  hsematuria  or  a  tumour  may 
occur  alone  or  conjointly  ;  or  both  may  be  absent,  in  which  case  the 
disease  runs  a  latent  course  and  cannot  be  diagnosed.  Pyelitis  and  pus 
cells,  hyaline  and  granular  casts  have  occasionally  been  observed.  Pain  is 
inconstant.  In  the  early  stages  the  child  looks  and  feels  quite  healthy. 
The  tumour  is  found  accidentally  or  attention  may  be  attracted  by 
hgeniaturia.  Abdominal  enlargement  is  often  the  first  sign.  Subsequently 
anorexia,  digestive  disturbances,  dyspncea  from  pressure,  ascites,  and 
fever  up  to  104°  F.  develop  ;  sometimes  diarrhoea,  retention  or  frequent 
micturition.     Cachexia  and  emaciation  are  late  symptoms. 

The  mean  duration  of  unoperated  cases  is  8  months,  of  those  operated 
on  it  is  16-17  months  (G.  Walker,  1897).  It  varies  between  10  weeks  and 
1  year  from  the  date  of  diagnosis.  The  older  the  child,  the  slower  is  the 
growth.  Death  results  from  exhaustion  or  pressure  effects.  The  ureters 
are  rarely  obstructed.  Calculi  are  not  infrequently  found  in  the  renal  pelvis. 
The  opposite  kidney  undergoes  hypertrophy  and  is  often  affected  with 
chronic  interstitial  nephritis.  Metastatic  growths  are  a  rare  and  late 
development,  and  occur  in  the  lungs,  renal  veins,  vena  cava  inferior, 
lymphatic  glands  and  liver  in  order  of  frequency. 

The  tumour  must  be  diagnosed  from  tuberculous  peritonitis  in  which 
the  matting  together  of  the  intestines  may  simulate  a  new  growth.  I 
have  known  such  a  case  explored.  It  may  be  mistaken  for  tuberculous 
glands,  enlarged  spleen,  tumour  of  some  other  organ,  hydronephrosis  or  a 
cyst.    The  semi-fluctuation  over  a  solid  tumour  is  a  source  of  error. 

Treatment. — The  only  hope  of  cure  is  early  removal.  The  prognosis 
then  depends  on  the  nature  of  the  growth  and  its  complete  removal.  Of 
Walker's  148  collected  cases  74  were  operated  on  ;  27  died  from  the 
operation,  28  from  early  recurrence,  15  recovered  but  the  subsequent 
history  was  incomplete,  and  4  were  well  when  seen  3  years  later.  Steffen 
states  that  18  out  of  88  cases  were  permanently  cured.  Others  regard  the 
outlook  as  still  more  hopeless.  Not  one  of  21  cases  was  cured  (Bland 
Sutton). 


CHAPTER    XLVIT. 

THE    GENITAL    SYSTEM. 

Affections  of  the  Male  Genitals — Malformations — The  Penis — Circum- 
cision—  The  Urethra — Testes — The  Mammce — The  Female  Genitals — 
Vulvo-vaginitis — The  Vagina,  Uterus  and  Ovaries — Masturbation — 
Menstruation — Puberty. 

Malformations. — Various  deformities  and  their  mode  of  development 
have  been  described  in  the  section  on  malformations  of  the  rectum  (p.  332). 
The  penis  is  developed  from  the  genital  eminence  which  appears  in  front 
of  and  within  the  orifice  of  the  cloaca  in  the  fifth  or  sixth  week  of  foetal  life. 
A  solid  cord  of  epithelium  is  formed  and  is  hollowed  out  into  a  groove, 
the  lips  of  which  unite  in  the  eleventh  or  twelfth  week  and  convert  it 
into  the  penile  or  spongy  urethra.  It  is  complete  about  the  fifteenth  week 
and  the  raphe  indicates  the  line  of  union.  In  rare  instances  the  urethra, 
or  both  the  penis  and  urethra  are  absent.  Volpa  (1903)  reported  a  case  of 
double  penis,  associated  with  double  scrotum,  a  double  bladder  with  two 
large  intestines  opening  into  it,  imperforate  anus,  one  kidney,,  one  ureter 
and  one  testis.  Malformation  of  the  raphe  may  occur  alone  or  in  conjunc- 
tion with  torsion  of  the  penis,  the  frsenum  being  on  one  side  of  the  median 
line  and  the  meatus  placed  obliquely. 

In  epispadias  the  urethra  opens  on  the  dorsal  surface  of  the  glans  or 
penile  portion.  Occasionally  there  is  no  symphysis  and  it  is  associated  with 
incomplete  development  or  exstrophy  of  the  bladder.  Incontinence  is  often 
present.    Do  not  operate  before  the  seventh  year. 

In  hypospadias  the  urethra  opens  on  the  under  surface  ;  most  fre- 
quently at  the  junction  of  the  glans  and  frsenum.  The  orifice  is  gutter-like 
and  may  present  a  meatal  dimple  ;  or  the  glans  grooved  and  the  orifice  at 
the  corona.  In  other  cases  the  opening  is  penile  or  peni-scrotal.  In  a  third 
variety  it  is  perineal,  and  the  aspect  of  the  parts  simulates  the  female 
genitals  if  the  testes  are  undescended  (hermaphroditism).  There  is  no  true 
hermaphrodite,  if  the  testes  and  ovaries  are  alone  regarded  as  the  sign  of 
sex.  A  male  may  have  Fallopian  tubes  and  a  well-formed  uterus,  with 
a  narrow  vagina  opening  at  the  sinus  pocularis.  Such  a  uterus  is 
occasionally  found  in  the  inguinal  canal  or  scrotum  (Bland  Sutton). 
Occasionally  the  penile  urethra  is  short,  though  the  groove  has  united, 
and  the  penis  curves  downward. 

The  prepuce  is  frequently  narrow  and  adherent ;    rarely  imperforate, 


592  Chapter   XL  VII. 

hooded,  and  bifid,  or  practically  absent.  It  may  be  so  short  as  to  simulate 
circumcision  ;  or  absent  on  the  under  surface  and  without  a  fraenum. 

The  urethra  may  be  stenosed  or  show  complete  atresia.  The  meatus 
may  be  absent  for  the  first  J;  in.  The  urethra  may  be  absent  entirely  or 
partially,  notably  in  the  glans,  or  closed  by  adhesions.  The  defect  pro- 
duces patent  urachus  and  umbilical  fistula,  or  ectopia  vesicae.  The  meatus 
may  be  congenitally  narrow.  Cylindrical  stricture,  membranous  duplica- 
tions of  the  urethra,  and  congenital  or  acquired  diverticula  are  very  rare. 

Priapism  is  due  to  local  irritation  by  retained  smegma,  highly  acid 
urine,  undue  excitability  of  the  lumbar  cord,  bad  habits,  and  rarely 
thrombosis  or  haemorrhage  into  the  corpora  cavernosa. 

Phimosis  and  Circumcision. — True  congenital  phimosis  is  uncommon. 
Often  the  orifice  is  constricted  and  rarely  it  is  absent.  Phimosis  may  be 
secondary  and  cicatricial.  The  actual  cause  is  often  a  constriction  of  the 
mucosa  and  not  of  the  skin.  Constriction  may  lead  to  ballooning  of  the 
foreskin  on  micturition.  A  long  and  narrow  foreskin  is  characteristic  of 
male  babies,  while  the  penis  is  small  and  undeveloped.  It  may  be  too  long 
and  too  narrow.  The  glans  and  prepuce  are  adherent  by  reason  of  the 
persistence  of  the  epithelial  agglutination  of  the  surfaces.  Few  babies  are 
born  with  the  adhesions  fully  separated,  but  separation  takes  place  in  the 
course  of  some  months.  The  adult  condition  is  reached  by  the  eighth  year. 
Extreme  constriction  of  the  orifice  may  lead  to  dilatation  of  the  urethra, 
bladder,  ureters  and  kidneys,  hydronephrosis  and  pyonephrosis,  and  atrophy 
of  the  renal  tissues.  Such  results  are  extremely  rare.  If  milder  in  degree,, 
it  may  cause  retention,  accumulation  and  decomposition  of  smegma, 
eczema  and  balanitis,  preputial  calculi,  adherent  prepuce,  meatal  stricture, 
enuresis,  urethritis,  cystitis  and  pyelitis.  In  prolonged  cases  of  local  irrita- 
tion the  foreskin  becomes  thickened  and  non-retractile,  leading  to  attacks 
of  balanitis  and  difficulty  in  coitus  in  later  life.  The  local  irritation  is- 
supposed  to  induce  restlessness,  irritability,  screaming  attacks,  frequent 
micturition,  dysuria,  colic,  masturbation,  insomnia  and  pavor.  The  strain- 
ing to  micturate  is  said  to  develop  or  maintain  hernia,  prolapsus  recti  and 
hydrocele.  On  the  whole  there  is  remarkably  little  evidence  that  these  various 
affections  depend  on  the  cause  assigned.  They  occur  independently,  and 
may  be  absent  although  the  supposed  cause  is  present  and  well  marked. 
Retained  smegma  and  local  irritation  are  the  two  most  frequent  sequels. 

However  advisable  for  hygienic  reasons  or  with  the  idea  of  diminishing 
the  risk  of  contracting  syphilis,  circumcision  is  by  no  means  always  required 
on  anatomical  grounds.  A.  long  foreskin  at  birth  may  be  insufficient  to  cover 
the  glans  when  the  penis  is  fully  developed.  If  it  can  be  retracted  with 
moderate  ease,  it  should  be  left  as  a  protection  for  the  sensitive  glans.  The 
irritation  from  retained  smegma  is  no  argument  in  favour  of  operation,  if  the 
prepuce  can  be  retracted,  but  it  is  a  slur  on  the  care  and  cleanliness  of  those 
responsible  for  the  welfare  of  the  child. 


The  Genital  System.  593 

In  many  babies  it  is  quite  sufficient  to  separate  the  adhesions  with  a 
blunt  probe,  without  causing  bleeding.  Others  can  be  treated  by  dilatation 
of  the  foreskin  with  dressing  or  artery  forceps,  until  it  can  be  easily  retracted. 
It  is  then  cleaned,  oiled  and  replaced.  The  retraction  and  oiling  is  done 
daily  by  the  attendant,  if  it  can  be  replaced  easily.  Otherwise  there  is  the 
prospect  of  being  summoned  hastily  to  cure  a  paraphimosis.  If  the  surface 
bleeds  on  separation,  adhesions  are  almost  certain  to  recur,  for  the  daily 
retraction  cannot  be  carried  out  without  pain  and  is  neglected.  If  simple 
measures  fail,  circumcise  ;  incise  the  mucous  membrane  only  on  each  side  ; 
or  make  a  longitudinal  dorsal  incision  through  the  foreskin.  Enlarge  the 
meatus,  if  it  is  unduly  narrow. 

Circumcision  is  the  best  operation,  though  neither  trivial  nor  always 
harmless.  Sepsis,  sloughing  of  the  skin  and  extensive  scarring,  sloughing 
and  gangrene  of  the  penis,  fatal  haemorrhage,  erysipelas  and  pyaemia  have 
ensued.  Haemorrhage  is  usually  due  to  neglect  to  tie  the  vessels  of  the 
fraenum.  Tuberculosis  and  syphilis  have  been  transmitted,  when  the 
operation  has  been  done  as  a  religious  rite  and  not  by  a  trained  surgeon. 
Haemorrhage  is  rare  in  this  mode  of  operating,  for  the  Jews  remove  the  skin 
only,  do  not  cut  the  mucous  membrane,  and  carefully  avoid  the  fraenum. 
Then  the  operator  takes  wine  in  his  mouth  and  sucks  the  penis.  Neither 
ligatures  nor  sutures  are  used.  Apart  from  the  dangers,  the  operation 
may  be  a  source  of  discredit  to  the  operator  and  of  subsequent  trouble  to 
the  child.  It  is  by  no  means  rare  to  find  an  excessive  amount  of  skin  re- 
moved ;  or  to  see  a  chronically  thickened  preputial  stump  or  a  mass  of 
redundant  skin  giving  the  penis  an  unkempt  ragged  appearance,  which 
spoils  the  surgeon's  reputation  for  years  and  is  a  constant  source  of  gossip 
among  the  female  members  of  the  family,  although  the  inartistic  appear- 
ance is  eventually  lost  or  forgotten.  Great  care  should  be  taken  not  to 
remove  too  much  skin  and  to  leave  enough  to  cover  the  corona.  Possibly 
the  friction  of  the  exposed  sensitive  glans  against  the  clothing  may  lead  to 
masturbation,  a  habit  quite  as  common  among  the  circumcised  as  the 
uncircumcised. 

Paraphimosis  is  the  result  of  forcible  retraction  of  a  narrow  foreskin 
and  constriction  of  the  penis  behind  the  glans,  unless  it  is  replaced.  It 
causes  pain,  oedema,  ulceration  and  gangrene.  Cold  alum  compresses  will 
lessen  the  congestion  in  early  cases,  if  they  cannot  be  reduced  in  the 
ordinary  manner.  In  others  it  will  be  necessary  to  incise  the  preputial 
ring  at  the  site  of  compression,  and  to  circumcise  later. 

Balanitis  or  balano-posthitis  is  a  purulent  inflammation  of  the  prepuce. 
It  becomes  swollen,  red,  and  shows  patchy  ulceration.  The  exudation  may 
be  profuse,  the  swelling  great,  and  gangrene  may  ensue.  It  gives  rise  to 
dysuria,  increasing  difficulty  in  micturition,  cystitis,  hydronephrosis,  etc., 
and  even  death  from  uraemia,  when  neglected.  The  treatment  is  on 
ordinary  surgical  principles. 

2q 


594  Chapter   XL  VI I. 

Urethritis  is  rare  in  infants.  It  is  due  to  trauma,  foreign  bodies, 
balanitis,  and  gonorrhoea.  Apert  and  Froget  (1906)  reported  gonorrhoea 
at  10  months,  with  secondary  phlegmonous  inflammation  of  the  whole 
posterior  half  of  the  scalp.  Urethritis  causes  dysuria  and  a  discharge  of 
mucus,  muco-pus  or  pus.  The  symptoms  and  treatment  are  the  same  as  in 
•adults. 

Rare  affections  are  tuberculosis  and  carcinoma.  Tuberculosis  of  the 
glans  may  be  a  sequel  of  circumcision.  Stiles  reports  a  case  in  a  child,  aged  6, 
occurring  after  an  interval  of  3  years.  It  may  cause  stricture  or  even 
necessitate  amputation.  The  careful  local  application  of  flowers  of  sulphur 
may  be  curative.  Carcinoma  of  the  penis  has  occurred  in  a  2-year  old  boy 
(Creite,  1906).  He  had  persistent  priapism  for  8  days.  The  tumour  was  as 
big  as  a  walnut.  The  corpora  cavernosa  and  posterior  half  of  the  corpus 
spongiosum  were  infiltrated.  Medullary  carcinoma  of  the  prostrate  may 
occur  in  the  first  7  years  of  life  and  as  early  as  6  months  of  age.  The 
inguinal  glands  are  soon  affected  and  metastasis  is  general.  A  few  cases 
of  sarcoma  and  myxosarcoma  are  on  record,  one  of  them  (Edington,  1909) 
in  the  second  year  of  life. 

Testes. — At  birth  the  testes  vary  in  size  from  an  orange  pip  to  a  small 
nut,  and  they  grow  little  until  puberty.  The  left  one  is  usually  larger  than 
the  right.  Tri-orchism  is  rare  ;  the  third  testis  small  and  atrophied.  The 
vas  can  be  felt  as  a  fine  cord  and  the  epididymis  is  loosely  attached.  Displace- 
ments are  due  to  maldevelopment. 

Undescended  Testis. — In  cryptorchism  the  testis  on  one  or  both  sides 
remains  within  the  abdomen  either  just  below  the  kidney,  in  the  foetal 
position,  or  in  the  iliac  fossa.  Ectopia  testis  is  the  descent  to  some  abnormal 
position  such  as  the  perineal,  scroto-femoral,  femoral  or  penile  regions. 
Partial  descent,  or  retentio  inguinalis,  is  the  most  common  type,  the  organ 
Temaining  in  the  inguinal  canal,  about  the  groin,  or  in  the  upper  part  of  the 
scrotum.  In  these  situations  it  is  small,  soft,  movable,  and  liable  to  be 
mistaken  for  inguinal  hernia.  Complete  descent  may  be  established  in 
later  life,  up  to  21  years  of  age. 

Non-descent  causes  failure  or  arrest  of  development.  Fibrotic  changes, 
due  to  chronic  inflammation  from  trauma  or  strangulation,  render  the 
organ  useless.  Semen  is  absent  in  bilateral  cases,  and  is  absent  from  the 
vesicula  seminalis  on  the  affected  side  in  unilateral  ones.  Sections  show 
fibrosis  and  atrophy,  and  absence  of  marked  development  of  the  tubules 
at  puberty.  Imperfect  development  is  likely  to  interfere  with  perfect 
development  of  masculine  characteristics.  The  skin  remains  soft  and 
white,  stature  tall  and  narrow,  muscles  poor,  and  larynx  small.  Intelligence 
is  defective,  temper  good,  courage  small,  and  the  letter  R  is  pronounced 
badly. 

f        In  inguinal  and  allied  types  of  partial  descent  a  hernia  is  present  in 
80  per  cent.    The  gland  is  liable  to  injury  in  all  extra-abdominal  situations. 


The  Genital  System.  595 

If  mistaken  for  hernia  the  pressure  of  a  truss  may  set  up  inflammation, 
with  swelling,  tenderness,  pain  and  vomiting  ;  a  condition  which  may  be 
wrongly  diagnosed  as  strangulated  hernia.  Torsion  of  the  cord  may  occur. 
Tumour  formation  is  said  to  be  more  frequent  in  retained  testis  than  the 
undescended  organ,  but  the  evidence  in  favour  of  this  is  slight.  Of  78  cases, 
4  under  12  years,  at  the  London  Hospital  in  20  years  (Russell  Howard, 
1907)  the  testis  was  undescended  in  12,  fully  descended  48,  not  noted  18. 
Atrophy  and  fibrosis  render  it  less  liable  to  orchitis  and  tuberculous  disease. 

Treatment. — An  attempt  must  be  made  to  bring  down  a  partially 
■descended  testis  into  the  scrotum  by  manipulation.  The  mother  must  be 
taught  to  press  it  down  toward  the  bottom  of  the  scrotum  several  times  a 
day  and  hold  it  in  position  for  a  few  minutes.  Fair  success  is  achieved  in 
infancy.  If  this  fails,  operate  after  the  age  of  2  and  before  5  years  of  age. 
Some  recommend  that  operation  should  be  postponed  until  puberty.  This 
is  inadvisable  for  fibrosis  may  occur  quite  early.  It  is  justifiable  to  wait 
until  the  eighth  year,  if  there  is  no  hernia  and  the  organ  can  be  preserved 
from  injury,  for  the  gland  may  reach  the  scrotum  unaided.  Sutures, 
.splints  and  mechanical  appliances  are  of  little  value.  The  organ  must 
not  be  sacrificed  without  due  consideration,  because  of  the  functional 
-effects  of  its  internal  secretion.  It  can  be  transplanted  into  the  scrotum 
and  inserted  between  the  scrotal  fascia  and  the  skin.  In  25  out  of  29  cases 
•of  scrotal  placement  the  ultimate  results  were  unfavourable  (L.  B.  Raw- 
lings,  1907),  for  the  testis  became  pubo-scrotal,  pubic  or  inguinal,  and 
.atrophic.  Increase  in  size  may  be  followed  by  atrophy.  It  may  succeed 
under  7  years  of  age.  An  inguinal  testis  is  a  source  of  discomfort  and  very 
liable  to  injury  and  torsion.  It  is  generally  useless  and  should  be  removed, 
if  unilateral.  The  remaining  organ  is  sufficient  for  all  purposes.  The 
associated  hernia  must  be  dealt  with  at  the  same  time.  It  is  useless  to 
•attempt  to  save  the  testis  if  the  epididymis  is  widely  separated  from  it, 
if  the  vessels  of  the  cord  have  to  be  severed  in  transplanting,  if  the  cord  is 
short  and  the  organ  fibrotic,  and  if  the  boy  is  over  10  years  of  age.  Repo- 
sition in  the  abdomen  is  valueless,  for  the  organ  does  not  develop  any 
better  in  that  position.  If  both  organs  are  in  the  inguinal  canal  they  are 
ibest  left  alone,  unless  they  become  troublesome.  Scrotal  placement  may 
>he  tried.  Reposition  in  the  abdomen  and  extra-peritoneal  fixation,  if 
done  early  in  life,  may  possibly  enable  them  to  develop  at  puberty  and 
.become  functional  for  a  short  time,  so  that  the  child  does  not  become  as 
.a  eunuch. 

Torsion  of  the  Spermatic  Cord  is  rare,  about  40  cases  on  record.  It 
may  occur  at  birth,  in  the  early  months  of  life  or  later.  The  testis  may  be 
in  the  abdomen,  imperfectly  or  fully  descended,  or  one  which  has  been 
replaced  in  the  abdomen.  Often  no  exciting  cause  can  be  found.  The  onset 
is  sudden,  sometimes  in  sleep.  It  causes  painful  swelling  of  the  testis, 
■bloody  hydrocele,  suppuration,  gangrene  and  atrophy.    Suppuration  is  not 


596 


Chapter   XL  VII. 


common  and  complete  atrophy  not  invariable.  There  is  considerable- 
vomiting  and  the  symptoms  suggest  strangulated  hernia,  but  the  bowels 
act  with  enemata  and  flatus  is  passed.  Recurrent  attacks  have  been  noted- 
Try  and  untwist  the  cord,  if  the  testis  is  in  the  scrotum  and  the  child 
is  seen  early.  Prescribe  rest,  elevation  of  the  organ,  and  morphia  for 
the  relief  of  pain  ;  and  tap  the  hydrocele.  Do  not  remove  the  organ 
unless  the  symptoms  are  very  urgent,  or  there  is  hernia  with  undescended 
testis.    Strangulation  may  occur  from  pressure  on  the  cord. 

Acute  Orchitis  is  due  to  injury,  gonorrhoea,  other  infections,  rarely 
infarction,  and  mumps  (q.v.).  The  testis  is  swollen,  very  painful,  and  the 
overlying  skin  is  inflamed.  It  must  be  elevated  and  supported,  an  icebag 
applied,  the  bowels  kept  open,  and  the  patient  in  bed. 

Syphilitic  Orchitis  is  not  infrequent  in  congenital  syphilis,  though 
apparently  overlooked  until  it  was  described  by  Despres  in  1875.  Still 
found  it  present  in  8  per  cent,  of  64  cases  and  regards  it  as  pathognomonic 
It  is  found  in  the  first  3  months  of  life  and  up  to  3  years  of  age.  Generally 
it  is  bilateral  and  associated  with  hydrocele.  Usually  the  testis  is  much- 
enlarged,  hard  and  painless.  It  is  not  necessarily  enlarged  and  in  such 
cases  the  diagnosis  depends  on  the  feeling  of  hardness.  It  never  suppurates.. 
The  epididymis  may  be  secondarily  affected.  Microscopically  there  is  a- 
diffuse  interstitial  cell  proliferation  ;  rarely  gummatous  and  causing  an 
irregular  outline.  Gummata  are  rare,  but  may  occur  in  the  testis  or  epididy- 
mis. The  disease  ends  in  atrophy,  not  necessarily  complete  ;  and  may 
result  in  infantilism,  impotence  and  sterility.  The  diagnosis  depends  on  the 
chronicity,  absence  of  pain,  stony  hardness,  and  other  evidence  of  congenital 
syphilis.  Tuberculous  testis  may  occur  in  this  disease.  The  treatment  is 
that  of  the  cause. 

Tuberculous  Testis  is  not  very  rare.  It  is  really  an  epididymitis.  A 
congenital  case  has  been  reported  by  Dreschfield  (1884),  and  one  at  a  few 
days  of  age  by  Giraldes.  It  is  most  common  under  2  years  of  age,  unilateral, 
and  more  frequent  on  the  left  side.  Generally  it  is  secondary.  Injury  is  a 
predisposing  factor.  Hydrocele  is  present  in  one-third  of  the  cases.  It 
may  begin  insidiously,  or  come  on  acutely  and  present  a  slight  urethral 
discharge.  It  may  remain  quite  localised.  The  tendency  in  babies  is  to 
early  abscess  formation  but  without  fistulas.  It  is  treated  on  general 
principles,  and  by  removal  if  suppuration  ensues. 

Tumours  of  the  testis  are  clinically  malignant.  Innocent  ones  are  very 
rare  ;  so,  too,  teratomata,  either  dermoids  or  sebaceous  cysts,  in  the  testis, 
scrotum  or  inguinal  canal.  Ten  per  cent,  of  malignant  tumours  occur 
under  10  years  of  age.  Not  one  out  of  114  cases  (Robert)  was  between  10 
and  15  years  old.  Some  are  congenital.  Of  16  cases  in  1932  tuberculous 
children  1  was  noted  at  one  and  2  at  two  months  (Demme).  Of  16  cases  in 
5566  children  6  were  in  the  first  and  6  in  the  second  year  (Jullien).  It  is  a 
trifle  more  frequent  on  the  right  side  and  occasionally  bilateral ;   right  47,. 


The  Genital  System.  597 

left  41,  bilateral  5  (Robert).  Injury  and  undescended  testis  are  the  chief 
predisposing  causes.  Many  are  embryomata,  derivatives  of  the  three 
embryonic  layers  and  analogous  to  certain  ovarian  tumours.  Others  are 
really  columnar  or  spheroidal-celled  carcinomata,  beginning  in  the  tubules 
of  the  testis  or  vas.  Chondrification,  mucoid  degeneration,  haemorrhage  and 
cyst  formation  are  liable  to  occur.  Fibro-cystic  tumours,  containing 
cartilage,  are  rare  in  infants.  A  few  are  sarcomata.  Usually  the  tumour  is 
soft  and  fleshy.  D'Arcy  Power  (1907)  states  that  sarcoma  occurs  in  boys 
of  10  years  and  over  ;   and  that  it  usually  starts  in  the  epididymis. 

The  swelling  is  gradual  and  painless.  Testicular  sensation  varies  as 
the  amount  of  testis  left  and  is  lost  early.  Dull,  aching  or  lancinating  pain 
is  caused  by  rapid  growth.  Dragging  pain  in  the  groins  and  pain  across  the 
loins  may  be  felt.  The  testis  retains  its  shape,  like  orchitis,  and  the  growth 
is  smooth  until  the  tunica  albuginea  is  perforated  by  bosses.  It  is  firm, 
heavy  and  hard  at  first.  Later  it  becomes  soft,  elastic  and  fluctuating,  like 
a  cyst.  It  may  be  masked  by  hydrocele  or  hematocele.  The  epididymis 
is  stretched  and  flattened.  The  scrotum  may  become  adherent  and  the 
growth  fungate  in  late  stages.  The  prognosis  is  grave  and  generally  fatal. 
Secondary  growths  often  occur  in  the  lumbar  glands  and  may  press  on  the 
vena  cava  inferior  and  on  the  portal  vein,  causing  oedema,  ascites  and 
dilated  superficial  abdominal  veins.  Deposits  in  the  cord  are  rare.  The 
peritoneum  may  be  diffusely  infiltrated.  The  only  hope  of  cure  is  early 
removal  of  the  tumour.  The  embryomata  are  not  always  malignant.  One 
tissue  only  may  become  malignant,  and  simulate  sarcoma  or  carcinoma. 
►Sarcomata  are  distributed  by  blood  vessels  and  are  more  malignant  than  the 
carcinomata  which  are  disseminated  by  lymphatics. 

Hydrocele  is  congenital  or  acquired.  The  former  type  has  been 
described  (p.  328).  Translucency  is  of  no  value  in  diagnosing  it  from  a 
congenital  hernia.  The  acquired  type  is  rare  and  like  that  of  adults,  but 
does  not  attain  a  great  size.  It  is  due  to  injury,  or  secondary  to  disease  of 
the  testis  or  epididymis.  It  may  simulate  hernia  or  an  enlarged  testis. 
Simple  puncture  with  sterile  needles  in  several  places  may  cure  it.  Opera- 
tion and  excision  of  the  sac  is  rarely  needed.  A  hematocele  is  still  more 
rare,  and  due  to  trauma  or  torsion  of  the  cord. 

The  Mammae. —  Amastia,  or  absence  of  the  glands,  is  very  rare.  Poly- 
mastia is  not  very  uncommon,  especially  among  the  Japanese,  being 
present  in  women  5*19  and  in  men  1-6  per  cent.  (Teizo  Iwai,  1907).  The 
statue  of  Diana  of  the  Ephesians  in  the  National  Museum  at  Naples  has 
multiple  mamma?.  Polymastia  may  be  atavistic  (p.  17).  Normally  many 
glands  are  developed  bilaterally  along  the  abdomen,  and  in  the  human 
female  all  but  two  atrophy.  Occasionally  it  is  a  spontaneous  variation,  or 
the  result  of  dichotomy  of  a  single  gland.  The  peculiarity  runs  in  families 
and  is  transmitted  by  females.  The  accessory  glands  may  be  on  any  part 
of  the  trunk,  commonly  in  the  pectoral  region,  and  have  been  seen  on  the 


598  Chapter   XL  VI I. 

arms,  thighs,  cheeks,  and  even  the  vulva.  They  are  rather  more  frequent 
on  the  left  side.  Rarely  more  than  3,  but  as  many  as  8  have  been  noted. 
In  structure  they  vary  from  a  normal  gland  with  a  nipple  to  a  mass  of 
connective  tissue  containing  a  few  acini.  The  mammary  gland  is  a 
modified  sebaceous  gland.  Accessory  ones  situated  out  of  the  mid-line  of 
the  body  are  probably  not  mammary  glands  but  really  giant  sebaceous  ones. 
Supernumerary  glands  with  nipples  may  secrete  milk.  According  to  Iwai, 
polymastia  is  more  common  among  the  tuberculous  and  those  with  poly- 
mastia are  more  liable  to  this  disease.  Supernumerary  nipples  are  not 
infrequent  (polythelia). 

Gynecomastia,  hypertrophied  breasts  in  the  male,  represents  an 
atavistic  tendency,  a  reversion  to  a  time  when  the  males  aided  the  females 
in  suckling  the  young.  These  glands  contain  a  large  amount  of  fibrous  tissue 
and  perhaps  as  many  acini  as  in  the  female  breast.  They  may  develop 
chronic  mastitis.  Humboldt  investigated  and  recorded  the  case  of  Francisco 
Lozano  who  nourished  his  infant  son  at  the  breast  for  several  months. 
Similar  instances  on  record  are  not  so  well  authenticated.  Precocious- 
lactation  and  mammary  enlargement  have  been  reported  in  a  male  childr 
3  months  old,  with  congenital  morbus  cordis.  The  breasts  were  about 
half  the  size  of  a  billiard  ball,  areolae  prominent  and  well  marked,  nipples 
large.  The  increase  in  size  began  at  5-6  weeks  of  age.  The  secretion 
resembled  milk  rather  deficient  in  fat.  There  was  no  evidence  of  mastitis- 
or  history  of  manipulation  of  the  breasts.  The  child  was  large,  the  penis- 
big,  and  the  anterior  fontanelle  closed.  On  section  after  death  the  glands 
were  normal  secreting  organs. 

Mammce  in  the  Neivborn. — The  breasts  are  almost  invariably  enlarged. 
The  increase  in  size  begins  on  the  second  or  third  day,  attains  its  maximum 
in  the  second  week,  and  disappears  in  another  week  or  two.  A  milky 
secretion,  "  witches  milk,"  can  be  squeezed  out ;  in  composition  like  colos- 
trum. The  secretion  may  persist  for  2-3  months.  If  the  breasts  are  unduly 
large,  give  a  purge  and  pot.  iod.,  and  apply  belladonna.  Such  treatment  is- 
rarely  necessary. 

Mastitis  and  Mammary  Abscess. — In  the  first  to  the  third  week  of 
life  the  breast  may  be  found  tender,  and  the  skin  reddened  and  cedematous. 
It  is  the  result,  almost  invariably,  of  the  pernicious  practice  known  as- 
"  breaking  the  baby's  nipple  strings."  This  is  based  on  the  superstition 
that  it  produces  wellformed  nipples,  whereas  it  is  probably  the  chief  cause- 
of  retracted  and  ill-developed  nipples.  The  nurse  manipulates  the  nipple 
with  the  fingers  and  thumb  until  a  little  secretion  is  squeezed  out.  This  is 
followed  by  painful  swelling  of  the  breast  and  abscess  formation,  if  infection 
is  conveyed  via  the  nipple.  In  addition  to  the  local  signs  the  mischief  causes- 
fever,  anorexia,  vomiting,  liquid  stools  and  restlessness.  The  ultimate 
results  may  be  bad  in  girls  because  of  partial  destruction  of  the  glandular 
tissue.     The  condition  must  not  be  confused  with  that  of  physiological 


The  Genital  System.  599 

enlargement  and  lactation.  Treatment  is  preventive  ;  the  local  application 
of  lead  lotion  ;  and  incision  if  pus  forms.  The  incision  should  be  made  as 
near  the  periphery  as  possible  and  in  a  line  with  the  ducts. 

Mammcc  at  Puberty. — The  physiological  enlargement  which  takes 
place  at  10-15  years  of  age  may  cause  painful  swelling  and  irritability  of 
the  mamma1.  It  does  not  lead  to  ill  results.  Active  treatment  is  un- 
necessary. The  breasts  must  be  protected  from  undue  pressure.  Sometimes 
the  pain  is  more  or  less  hysterical  in  its  causation.  A  similar  condition  of 
the  breasts  may  occur  in  boys  at  puberty.  Angeioma,  adenoma  and  other 
tumours,  and  tuberculosis  of  the  mamma,"  are  rare  diseases  in  early  life. 

The  Female  Genitals. — Adhesion  of  the  prepuce  of  the  clitoris  is 
probably  more  frequent  in  girls  than  boys,  and  neglected  on  grounds  of 
modesty.  It  usually  gives  rise  to  no  symptoms  ;  sometimes  to  nervous 
irritability,  capricious  appetite,  poor  health,  enuresis  nocturna,  onanism, 
and  possibly  epileptiform  convulsions  and  reflex  paresis  of  the  lower  limbs. 
Other  causes  must  be  carefully  excluded  before  blaming  an  adherent  prepuce 
for  any  of  these  symptoms.  I  have  known  ulceration  at  the  base  of  the 
clitoris  a  cause  of  painful  micturition.  If  local  irritation  in  infants  under 
one  year  is  suspected,  the  parts  must  be  examined.  Adhesions  can  be 
separated  by  a  probe  but  they  are  liable  to  recurrence.  Circumcision  is 
rarely  needed.  It  must  be  done  under  a  general  ancesthetic  and  the 
haemorrhage  controlled  by  a  compress. 

The  urethra  and  clitoris  may  show  a  congenital  fissure.  The  urethra 
may  open  abnormally  into  the  vagina  or  rectum,  or  present  other  develop- 
mental defects  as  in  the  male.  Prolapse  is  rare.  The  everted  urethra 
forms  a  red,  oozing,  projecting  mass  which  may  be  mistaken  for  a  carbuncle. 
It  causes  genital  irritation,  straining,  and  the  discharge  of  bloody  mucus. 
Urethritis  is -part  of  a  vulvo- vaginitis. 

The  Vulva  and  Vagina. — Occasional  malformations  are  atresia  of  the 
anus  and  vulva,  of  the  anus  and  vagina,  simple  epithelial  adhesion  of  the 
labia,  atresia  of  the  vagina,  imperforate  hymen,  and  congenital  cysts  of  the 
hymen.  Some  of  these  are  described  in  connection  with  malformations  of 
the  rectum  and  anus  (p.  333).  The  bladder  may  open  directly  into  the 
vagina.  As  many  as  3  septa  have  been  found  in  the  vagina,  exclusive  of 
the  hymen.  One  is  not  uncommon  and  is  situated  about  an  inch  within 
the  canal.  The  vagina  may  be  occluded  by  a  dense  hymen  or  by  a  tense 
membrane  immediately  above  a  well-formed  hymen.  The  latter  structure 
may  be  absent.  All  these  septa  depend  on  incomplete  absorption  of  the 
tubular  downgrowth  from  which  the  vagina  develops. 

Herpes  Vulvce. — A  herpetic  eruption  may  break  out  on  the  mucous 
membrane  of  the  vulva  alone,  or  in  conjunction  with  a  like  eruption  on  the 
cutaneous  surface  of  the  vulva,  and  perhaps  on  the  perineum  and  about  the 
anus.  The  rash  and  symptoms  are  similar  to  those  of  herpes  elsewhere. 
On  the  mucous  membrane  the  vesicles  break  down  and  form  small  ulcers, 


fiOO  Chapter   XL  VII. 

which  may  heal  in  2-3  days  or  extend  and  coalesce  into  large,  superficial, 
painful  ulcers,  with  pain,  itching  and  discharge.  Single  vesicles  may  be 
mistaken  for  condylomata,  hut  they  are  much  smaller  and  more  transparent. 
A  diagnosis  from  vulvo- vaginitis  is  easily  made  on  inspection  of  the  parts. 
It  is  not  uncommon  for  herpetic  ulcers  to  develop  on  the  perineum,  thighs 
and  buttocks.  The  affection  is  readily  cured  by  cleanliness  and  the  free 
application  of  a  drying  powder,  composed  of  calomel,  zinc  oxide,  talc 
and  starch.  Mild  ointments  must  be  applied,  if  ulceration  has  taken  place, 
spread  freely  on  lint  and  inserted  between  the  labia  to  prevent  friction. 
It  may  be  necessary  to  keep  the  child  in  bed  for  a  few  days.  The  youngest 
case  under  my  observation  was  11  months  old. 

Noma  Vulvce  is  a  gangrenous  process,  similar  to  cancrum  oris  and 
sometimes  called  gangrenous  vulvitis.  The  chief  causes  are  malnutrition, 
bad  hygiene,  and  measles.  It  may  follow  herpes  or  catarrhal  vulvitis. 
The  bacteriology  is  the  same  as  in  cancrum  oris  (p.  220).  Probably  a  simple 
infection  is  followed  by  a  mixed  one.  Some  cases  are  due  to  the  diphtheria 
bacillus,  and  recovery  has  ensued  under  antitoxin  treatment.  It  begins  as 
a  slight  ulceration  of  the  mucosa  with  a  surrounding  area  of  intense  hardness. 
Or  tense  brawny  induration  is  first  noted,  and  the  mucous  membrane  is 
shiny  and  swollen  over  the  most  prominent  part.  The  centre  of  the 
swelling  becomes  dark  purplish  in  colour,  and  finally  gangrenous,  breaking 
down  and  discharging  offensive  matter.  The  induration  and  subsequent 
gangrene  spread  and  may  involve  the  whole  labium,  the  mons  veneris  and 
the  perineum.  Such  an  extensive  disease  is  usually  fatal.  Milder  cases 
racover,  with  considerable  local  deformity  from  the  sloughing,  destruction, 
and  secondary  cicatrisation.  Stenosis  and  atresia  of  the  vagina  may 
result.  For  details  of  the  treatment  and  a  fuller  description  of  the  process 
reference  must  be  made  to  the  mouth  affection. 

Vulvo-vaginitis. — Vulvitis  or  vulvo- vaginitis  is  an  inflammation  of  the 
vulva  and  adjacent  parts.  It  may  affect  the  urethra  and  vagina,  and 
extend  to  the  cervix  uteri.  It  is  catarrhal,  the  result  of  dirt  (?),  chemical 
irritation,  debility,  and  traumatism,  such  as  direct  injury  and  mastur- 
bation ;  or  parasitic,  due  to  saphrophytes  in  delicate  children  and  after 
infective  disease,  oxyurides  (?),  and  pathogenic  bacteria,  notably  the 
gonococcus.  The  gonococcal  form  is  more  frequent  than  generally  suspected, 
more  dangerous  than  commonly  realised,  and  sometimes  appalling  in  its 
results.  Leucorrhoea  does  not  occur  in  healthy  children,  and,  therefore, 
requires  treatment.  Normally  the  vagina  contains  a  bacillus  producing 
lactic  acid  which  prevents  the  development  of  staphylococci  and  streptococci, 
and  to  a  less  extent  the  gonococcus. 

Simple  or  Catarrhal  Vulvo-vaginitis  includes  all  cases  not  of  gonococcal 
origin.  It  is  most  common  after  the  first  dentition,  but  may  occur  in  infants. 
Saprophytic  cases  are  liable  to  spread  from  child  to  child,  where  many  are 
living  under  the  same  conditions,  being  spread  by  direct  inoculation  or  by 


The  Genital  System.  601 

medium  of  sponges,  towels,  thermometers,  etc.  Masturbation  is  a  doubtful 
cause,  though  it  may  produce  a  mild  degree  of  local  redness  and  irritability, 
predisposing  to  secondary  infection.  Feeble-minded  children  may  mastur- 
bate to  a  sufficient  extent  to  produce  excoriation  of  the  vulva,  without 
setting  up  vulvo-vaginitis.  The  discharge  consists  of  epithelial  and  pus 
cells,  many  varieties  of  bacteria  and  cocci,  often  a  few  diplococci.  Cocci  are 
found  in  normal  vaginal  secretion.  It  is  as  well  to  regard  all  cases  as 
infectious,  though  about  one-third  are  due  to  non-infective  organisms. 

Gonorrheal  Vulvo-vaginitis. — The  mucous  membrane  of  babies  is  very 
;susceptible  to  gonococcal  infection.  Some  cases  are  due  to  mixed  infections 
by  the  gonococcus  and  other  diplococci.  The  disease  is  most  frequent  in  the 
newborn  and  in  the  first  5  years  of  life,  and  may  have  been  in  existence  for 
.some  time  before  the  child  comes  under  observation.  It  increases  in 
frequency  at  puberty.  Out  of  600  cases  admitted  into  the  New  York 
Babies'  Hospital  during  one  year  70  were  affected  and  9  others  had  gonococcal 
arthritis.  (Kimball,  1903).  The  disease  is  certainly  not  as  prevalent  in 
London  Hospitals. 

The  infection  is  conveyed  by  the  mother  during  parturition,  by 
the  fingers  or  infected  garments  of  attendants,  from  the  clothes  or  fingers  of 
•a  bedfellow,  attempted  rape,  public  baths,  bathing  water,  chamber  utensils, 
sponges,  towels,  diapers  and  rectal  thermometers.  The  affection  is  by  no 
means  always  due  to  attempted  rape,  even  in  older  girls.  Undue  impor- 
tance is  given  to  this  cause  on  account  of  the  prevalence  of  a  popular 
superstition  that  sexual  congress  with  a  virgin  will  cure  gonorrhoea  in  the 
male.  Nevertheless  infection  is  usually  direct,  from  the  fingers,  rather  than 
indirect.  In  most  cases  it  will  be  found  that  some  other  member  of  the 
family  is  affected,  usually  the  mother,  and  that  the  liability  to  infection  has 
•been  great,  apart  from  sexual  causes.  The  older  the  child  the  greater  is 
the  possibility  of  a  sexual  origin. 

The  incubation  period  is  about  3  days.  In  the  early  stage  the  symptoms 
■are  those  of  simple  catarrh,  a  subacute  inflammation  of  the  genitalia  often 
not  extending  beyond  the  hymen  ;  with  thin  yellowish- white  discharge, 
a  sensation  of  burning,  pain  on  micturition,  genital  itching  and  eczema, 
and  pain  on  walking  in  the  more  severe  attacks.  The  simple  catarrhal 
variety  is  usually  purulent,  seldom  very  acute,  and  rarely  extends  to  the 
vagina,  the  hymen  being  a  sufficient  barrier.  In  more  severe  forms  the 
•discharge  is  thicker  and  dries,  forming  crusts  and  causing  adhesion  of  the 
labia,  and  is  offensive. 

In  the  gonococcal  variety  there  is  a  thick  yellowish  or  whitish  dis- 
charge, which  on  pressure  seems  to  exude  from  the  vagina.  The  vulva, 
urethra,  hymen  and  vagina  become  red,  swollen,  and  painful.  Erosions 
may  form  and  the  parts  bleed  readily.  The  discharge  forms  thick  crusts 
on  the  labia.  It  is  much  more  apt  than  the  simple  type  to  spread  up  the 
vagina  and.  involve  the  cervix  uteri,  endometrium,  Fallopian  tubes  and 


602  Chapter   XL  VII. 

peritoneum.  Painful  micturition  is  by  no  means  constant  in  either  variety 
and  may  be  absent  throughout.  Often  there  are  no  subjective  symptoms,, 
yellow  spots  on  the  garments  being  the  only  point  noted  by  the  mother. 
Usually  there  is  a  slight  rise  of  temperature  and  a  little  general  malaise,, 
a  marked  contrast  to  the  effects  seen  in  adults.  Prolonged  cases  cause- 
failure  of  general  health. 

Complications  are  less  frequent  than  in  adults  and  of  the  same  character.. 
Extension  may  take  place  to  the  urethra  and  bladder,  but  cystitis  is  rare. 
Inguinal  adenitis  (bubo)  has  been  noted.  Rectal  infection  may  occur  and 
set  up  proctitis  (p.  338).  In  babies  arthritis  and  pysemia  are  not  uncommon.. 
Out  of  600  babies  10  had  arthritis.  One  of  these  had  vulvo-vaginitis 
(Kimball),  and  8  developed  pysemia  under  3  months  of  age ;  and  6  died.. 
He  ascribed  the  infection  to  gonorrhceal  stomatitis.  Purulent  ophthalmia 
is  the  most  frequent  complication  (p.  137).  Iritis,  apt  to  be  regarded  as 
rheumatic  iritis,  and  endocarditis  may  occur.  Extension  of  the  disease 
to  the  uterus  and  tubes  may  give  rise  to  salpingitis,  pyosalpinx  and  peri- 
tonitis. Many  cases  of  unexplained  pelvic  disease  in  virgins  might  be 
due  to  an  infantile  gonorrhceal  salpingitis  which  has  remained  quiescent 
until  puberty.  Possibly  sterility  and  some  instances  of  deformed  or 
undeveloped  uteri,  associated  with  dysmenorrhea,  have  a  like  origin. 

Course. — The  simple  type  lasts  for  1-6  weeks  ;  the  gonococcal  may 
persist  for  as  many  months  or  for  years,  with  periods  of  latency.  The- 
prognosis  is  serious  as  regards  duration,  and  guarded  in  view  of  possible 
complications. 

Diagnosis. — The  differentiation  of  the  gonococcal  from  the  simple- 
variety  depends  on  bacteriological  examination.  Take  the  pus,  from 
the  urethra  if  it  is  affected,  and  make  smear  preparations  and  cultures.  The- 
organisms  are  found  in  the  polymorphs.  They  are  small  diplococci,  flat- 
tened or  slightly  concave  on  their  opposed  sides,  like  two  little  kidneys. 
They  are  Gram-negative,  form  acid  in  glucose  and  galactose  media,  and 
are  readily  stained  by  carbol  thionin,  pyronine  methylene  green,  and  alco- 
holic methyl  violet  2  per  cent,  solution.  Schutz  recommends  the  following 
differential  stain  ;  a  saturated  aqueous  solution  of  methylene  blue  with 
carbolic  acid  5  per  cent.  Stain  for  5-10  minutes,  wash  and  decolourise  with, 
acetic  acid,  5  drops  in  20  c.c.  water,  for  3  sees.  ;  wash,  dry  and  mount.. 
The  gonococci  are  stained  blue  and  other  organisms  are  unstained.  The 
normal  diplococci  of  the  vagina  are  not  decolourised  by  Gram  (Heiman). 
Culturally  the  gonococcus  grows  on  serum,  and  on  a  mixture  of  hydrocele - 
fluid  and  agar  agar,  but  not  on  agar  agar  alone. 

Treatment. — The  patient  must  be  isolated  and  care  taken  to  prevent 
indirect  spread  of  infection.  Napkins  must  be  sterilised.  These  precau- 
tions should  be  taken  in  even  simple  cases.  The  slightest  suspicion  of  con- 
junctivitis must  be  at  once  attended  to,  as  in  ophthalmia  neonatorum.  The 
instillation  of  protargol  0*5  per  cent,  solution  into  the  eyes,  and  the  use  of  a. 
vulvar  pad  and  T-bandage  are  preventive  measures. 


The  Genital  System.  603- 

Keep  the  bowels  open.  Give  quinine,  syr.  ferri  iod.,  or  cod-liver  oil ; 
and  alkalies,  if  the  urine  is  highly  acid  and  irritating.  Sit  the  child  in  a 
bath  or  basin,  containing  milk  or  water  with  borax  or  liq.  plumbi  subacetat., 
several  times  daily  ;  or  tannic  acid,  1  in  1000,  once  a  day.  Dry  well  and 
apply  with  a  soft  brush  or  wool,  calamine  dr.  1|,  almond  oil  oz.  2,  lime  water 
to  oz.  8  ;  or  wool  soaked  in  boric  acid  grs.  20,  glycerine  dr.  2,  liq.  plumbi 
oz.  -|,  fresh  milk  to  oz.  8.  It  is  not  advisable  to  wipe  away  secretion  with 
mops  because  of  the  tenderness  ;  nor  to  keep  lint  between  the  labia,  for  it 
prevents  the  free  escape  of  the  discharge.  Irrigation  is  of  doubtful  value. 
It  attracts  too  much  attention  to  the  parts,  may  convey  infection  up  higher,, 
and  may  cause  severe  pain.  It  is  permissible  to  syringe  away  superficial 
discharge  with  saturated  solution  of  boric  acid,  separating  the  labia. 
If  necessary  the  lower  part  of  the  vagina  may  be  irrigated.  Irrigation 
should  be  preceded  by  a  hip  bath  and  thorough  cleansing  with  soap  and 
water.  Use  a  douche,  held  2  feet  above  the  level  of  the  vaginal  orifice,, 
and  a  soft  rubber  catheter  ;  and  have  the  thighs  flexed  and  fully  abducted. 
Use  saturated  boric  acid  solution,  sodium  carbonate  5  per  cent.,  perman- 
ganate of  potash  1  in  1000,  ordering  a  1  per  cent,  solution  and  mixing 
4  oz.  with  2  pints  of  water,  or  1  in  10,000  bichloride  of  mercury.  Douche 
twice  daily,  then  blow  powdered  boric  acid  into  the  vagina  and  vulva, 
and  put  on  a  large  pad  of  antiseptic  wool  and  a  T-bandage.  Irrigation  with 
sodium  carbonate  may  be  followed  by  the  injection  of  protargol  0-5-2-0  per 
cent.,  and  a  tampon  of  ichthyol  10  per  cent,  solution.  In  gonorrhceal  cases 
douche  every  4-6  hours.  Apply  a  simple  ointment  to  the  surrounding- 
parts.  Bougies  of  iodoform,  or  alumnol  2  per  cent.,  and  the  insufflation  of 
iodoform  are  useful  in  early  stages.  In  chronic  cases  lotions  of  sulphate  or 
sulphocarbolate  of  zinc  and  alum,  aa  dr.  1  to  the  pint  of  water,  are  required. 
Or  it  may  be  necessary  to  inject  silver  nitrate  solution,  dr.  1-4,  beginning 
with  1  in  2000  and  reducing  the  strength  50  per  cent,  daily  down  to  1  in  125- 
on  the  fifth  day.  A  2  per  cent,  solution  may  be  applied  direct  to  the  vaginal 
mucosa  through  a  speculum  every  3  days.  The  cases  are  tedious  and 
relapses  common,  unless  the  treatment  is  carried  out  thoroughly.  Packing 
the  vagina  may  be  necessary.  Vaccine  may  be  used  in  chronic  cases. 
No  patient  is  cured  until  the  gonococcus  cannot  be  grown  on  culture  media. 

Hydrocolpos  may  result,  in  infants  with  imperforate  hymen,  from 
excessive  secretion  of  a  watery  or  white  viscid  fluid.  The  vagina  alone  may 
be  dilated,  but  if  the  secretion  is  watery,  the  uterus  is  usually  dilated  as 
well.  The  condition  has  been  noted  on  the  day  after  birth,  causing  a  pro- 
trusion like  a  prolapse  at  the  vulva  ;  31  oz.  were  let  out  (Commandeur, 
1904).  Hcematocolfos  and  hcematosalpynx  may  occur  after  the  onset  of 
menstruation.  Tumours  of  the  vagina  are  almost  always  sarcomata.  They 
occur  in  the  very  young,  and  are  occasionally  congenital.  Of  24  collected 
cases  the  oldest  was  only  3  years.  Few  cases  are  under  6  months,  and  it  is- 
rare  after  the  seventh  year.    It  begins  as  a  small,  flat,  sessile  growth,  or  a 


604  Chapter   XL  VII. 

smooth  convex  swelling,  in  the  anterior  wall ;  spreads  very  rapidly  by  con- 
tinuity ;  may  involve  the  cervix  uteri,  urethra  and  bladder  ;  and  causes 
haemorrhage,  disturbed  micturition,  constipation,  and  abdominal  or  pelvic 
pain.  Bleeding  is  the  first  sign.  The  vagina  becomes  filled  with  soft, 
friable,  sometimes  pedunculated,  masses.  The  chief  complications  are 
retention,  cystitis,  peritonitis,  pyaemia,  pyelitis,  pyelo-nephritis,  pyornetra 
and  sepsis.  The  average  duration  is  12  months.  It  is  almost  always 
fatal,  for  it  is  detected  too  late  on  account  of  the  absence  of  early  symptoms. 
Israel,  Hollander  and  Schuchardt  report  cures  after  operation.  Usually 
operation  is  followed  by  recurrence  in  6-8  weeks,  and  the  recurrent  growth 
grows  and  degenerates  more  rapidly.     Metastases  are  infrequent. 

Rectovaginal  fistula  is  due  to  inflammatory  mischief  and  abscess.  Some- 
times no  cause  can  be  found.  In  a  7-month  old  girl  the  stools  had  been 
passed  per  vaginam  with  much  pain  for  a  week.  In  a  girl,  16  years  old, 
the  fistula  appeared  in  the  third  week  of  enteric  fever.  Both  cases 
recovered.  The  prognosis  is  always  good.  Vulvar  abscess,  the  result  of 
suppuration  of  Barfcholini's  glands,  is  occasionally  seen. 

Uterus  and  Fallopian  Tubes. — The  uterus  may  be  absent  or  rudimen- 
tary, so  small  as  to  be  even  overlooked  after  death  and  incapable  of  palpa- 
tion during  life  on  bimanual  examination.  It  is  a  rare  condition,  except  in 
monsters,  and  usually  associated  with  absence  or  deformity  of  the  appen- 
dages and  vagina,  of  the  bladder,  kidneys,  clitoris  and  labia.  Cases  of 
apparent  absence  have  been  recorded  in  2  or  3  sisters,  and  in  cousins,  exam- 
ined during  life,  with  no  other  defect  and  no  heredity  of  the  peculiarity. 
Sentiment,  puberty,  sexual  desire  and  development  were  normal,  except 
for  the  absence  of  menses.  Prolapse  of  the  uterus  and  vagina  has  been 
reported,  e.g.,  in  a  case  of  spina  bifida  (Burger,  1904).  It  is  due  to  imperfect 
development  of  the  pelvic  floor  and  may  be  congenital.  New  growths  of  the 
nterus  are  rare. 

The  Fallopian  tubes  may  be  affected  with  pyosalpynx  or  hseinato- 
salpynx.  Tuberculosis  is  occasionally  seen.  It  is  due  to  secondary  infection 
from  the  peritoneum,  and  almost  certainly  is  never  the  result  of  an  ascending 
genital  infection.    From  the  tubes  it  may  spread  to  the  uterus. 

Ovaries. — Complete  absence  is  very  rare.  Occasionally  one  is  wanting. 
Exceptionally  there  are  three.  The  glands  rest  on  the  pelvic  brim  at  birth 
and  gradually  descend  to  the  sides  of  the  pelvis.  Abnormally  one  may  be 
found  in  the  inguinal  canal  or  even  in  the  labium  majus  (ovarian  hernia). 
Strangulation  may  occur  in  the  sac  of  an  inguinal  hernia,  even  in  the  new- 
born. 

Numerous  cases  of  tumours  and  cysts  are  on  record.  Alban  Doran 
reported  double  ovarian  tumour  in  a  7-month  fa-)tus.  Cystic  follicles  are 
not  very  uncommon  in  the  first  year  of  life  and  must  not  be  confused  with 
cystic  adenomata. 

The  chief  varieties  are  simple  cysts,  adenomata,  dermoid  cysts  and 
sarcomata.      Papuliferous   cysts   and   parovarian   cysts   are   unknown   or 


The  Genital  System.  605 

exceptional.     Bland  Sutton's  statistics  of  100  collected  cases  operated  on 
under  15  years  of  age,  and  the  operative  mortality,  are  : — 

(1)  Simple  cysts  and  adenomata  41  ;    deaths  3. 

(2)  Dermoid  cysts  38  ;    deaths  5. 

(3)  Sarcomata  21  ;   deaths  7. 

Howard  Kelly  (1901)  recognises  two  groups  : — (1)  Cystic  ;  adeno- 
cystomata,  unilocular  cysts,  dermoids  and  teratomata.  (2)  Solid  tumours  ; 
sarcomata  and  carcinomata.  He  gives  the  mortality  under  4  years,  inde- 
pendent of  the  character  of  the  tumour,  as  50  per  cent.  Of  55  cases  of  uni- 
and  multi-locular  cysts  4  died  ;  10  out  of  47  dermoids  ;  and  8  out  of  24 
solid  tumours.  Of  the  55  cystic  cases  51  were  over  4  years  of  age  and  only 
one  of  these  died.  A  good  many  cases  have  been  recorded  since.  Some 
show  precocious  development  (p.  200).  Under  the  age  of  3  years  the  tumour 
is  usually  a  dermoid  or  a  sarcoma  ;  after  that  age,  an  adenocystoma. 
These  tumours  have  to  be  diagnosed  from  tuberculous  peritonitis,  cystic 
kidney,  sacculated  exudations  and  hydatids. 

Torsion  of  Ovarian  Pedicle. — In  25  collected  cases  of  ovarian  hernia  in 
the  inguinal  region,  usually  on  the  right-side,  the  pedicle  has  been  twisted. 
All  were  infants  in  the  first  few  months  of  life  ;  one  over  6  months.  Its 
effects  are  the  production  of  a  tender  swelling,  irreducible,  and  without  an 
impulse  on  cough.  The  skin  may  be  inflamed  and  slightly  cedematous. 
The  ovary  may  be  gangrenous.  There  is  no  intestinal  obstruction  and  no 
peritonitis.  Vomiting  is  almost  always  absent.  Torsion  of  the  pedicle  within 
the  abdomen,  generally  in  connection  with  a  tumour,  causes  vomiting, 
abdominal  pain,  constipation  and  tympanites.  Operative  results  are 
excellent. 

Masturbation. — Syn.  :  Onanism,  Manustwpration,  Thigh-friction. — 
True  masturbation  must  be  regarded  as  simply  a  bad  habit,  the  result  of 
education  or  local  irritation  leading  to  manipulation  of  the  penis  or  vulvar 
region.  In  infants,  particularly  females,  it  takes  the  form  of  thigh-friction. 
A  neurotic  heredity  is  a  predisposing  cause  but  is  often  absent.  The  exciting 
factor  is  almost  invariably  local  irritation  by  retained  and  decomposing 
smegma.  This  is  apt  to  occur  in  boys  with  long  narrow  foreskins  or  par- 
tially adherent  ones,  the  smegma  collecting  in  pouches.  Irritating"  vaginal 
secretions  or  excessive  secretion  of  smegma  and  adhesions  of  the  preputium 
clitoridis,  and  other  causes  of  prutitus  vulvae,  are  the  main  factors  in  girls. 
Possibly  a  few  cases  depend  on  reflex  irritation  from  the  rectum,  bladder 
or  kidneys.  In  some  instances  the  habit  is  practised  by  nurses,  generally 
on  boys,  as  a  means  of  soothing  the  child.  The  friction  of  rough  diapers, 
hard  sponges  or  towels  may  first  start  the  habit ;  or  even  an  excess  of 
irritating  dusting  powder.  In  older  boys  it  may  originate  from  friction  by 
tight  or  ill-fitting  knickerbockers,  riding  a  wooden  horse,  or  ordinary  horse 
exercise.  The  friction  of  the  glans  penis,  exposed  by  circumcision,  is 
another  cause. 


•606  Chapter  XL  VII. 

Cases  have  occurred  in  babies  at  the  breast,  as  early  as  the  fourth  month, 
but  more  commonly  begin  at  6  months  to  2  years  of  age.  As  a  bad  habit  it 
is  acquired  about  puberty,  or  earlier  from  evil  companions.  It  is  often  over- 
looked in  girl  babies,  for  the  nature  of  the  movements  is  not  recognised  and 
they  are  ascribed  to  other  causes.  It  takes  the  form  of  thigh-friction,  the 
thighs  being  rubbed  together  and  sometimes  crossed,  or  of  wriggling  move- 
ments of  the  body,  or  manipulation  of  the  lower  abdominal,  iliac  or  pubic 
Tegions.  Some  make  to-and-fro,  body-rocking  movements,  while  seated 
on  a  chair,  or  rub  the  vulvar  region  against  the  leg  of  a  chair,  etc.  In  a 
4-month  old  baby  the  vulva  was  rubbed  against  the  nurse's  breast  (Strasser). 
Barely,  the  orgasm  is  induced  by  mental  suggestion.  Sometimes,  if  the 
child  is  prevented  from  carrying  out  one  kind  of  movement,  she  develops 
another.  During  each  act  of  indulgence  the  attention  is  preoccupied, 
abstracted  from  surrounding  objects  ;  the  face  becomes  red  and  injected, 
^nd  covered  with  sweat ;  the  eyes  glitter,  the  expression  is  strained,  and  at 
times  a  grin  overspreads  the  features  ;  and  sometimes  the  child  grunts  or 
pants.  Visible  annoyance  is  expressed  if  she  is  stopped.  After  a  variable 
period  the  child  sighs  and  sinks  back  pale  and  exhausted,  and  may  fall  into 
-a  sound  sleep.  The  usual  position  taken  up  is  on  the  back  or  half  reclining, 
sometimes  a  sitting  posture  on  the  floor.  In  male  infants  the  signs  of  orgasm 
•are  rare.  Erection  of  the  penis  and  exudation  of  a  glairy  fluid  may  occur. 
At  first  it  only  occurs  occasionally  ;  then  more  and  more  frequently, 
■even  50  times  a  day,  until  it  is  impossible  to  leave  the  child  unoccupied 
lest  it  indulges.    It  may  take  place  during  sleep. 

Examination  reveals  nothing  positively  indicative  of  the  habit. 
Erection  on  slight  manipidation  is  suggestive  ;  so,  too,  redness  and  irrita- 
tion of  the  genitalia,  and  enlargement  of  the  clitoris  or  penis,  conditions 
which  are  a  result  or  a  cause.  These  children  may  be  apparently  healthy. 
More  often  they  are  excitable,  neurotic,  or  show  signs  of  mental  back- 
wardness. Many  are  pale  and  debilitated.  On  the  whole  the  habit  must  be 
regarded  as  not  conducive  -to  mental  debility,  and  that  psychical  defect 
is  a  cause  not  a  sequel.  I  have  never  seen  any  definite  evil  results,  even  in 
■cases  which  have  continued  for  some  years. 

At  a  later  period  the  habit  is  most  common  in  boys  and  those  mentally 
•defective  or  highly  neurotic,  especially  about  puberty.  In  them  the  chief 
causes  are  local  irritation,  constipation,  overfeeding,  late  suppers,  alcohol, 
highly  stimulating  food,  evil  education  and  pernicious  literature.  There  are 
no  definite  local  signs.  These  boys  may  show  anaemia,  general  exhaustion, 
absent-mindedness  and  lack  of  memory.  Pallor,  dilated  pupils,  languor, 
■debility,  vague  pains,  capricious  appetite,  disinclination  for  work  or  play, 
headaches,  depression,  irritability,  shyness,  loneliness,  morbidness  and 
apathy  have  also  been  ascribed  to  excessive  indulgence  in  the  habit.  These 
are  symptoms  of  neurasthenia  and  may  occur  quite  independently.  Sexual 
.neurasthenia  often  begins  at  puberty. 


The  Genital  System.  607 

Diagnosis. — The  habit  is  easily  recognised  by  the  description,  and  not 
infrequently  will  be  practised  by  a  female  infant  while  under  observation. 
Many  cases  are  wrongly  diagnosed  as  'petit  mal  on  account  of  the  sequence 
of  spasmodic  movements  for  a  few  moments  and  sound  sleep. 

Prognosis  is  excellent  in  babies.  The  cure  depends  on  the  surround- 
ings of  the  child  and  the  amount  of  care  and  attention  which  it  receives. 
The  attention  must  be  constant  and  never  waver  by  day  or  night.  The 
child  must  never  be  left  alone,  unless  asleep.  If  there  is  mental  impairment, 
.so  often  present  in  cases  seen  in  young  children  beyond  the  age  of  infancy 
and  occasionally  in  the  infantile  cases,  the  outlook  is  bad  ;  but  the  prog- 
nosis is  that  of  the  mental  condition,  not  that  of  the  habit  which  may  persist 
and  do  little  harm,  unless  extreme.  Some  of  these  patients  practise  the 
habit  in  public.  A  boy,  6  years  old,  with  a  family  history  of  insanity,  had 
masturbated  for  4  years,  by  manustupration.  He  was  shy,  emotional, 
untruthful,  dyspeptic  and  thin.  Although  he  had  a  sense  of  shame  he  would 
masturbate  in  the  presence  of  other  children  and  adults.  The  penis  was 
large,  the  prepuce  contracted  and  partially  adherent,  and  there  was  much 
smegma  preputii.  It  is  criminal  to  alarm  parents  about  the  supposed  evil 
effects  of  this  habit,  and  they  are  very  grossly  exaggerated  by  the  quacks 
who  prey  upon  the  public. 

Treatment. — Every  possible  source  of  local  irritation  must  be  attended 
"to.  Circumcision  is  advisable  if  the  prepuce  is  narrow  and  adherent,  but  care 
must  be  taken  to  leave  enough  skin  to  cover  the  corona.  The  operation,  as 
sometimes  done,  is  in  my  opinion  a  not  uncommon  cause.  The  few  days 
rest,  and  the  impossibility  of  practising  the  habit  until  the  wound  is  healed, 
may  permanently  break  the  habit.  Clitoridectomy  is  not  permissible. 
It  has  been  followed  by  cure  but  there  is  no  evidence  that  the  result  was  due 
to  the  operation.  The  source  of  irritability  and  gratification  is  merely 
transferred  to  some  other  part  of  the  genitalia.  The  most  important  part 
•of  the  treatment,  after  attending  to  local  irritation,  is  to  keep  the  baby 
under  constant  observation  and  to  stop  her  as  soon  as  she  begins  the 
peculiar  movements.  The  thighs  can  be  kept  separated  by  very  large 
napkins,  made  of  non-irritating  material,  or,  if  napkins  are  the  supposed 
source  of  irritation,  by  a  mechanical  appliance,  such  as  a  couple  of  padded 
Jeather  cup-shaped  discs  applied  to  the  inner  surface  of  the  knees  and 
•connected  by  an  iron  rod  working  in  ball-and-socket  joints.  In  manu- 
stupration the  hands  must  be  fixed  so  that  they  cannot  be  used. 

Locally,  apply  to  the  vulvar  region  carbolic  lotion  1  per  cent.,  lead  or 
lead  and  opium  lotion,  or  salicylated  talc  powder.  Keep  the  bowels  open, 
attend  to  the  general  health  and  give  tonics,  bromides,  belladonna,  and 
alkalies.  Still  recommends  the  liquid  extract  of  salix  nigra.  Camphor, 
■chloral  and  cannabis  indica  may  be  useful. 

Similar  treatment  is  necessary  for  older  children.  Boys  must  not  be 
•allowed  to  sit  on  feather  cushions  or  soft  chairs,  or  sleep   on  feather  beds, 


608  Chapter   XL  VI I. 

nor  have  their  knickerbockers  too  warm  or  too  tightly  braced.  Combina- 
tion garments  are  often  unsuitable,  the  penis  being  subjected  to  friction 
through  slipping  in  and  out  of  the  opening.  Cold  baths  are  valuable 
for  children  over  4  years,  and  under  this  age  the  judicious  use  of  cold 
douching  in  the  lumbar  region  is  beneficial.  Let  the  child  have  plenty 
of  exercise,  except  riding  and  swarming  up  ropes  or  poles.  Allow  little 
animal  food,  no  alcohol  and  no  late  meals.  Put  to  bed  only  when  sleepy 
and  watch  the  child  until  asleep.  See  that  he  gets  up  immediate!}^  on  waking 
in  the  morning.    Allow  no  heavy  bedclothes. 

The  habit  must  be  regarded  and  treated  as  a  disease  in  infants,  and  as 
a  vice  only  when  it  develops  in  older  children  free  from  mental  defect. 
Such  cases  must  be  treated  by  moral  influence  as  a  bad  habit,  a  breach  of 
good  manners,  and  a  cause  of  physical  unfitness  for  games.  Keep  the 
child's  thoughts  away  from  it  by  providing  plenty  of  amusement,  constant 
occupation,  and  change  of  surroundings.  Above  all  do  not  be  alarmist  in 
talking  about  it  to  neurotic  children.  The  so-called  "  straight  talks  "  may 
do  more  harm  than  the  habit,  especially  if  a  religious  element  is  introduced. 
Punishment  is  useful,  even  in  early  cases,  and  must  not  be  neglected,  if 
the  child  is  old  enough  to  understand  that  the  habit  must  not  be  indulged 
in.  Blistering  the  penis  with  iodine  liniment  is  a  punitive  rather  than  a 
curative  treatment,  and  has  little  to  recommend  it.  Punitive  measures 
must  be  used  with  great  judgment  and  moderation.  Some  cases  are  good 
illustrations  of  the  old  maxim  that  "  to  spare  the  rod  is  to  spoil  the  child." 
Such  measures  must  only  be  adopted  and  carried  out  under  medical  advice 
and  supervision.  As  in  cases  of  enuresis  they  are  apt  to  be  overdone  and 
to  be  abominably  cruel. 

Menstruation. — Abnormal  discharge  of  blood  from  the  vagina  is  not 
always  precocious  menstruation.  It  may  result  from  injury,  foreign  bodies, 
inflammation,  tumours,  sepsis  or  various  blood  states ;  and  may  be 
simulated  by  bleeding  from  a  prolapsed  urethral  mucosa  or  from  other 
portions  of  the  genitalia.     ■  "  i 

Foetal  menstruation  is  a  red  vaginal  discharge  occasionally  noted  in 
newborns,  usually  on  the  5th-7th  day,  and  consisting  of  blood- 
stained mucus  and  clots.  It  lasts  for  1-7  days  and  does  not  recur.  It 
must  not  be  confused  with  haemorrhage  from  the  vagina  in  sepsis  neona- 
torum. Halban  (1904)  believes  that  it  is  analogous  to  true  menstruation. 
All  the  stages  from  premenstrual  hyperemia  up  to  subepithelial  haemor- 
rhages and  the  escape  of  blood  into  the  uterine  cavity  can  be  recognised, 
just  as  in  menstruation  of  ovarian  origin.  Changes  also  occur  after  the 
eighth  month  in  the  mammary  glands,  similar  to  those  in  the  mother's 
breasts,  and  the  uterus  enlarges.  The  involution  of  the  breast  and  uterus 
after  birth  takes  about  3  weeks.  Halban  states  that  comparative  changes 
occur  in  the  mammoe  and  prostrate  of  male  infants.  He  ascribes  it  to  some 
placental  secretion.    More  probably  it  is  due  to  some  substance  transferred 


The  Genital  System.  609 

from  the  mother.  (Edema  of  the  vulva  may  occur  from  the  same  cause  and 
be  analogous  to  oedema  of  the  penis  and  scrotum  sometimes  seen  in  boys, 
even  when  delivered  by  Caesarian  section. 

Precocious  menstruation  (menstruatio  praecox)  is  rarely  seen  before 
18  months  of  age.  It  is  commonly  associated  with  precocious  puberty, 
viz.,  hair  on  the  pubes  and  in  axillae,  erectile  nipples,  large  mamma;,  fully 
developed  genitals,  large  and  pigmented  labia  minora,  and  generally  an 
ovarian  or  adrenal  tumour  (p.  200).  Occasionally  it  takes  place  in  the 
absence  of  tumour  formation  ;  sometimes  in  imbeciles  ;  and  has  been 
reported  in  a  cretin,  aged  9  years,  with  reversion  to  a  more  infantile  state 
on  taking  thyroid  extract  (Kemble,  1905).  Senile  changes  commence  at 
a  much  earlier  age  than  normal.  The  mothers  of  some  of  these  children 
have  been  remarkably  fertile. 

Delayed  menstruation. — Normally  the  catamenia  appear  at  10-20  years 
of  age  ;  earlier  in  the  well-nourished  and  in  hot  climates  than  in  the  under- 
fed and  in  colder  regions.  The  usual  age  is  this  country  is  14-17  years. 
Amenorrhcca  may  be  due  to  congenital  defects,  such  as  atresia  of  the 
vagina,  aplasia  of  the  uterus  or  ovaries  ;  pulmonary  stenosis  or  morbus 
cordis,  leading  to  delayed  development  ;  and  functional  or  constitutional 
anomalies.  A  foetal  uterus  is  associated  with  lack  of  pubic  hair  and  of 
mammary  enlargement. 

Puberty. — Sexual  maturity  depends  on  race,  climate,  nutrition,  growth 
and  other  factors.  It  occurs  earlier  in  some  families  than  others,  earlier 
in  girls  than  in  boys,  and  is  stimulated  by  alcohol  and  premature  sexual 
intercourse.  It  is  present  before  the  onset  of  the  catamenia  in  so  far  as 
the  possibility  of  impregnation  is  existent.  Maternity  has  been  reported 
at  8  years  of  age.  Probably  in  remote  ages  females  did  not  menstruate, 
being  impregnated  first,  and  the  development  of  the  function  is  the  result 
of  the  customs  of  civilisation  postponing  impregnation  to  a  more  mature 
age. 

Puberty  is  characterised  by  enlargement  of  the  thyroid  gland,  growth  of 
hair  on  the  pubes  and  axillae,  development  of  the  sexual  organs  and 
functions,  and  mental  and  psychical  changes.  In  girls  the  mammae  develop, 
pelvis  enlarges,  buttocks  and  thighs  become  fatter,  respiration  more  costal, 
and  the  larynx  enlarges  in  a  vertical  direction,  the  voice  occasionally 
cracking.  In  boys  hair  begins  to  appear  on  the  face,  back  and  chest ;  the 
larynx  grows  chiefly  in  its  transverse  diameter  and  the  voice  cracks,  the 
thorax  increases  in  breadth  and  circumference,  breathing  is  more  abdominal ; 
and  semen  appears  in  the  fourteenth  year.  Growth  of  bones  and  muscles 
is  very  rapid  at  this  period.  It  is  most  marked  in  girls  at  12-15,  and  in 
boys  at  14-17  years  of  age,  beginning  rather  earlier  in  large  than  in  small 
children.  Both  physical  and  psychical  development  take  place  by  leaps  and 
bounds,  rather  than  by  steady  progression,  and  vary  much  in  different 
children.     Overgrowth  leads  to  undue  strain  on  the  heart,  and  perhaps 

2   R 


610  Chapter  XL  VI I. 

relatively  unequal  development  of  the  body,  heart  and  blood  vessels.  Yet 
the  heart  nearly  doubles  itself  in  size  and  the  left  ventricle  may  be  hyper- 
'trophied.  Hence  arise  feeble  pulse,  palpitations,  dilatation  and  irregularity, 
shortness  of  breath,  syncopal  attacks  and  vertigo.  Nervous  palpitations, 
anorexia,  dyspepsia,  constipation,  inertia,  irritability  and  insomnia  are  not 
infrequent  for  some  weeks  or  months  before  the  first  menstruation. 
Stooping,  lateral  curvature  and  genu  valgum  depend  on  muscular  debility 
and  unnatural  attitudes.  Vasomotor  instability  shows  itself  in  blushing, 
functional  albuminuria,  angioneuroses,  syncope,  etc.  Anaemia,  headache 
and  epistaxis  are  common.  Chlorosis  in  girls  is  possibly  due  to  the  with- 
drawal of  iron  from  the  blood  and  its  storage  in  the  liver  in  preparation  for 
maternity.  Vague  pains  and  sensations  are  felt  in  the  breasts  and  lower 
abdomen.  Acne,  styes,  frequent  urination,  and  the  effects  of  constipation, 
the  result  of  shyness  and  false  modesty,  are  quite  common.  Boys  develop 
a  sense  of  superiority  and  girls  one  of  protective  duties.  Malnutrition  and 
exaltation  of  the  cerebral  processes  lead  to  neurasthenia,  hysteria  and  even 
epilepsy. 

The  age  of  puberty  or  adolescence  lasts  from  12-18  years,  and  the  vital 
processes  are  exalted  throughout  but  chiefly  at  the  periods  of  most  active 
growth.  Important  functions  arise  and  develop.  The  mortality  is  low  but 
the  tendency  to  disease  is  high.  The  development  of  normal  periodicity 
in  girls  is  of  the  utmost  importance  and  should  take  precedence  of  that  of 
mind  and  muscle.  There  is  a  craving  for  knowledge  of  mind  and  body, 
and  a  delight  in  rhythm,  music  and  singing.  Sentiment,  self-consciousness, 
love,  religious  feeling  and  ambition  arise.  It  is  the  age  of  hopes,  ideals  and 
tender  sentiments.  Yet  the  ideas  are  inchoate,  the  mind  lacking  in  precision 
and  conscious  power,  there  is  a  liability  to  exaggeration  and  excess,  and  the 
feelings  fluctuate  rapidly  in  character.  The  birth  of  imagination  leads  to 
reverie,  inner  absorption,  musing,  brooding  and  even  illusions.  Vivid 
ideas  seem  realities  to  some  imaginative  children.  The  critical  faculties  are 
defective,  yet  there  is  a  consciousness  of  self,  over-sensitiveness  and  self- 
criticism.  This  leads  to  over-assertion  and  the  bumptiousness  of  youth. 
The  vocabulary  is  enlarged  and  words  have  a  more  definite  meaning.  It  is 
the  age  of  folly,  of  imitation,  of  dramatic  rules  and  poses.  Even  now  the 
general  tendency  is  objective  rather  than  subjective,  and  training  should  be 
manual,  gymnastic,  in  sports  and  games,  and  industrial  as  well  as  mental 
and  moral.  The  disorders  of  this  period  of  life  are  commonly  those  of  arrest, 
defect  or  excessive  development  of  some  organ  or  function.  Hence  arise 
hooliganism,  perversions,  juvenile  crime  and  secret  vice.  Many  of  the 
ailments  at  this  period  depend  on  the  mode  of  life,  notably  school  life, 
rather  than  the  age  itself. 

Hysterical  symptoms  are  very  common,  and  include  abnormal  appetite, 
pica,  fasting,  barking  cough,  stuttering  and  convulsive  disorders.  Hysteria 
is  often  due  to  a  sexual  shock  which  is  brooded  over  in  secret  and  can  be 


The   Genital  System.  611 

■cured  by  talking  about  it.  In  the  mentally  defective,  a  state  sometimes 
first  noted  at  puberty,  there  may  arise  all  kinds  of  mental  and  psychical 
•disorders.  Vicious  habits  may  be  unduly  developed  by  imitation,  bad 
companionship,  and  insufficient  supervision  in  the  organisation  of  school 
life.  Excess  depends  mainly  on  inherited  nervous  instability.  Excessive 
■dieaming,  somnambulism  and  migraine  may  occur.  Troublesome  disorders 
•of  menstruation  begin.  The  first  period,  more  often  a  subsequent  one,  may 
be  profuse  and  even  fatal.  I  have  known  it  cause  profound  aneemia.  It 
should  be  treated  by  calcium  salts,  ergot  and  bromides.  Possibly  horse 
,-serum  may  do  good.  Irregularity  at  the  onset  and  for  some  months  is 
frequent  and  quite  unimportant.  Signs  of  imperforate  hymen  will  appear 
.at  this  age. 

Treatment. — The  diet  must  be  liberal  and  may  err  on  the  side  of  excess 
as  long  as  it  is  limited  to  simple  foods.  It  should  contain  an  ample  supply  of 
calcium  for  the  growing  bones,  phosphorus  for  the  brain,  protein  for 
muscles,  carbohydrates  for  exercise,  and  fat  for  heat.  A  free  supply  of 
oxygen  is  needed  for  metabolism.  Milk,  eggs,  cheese,  fruit  and  vegetables 
should  be  allowed  freely.  The  dress  must  be  arranged  so  that  there  is  no 
compression  of  the  neck,  chest  or  abdomen  ;  and  the  weight  be  chiefly 
supported  by  the  hips  and  shoulders.  From  9-10  hours  sleep  are  needed. 
The  work,  posture  at  work,  games  and  exercise  should  be  carefully  regulated ; 
guarding  against  mental  and  physical  overstrain,  as  in  cycling  and  long 
-distance  running.  Judicious  guidance  is  of  the  utmost  value  in  directing 
~the  emotional,  psychical  and  mental  development.  Fortunate  is  the  child, 
who  is  under  a  suitable  and  sympathetic  teacher,  for  the  future  may  be 
jnade  and  still  more  easily  marred. 


CHAPTER    XLVIII. 

THE    NERVOUS    SYSTEM. 

Peculiarities — Examination — Reflexes    and    Special    Signs    of   Disease — 
Cerebrospinal   Fluid — Electricity — Classification  of    Diseases. 

The  brain  at  birth  is  immature  and  its  convolutions  are  flattened  and 
badly  defined.  It  weighs  from  9-12  oz.,  being  roughly  about  one-twelfth 
of  the  body  weight  but  not  directly  proportionate  thereto.  It  grows  and 
develops  rapidly  and  at  the  end  of  the  first  year  weighs  about  30  oz.  Up 
to  the  seventh  year  it  grows  less  rapidly  and  then  quite  slowly.  At  all. 
ages  the  male  brain  is  heavier  than  the  female.  In  the  newborn  the  frontal 
lobes  are  inconspicuous  and  the  Island  of  Reil  is  not  well  differentiated. 
On  section  it  is  much  more  grey  because  of  the  deficiency  in  myelin.  The 
special  centres  are  hardly  defined  during  the  first  2  years  of  life  and  cerebral, 
lesions  are  localised  with  much  greater  difficulty  than  in  adults. 

The  dura  mater  is  peculiar  in  early  life  in  that  it  is  closely  adherent  to 
the  skull  and  can  with  difficulty  be  separated  from  it ;  thus  preventing 
extravasations  between  the  membranes  and  the  hone.  The  amount  of 
subarachnoid  fluid  is  relatively  laiger  than  in  later  life.  There  are  no. 
Pacchionian  bodies. 

The  spinal  cord  measures  14  cm.  and  extends  to  the  lower  extremity  of 
the  vertebral  canal  up  to  the  end  of  the  third  month  of  foetal  life.  There 
is  no  cauda  equina.  At  birth  the  termination  is  opposite  the  body  of  the 
third  lumbar  vertebra  and  it  gradually  ascends  until  in  adult  life  it  is. 
opposite  the  body  of  the  first  lumbar  vertebra.  The  vertebral  canal  grows, 
more  rapidly  than  the  spinal  cord. 

In  structure  the  nervous  system  differs  in  its  immaturity  in  early  life 
from  that  of  adults.  Neither  its  nerve  centres  nor  its  nerve  tracts  are 
fully  localised  or  developed.  The  spinal  cord  possesses  almost  its  full 
complement  of  myelin  at  birth  but  some  of  the  axis  cylinders  have  not 
acquired  their  medullary  sheaths.  The  brain  stem,  cerebellum  and  large 
portions  of  the  cerebrum  are  devoid  of  myelin,  and  myelinisation  is  not. 
complete  before  the  ninth  month.  Seeing  that  the  higher  centres  are 
imperfectly  developed  and  the  nerve  tracts  ill-defined,  the  lower  centres  are 
incompletely  controlled.  Hence  arise  defective  co-ordination,  spasmodic 
muscular  contractions  and  unchecked  reflex  excitability.  Development 
is  very  rapid,  and  there   is   great  liability  to   temporary  or  permanent- 


The   Nervous  System.  613 

disturbance  of  function  and  to  organic  disease.  The  whole  nervous  system 
is  peculiarly  sensitive,  very  excitable,  and  responds  with  immense  energy 
to  all  forms  of  stimulation.  It  lacks  stability  and  its  inhibitory  powers 
are  not  developed.  At  birth  and  for  many  months  after  the  infant  responds 
freely  to  all  kinds  of  reflex  irritation.  The  response  is  irregular  in  its 
manifestation  and  the  symptoms,  arising  from  causes  which  in  adults  would 
produce  no  effect,  may  be  serious  and  even  fatal,  as  is  the  case  in  con- 
vulsions due  to  errors  of  diet.  Convulsions,  unconsciousness  and  many 
functional  disorders  may  be  due  to  various  kinds  of  simple  reflex  irritation. 
Twitchings  and  deliiium  are  common  in  fever. 

Organic  lesions  in  early  life  produce  a  profound  effect  from  the 
immediate  destruction  of  tissue  and  from  interference  with  the  subsequent 
development  of  the  damaged  parts.  Thus  embolism,  thrombosis  or 
haemorrhage  may  hinder  the  development  of  the  brain  and  cause  paralysis 
and  varying  degrees  of  idiocy.  On  the  other  hand  damage  to  the  brain  in 
infancy  may  be  recovered  from  more  readily  than  in  adults.  For  instance, 
aphasia  due  to  destruction  of  the  speech  centre  on  the  left  side  during  the 
first  three  or  four  years  of  life  may  be  repaired  by  the  education  of  the 
speech  centre  on  the  opposite  side.  Aphasia  in  early  infancy  is  rarely 
permanent.  Bearing  in  mind  the  immaturity  of  the  brain  it  is  important 
that  it  should  not  be  overstrained  or  overstimulated.  Functional  strain, 
especially  when  combined  with  malnutrition,  is  a  fruitful  source  of  functional 
nervous  disorders  such  as  headache,  pavor  nocturnus,  somnambulism, 
neurasthenia,  chorea,  and  possibly  epilepsy  and  insanity.  Alcohol,  tea, 
coffee  and  other  stimulants,  and  highly  seasoned  foods  are  to  be  avoided 
during  early  life,  as  well  as  all  those  forms  of  mental  stimulation  included 
under  over-education  and  the  amusements  of  city  life.  To  these  causes  are 
due  many  of  the  neurotic,  excitable  children  seen  in  large  towns. 

Examination  of  the  Nervous  System. — The  younger  the  child  the 
greater  is  the  dependence  of  the  doctor  upon  objective  symptoms  and  his 
own  powers  of  observation.  Once  the  child  is  able  to  talk  a  certain  value 
■can  be  attached  to  what  it  complains  of,  bearing  in  mind  that  children  have 
not  learned  to  give  accurate  expression  to  their  feelings.  There  is  nearly 
always  exaggeration  of  all  subjective  symptoms,  especially  pain.  Atten- 
tion must  be  paid  to  the  family  history  for  some  organic  diseases  and  psychical 
disorders  depend  upon  heredity.  Alcoholism,  syphilis,  tuberculosis,  hysteria, 
epilepsy  or  insanity  in  one  or  other  parent  may  have  an  important  bearing 
on  the  diagnosis. 

A  past  history  of  febrile  disorders,  specific  fevers,  rheumatism,  sore- 
throat  or  injury,  may  indicate  the  possibility  of  meningitis,  acute  polio- 
myelitis, peripheral  neuritis,  embolism  and  such  like  diseases.  Over- 
excitement  or  errors  in  diet  may  point  to  the  possibility  of  severe  nerve 
storms  being  purely  functional.  On  the  other  hand  many  serious  and 
permanent  affections,  e.g.  infantile  paralysis  and  muscular  dystrophies, 


614  Chapter   XL  VIII. 

may  come  on  so  insidiously  as  not  to  attract  the  attention  of  either  the 
parents  or  the  nurse,  and  it  is  frequently  impossible  to  ascertain  the  date 
of  their  origin.  The  presence  of  rickets  and  the  nature  of  the  environment- 
must  be  noted. 

Superficial  examination  may  give  valuable  information.  Thus  the 
lateral  decubitus  and  retraction  of  the  head  suggest  basal  meningitis. 
Constantly  putting  the  hand  to  the  head  or  ear  may  indicate  headache  or 
otitis  media.  Involuntary  signs  of  pain  when  a  limb  is  moved  or  absolute 
flaccidity  of  one  or  more  limbs,  while  the  others  are  moved  freely,  are  also 
suggestive.  Cranial  and  facial  peculiarities  are  sometimes  present  in 
cerebral  disease.  Among  these  may  be  mentioned  macrocephaly,  micro- 
cephaly, hydrocephaly,  asymmetry,  brachycephaly  and  dolichocephalyr 
the  facial  aspect  of  the  Mongolian  imbecile,  and  the  fatuous,  stupid  or 
blankly  pleasant  expression  of  some  other  forms  of  imbecility.  A  large 
tense  fontanelle,  or  a  prematurely  closed  one,  and  separation  of  the  sutures- 
may  be  of  great  significance. 

Sensory  disturbances  are  difficult  to  estimate.  In  the  very  young 
many  sensory  variations  cannot  even  be  recognised.  Pain  is  often  exagger- 
ated and  may  be  very  vaguely  localised  and  described  by  intelligent 
children.  It  almost  invariably  signifies  disease  and  in  the  very  young  should 
not  be  ascribed  to  neuralgia.  Headache  must  never  be  disregarded  for 
it  is  often  the  first  and  for  some  time  the  only  symptom  of  organic  brain 
disease  or  febrile  disorders,  notably  typhoid  fever.  After  school  age 
headache,  neuralgia  or  migraine  may  arise  from  overwork.  A  facial 
neuralgia  may  be  due  to  a  bad  tooth.  In  a  boy,  8  years  old,  it  was  a 
troublesome  symptom  and,  although  a  dental  surgeon  could  find  nothing 
the  matter  with  the  teeth,  a  stopping  subsecpiently  became  loose  and 
revealed  underlying  caries.    This  was  attended  to  and  the  neuralgia  ceased. 

Visual  disturbance  may  be  uniecognised  until  the  end  of  the  first  year 
or  later.  Photophobia  is  obvious.  Temporary  or  permanent  amaurosis 
is  shown  by  the  fact  that  the  infant  pays  no  attention  to  a  bright  light, 
will  not  follow  a  light  or  other  object  held  in  front  of  the  eyes,  does  not 
blink  under  these  conditions,  and  still  more  so  if  the  pupils  do  not  react 
to  light.  Deafness  is  difficult  to  determine  in  infancy.  It  is  suspected  when 
no  attention  is  paid  to  sudden  loud  sounds.  In  testing  the  hearing  care 
must  be  taken  to  exclude  vibrations  which  might  attract  the  attention 
although  the  child  is  deaf.  The  senses  of  taste,  smell,  temperature  and 
muscular  sense  are  so  difficult  to  estimate  in  infants  that  it  is  rare  for  any 
information  to  be  gained  from  a  most  thorough  examination  of  these 
functions.  The  intellectual  faculties  can  only  be  roughly  estimated.  An 
intelligent  mother  will  note  whether  the  infant  is  more  backward  than 
her  other  children  were  at  the  same  age,  or  in  comparison  with  those  of  her 
friends.  She  may  note  vacancy  of  expression,  clumsiness  or  inco-ordination 
of  movement,  and  lack  of  interest  in  toys  and  surroundings.     The  doctor 


The  Nervous  System.  615 

may  make  similar  observations  but,  unless  he  sees  the  child  on  several 
occasions,  it  is  extremely  difficult  to  ascertain  whether  the  mental  condition 
is  imbecile  or  merely  backward. 

The  motor  junctions  are  more  easily  studied.  It  is  easy  to  recognise 
partial  or  complete  immobility  of  a  limb.  Care  must  be  taken  to  make  sure 
that  the  immobility  is  due  to  true  paralysis  and  not  to  local  disease,  such  as 
epiphysitis,  scurvy,  etc.  It  is  then  necessary  to  ascertain  whether  the 
paralysis  is  cerebral,  spinal  or  neural  in  origin,  or  due  to  primary  muscular 
dystrophy.  The  association  of  paralysis  with  atrophy  or  spasticity,  the 
condition  of  the  reflexes,  and  the  electrical  reactions  are  of  great  value,  but 
electrical  reaction  is  difficult  to  test  in  early  life.  Fibrillary  and  idio- 
muscular  contraction,  tremor,  inco-ordination  and  athetosis  must  be 
noted. 

Reflex  action  can  be  tested  without  difficulty.  Certain  special  signs  of 
nervous  irritability  must  be  mentioned. 

1.  The  Babinshi  Sign,  sometimes  called  the  plantar  or  great  toe 
reflex. — Babinski  found  that  in  disease  of  the  motor  tract  dorsal  flexion,  i.e., 
extension  of  the  toes  especially  the  great  toe,  resulted  from  reflex  irritation 
of  the  sole  of  the  foot.  Normally  two  reflexes  can  be  obtained  on  irritating 
the  sole  ;  viz.  simple  plantar  flexion,  due  to  a  weak  stimulus  and  ascribed 
to  a  cortical  reflex  ;  and  dorsal  flexion  of  the  toes  and  combined  movements 
of  the  leg,  due  to  a  strong  stimulus  and  ascribed  to  a  spinal  reflex.  In 
Babinski's  sign  dorsal  flexion  results  from  a  slight  stimulus  and  therefore 
the  spinal  reflex  is  exaggerated.  It  may  be  due  to  increased  excitability 
of  the  cord  by  strychnia,  or  diminished  excitability  of  the  coitex  as  in 
stupor  and  bromism  ;  or  it  may  depend  upon  interruption  of  the  motor 
tract.  The  sign  does  not  necessarily  indicate  disease  of  the  motor  tract 
and  it  is  frequently  present  if  the  excitability  of  the  cord  is  increased.  It 
is  constantly  present  in  the  newborn  for  the  cord  is  excitable  and  the 
motor  tract  imperfectly  developed.  Of  babies  under  2  years  of  age  the 
plantar  reflex  is  absent  in  one-third  ;  in  one-fourth  there  is  bilateral  dorsal 
flexion  and  in  one-fourth  bilateral  plantar  flexion.  In  the  remainder  the 
reflex  may  be  absent  on  one  side  and  cause  flexion  or  extension  on  the 
other ;  or  there  may  be  flexion  on  one  side  and  extension  on  the  other. 
There  is  no  constant  reflex  duiing  the  first  year,  and  during  the  second 
year  it  is  inconstant  but  approaches  the  adult  type.  Dorsal  flexion  is  present 
in  50  per  cent,  at  the  end  of  the  fiist  year.  In  the  third  year  plantar  flexion 
is  found,  unless  delayed  by  rickets.  The  extensor  response  is  common  in 
children  during  sleep,  so  the  test  must  be  applied  while  awake.  The  sign 
is  of  no  practical  value  before  the  third  year  of  life. 

2.  MendeVs  Reflex  is  said  to  be  of  more  value  than  Babinski's.  Place 
the  foot  with  its  inner  surface  on  a  firm  basis  and  percuss  the  dorsal  tendons. 
The  normal  response  is  dorsal  flexion  of  the  second  to  the  fifth  toes  and  is 


616  Chapter   XL  VIII. 

present  in  functional  affections.    Plantar  flexion  occurs  in  organic  disease, 
except  tabes. 

3.  Schafeis  Reflex  is  an  extensor  toe  response  obtained  by  pressure 
over  the  insertion  of  the  gastrocnemius  or  by  pinching  the  overlying  skin. 
It  indicates  pyramidal  degeneration. 

4.  Oppenheimer' 's  Sign. — Tapping  the  middle  of  the  posterior  surface 
of  the  tibia  from  above  downward  with  a  hammer  causes  plantar  flexion 
of  the  toes  in  the  healthy  and  contraction  of  the  extensors  of  the  leg  in 
the  spastic. 

5.  BrudzinsJci's  Contra-lateral  Reflexes  in  the  lower  limbs  are  of  two 
kinds.  On  flexing  the  sound  limb  forcibly  in  hempilegia  the  paralysed 
limb  executes  a  movement  of  extension.  This  is  called  the  "  reciprocal  " 
reflex.  In  the  other  type,  known  as  the  "  identical  "  reflex,  flexion  of  the 
sound  limb  induces  flexion  instead  of  extension  ;  and  in  other  cases 
extension  induces  extension.  The  identical  reflex  is  said  to  be  constant  in 
tuberculous  and  cerebrospinal  meningitis,  disappearing  during  recovery. 
One  or  other  may  be  found  in  backward  children,  Mongols,  idiots  and 
Little's  disease. 

6.  Kernigs  Sign  was  first  described  in  1880.  With  the  thigh  flexed 
at  a  right  angle  to  the  trunk  the  leg  cannot  be  straightened  without  pain 
on  account  of  contraction  of  the  flexors.  It  is  ascribed  to  increased 
irritability  of  the  lumbar  and  sacral  nerve  roots,  due  to  meningeal  inflam- 
mation. Flexion  of  the  thigh  stretches  these  roots,  increases  their 
irritability  and  causes  reflex  contraction  of  the  flexors.  It  is  especially 
apt  to  occur  in  meningitis  of  the  cerebrospinal  type  and  has  been  noted  in 
cerebellar  tumour,  subdural  and  intracerebral  haemorrhage,  thrombosis 
of  the  lateral  sinus,  and  occasionally  in  other  diseases  such  as  enteric  fever 
and  uraemia.  It  is  a  fairly  constant  sign  in  meningitis  but  its  absence  does 
not  exclude  this  diagnosis.  It  is  more  often  absent  in  the  tuberculous  than 
other  varieties  of  meningitis.  It  may  vary  from  time  to  time  in  the  course 
of  the  disease,  is  not  associated  with  increased  rigidity  elsewhere,  and 
usually  persists  for  some  time  during  convalescence.  The  sign  has  been 
noted  in  the  arms.  Possibly  it  is  not  a  reflex  and  is  due  to  exaggeration  of 
a  normal  condition,  the  effect  of  hypertonicity  of  the  muscles. ' 

7.  Trousseau's  Phenomenon,  or  the  "  median  nerve  reflex." — Pressure 
on  the  internal  bicipital  groove,  or  elastic  compression  of  the  arm  for  a  few 
minutes  sufficient  to  cause  cyanosis  and  pain,  produces  the  gynaecological 
hand  in  tetany.  It  is  due  to  pressure  on  the  blood  vessels  or  nerves.  In 
children  pronation  of  the  hand  and  some  adduction  of  the  fingers  is  the 
usual  response.  It  is  a  sign  of  nerve  irritability.  A  contraction  of  the 
hand  in  infants  of  6-8  weeks  old,  induced  by  pressure  on  the  nerves  of  the 
brachial  plexus,  has  been  described  by  Hochsinger  as  the  ''''phenomenon  of 
the  fist,''''   or   "  myotonia  of  the  newborn."     In   a   marked  case  flexor  or 


The   Nervous  System.  617 

•extensor  spasm  is  persistent,  varying  in  intensity  and  lasting  for  a  few  days 
to  several  weeks.  Usually  the  child  "  makes  a  fist."  It  may  simulate  the 
tetanoid  position.  Apparently  it  is  ot  the  same  nature  as  Trousseau's 
sign,  and  occurs  in  gastro-intestinal  auto-intoxication,  severe  nutritional 
•disturbance  and  tetany  in  the  first  few  months  of  life.  But  it  is  not 
.associated  with  the  other  signs  of  nerve  irritability.  Probably  it  is  a  mild 
type  of  tetany. 

8.  ChvosteJcs  Sign,  or  the  Facial  Phenomenon,  is  an  exaggerated 
•excitability  of  the  facial  nerve  and  muscles.  A  slight  touch,  tap  or  pressure 
•on  the  seventh  nerve  in  front  of  the  ear,  or  a  tap  on  the  face  below  the  malar 
bone,  causes  rapid  contraction  of  the  eyelids  and  mouth  and  twitching  of 
the  side  of  the  face.    Other  exposed  nerves  are  similarly  excitable. 

9.  ErUs  Sign  is  an  increased  irritability  of  the  nerve,  especially  the 
-ulnar  nerve,  and  muscles  to  electrical  currents,  notably  galvanism. 
Finkelstein  asserts  that  it  exists  in  30  per  cent,  of  infants  fed  on  cow's 
milk  or  whey. 

10.  The  Phenomenon  of  the  Phrenics  is  a  name  given  by  Solovieff 
to  rhythmical  contractions  of  the  diaphragm,  synchronous  with  the 
movements  of  the  heart. 

Trophic  disturbance  is  indicated  by  wasting  of  muscles,  glossy  skin, 
bed-sores,  pigmentation  and  skin  eruptions,  disorders  of  the  nails  and 
hair,  and  ulceration  of  the  cornea.  Variations  in  surface  temperature, 
•coldness  of  paralysed  limbs,  liability  to  chilblains,  and  patchy  redness  or 
lividity  of  the  affected  limb  are  partly  trophic,  partly  vasomotor  in  origin. 

Cerebrospinal  Fluid  is  a  true  secretion,  probably  from  the  choroid 
plexus.  It  passes  through  the  foramen  of  Majendie  into  the  subarachnoid 
space.  It  is  obtained  from  the  ventricles  after  death,  and  during  life  by 
tapping  the  vertebral  canal  in  the  lumbar  region.  Examination  of  the 
fluid  is  valuable  in  diagnosis.  Lumbar  juncture  was  introduced  by  Quincke 
in  1891  for  the  relief  of  chronic  hydrocephalus.  It  had  been  utilised  by 
Essex  Wynter  at  the  Middlesex  Hospital  in  1889.  It  is  almost  free  from 
risk,  if  properly  carried  out.  Ossipow  (1901)  collected  12  fatal  cases. 
Headache,  nausea  and  vomiting,  giddiness,"  palpitations,  haemorrhage 
into  the  canal  and  sudden  death  have  been  observed.  Although  I  have  used 
the  method  in  a  large  number  of  children  I  have  never  seen  any  bad 
symptom.  The  patient  should  be  kept  quiet  for  24  hours  afterwards,  so  the 
operation  is  not  available  for  out-patients. 

The  strictest  antiseptic  precautions  must  be  adopted.  Place  the 
•child  on  the  right  side  with  the  knees  and  thighs  well  flexed,  the  head 
and  trunk  bent  forward  and  the  left  shoulder  depressed,  in  order  to  separate 
the  intervertebral  spaces  as  widely  as  possible  ;  or  in  the  sitting  posture 
with  the  head  and  trunk  bent  forward.  An  anaesthetic  is  rarely  needed. 
If  required,  give  a  whiff  of  chloroform  or  apply  the  ethyl  chloride  spray  or 


618  Chapter  XL  VIII. 

cocaine  locally.  Use  an  antitoxin  or  small  exploring  needle,  about  5  cm. 
long,  attached  to  a  syringe  as  a  handle.  Cleanse  the  site  of  puncture 
thoroughly.  Insert  the  needle  vertically  to  the  surface,  1  cm.  from  the^ 
middle  line  in  the  space  between  the  second  and  third,  or  the  third  and 
fourth  lumbar  vertebrae  opposite  the  upper  edge  of  the  lower  spinous- 
process,  and  direct  it  slightly  upward  and  inward.  Or  the  median  line  may 
be  chosen  and  the  needle  inserted  between  the  third  and  fourth  lumbar- 
vertebra?,  through  the  interpeduncular  ligament  which  is  soft  and  yielding. 
in  children.  In  older  subjects  the  ligamenta  subnava  are  thick  and  tough,, 
like  indiarubber,  and  resistant.  The  depth  of  the  canal  from  the  surface 
varies  with  the  age  and  nutrition  of  the  child.  In  babies  the  needle  enters- 
the  subarachnoid  space  at  a  depth  of  2-3  cm.  If  it  is  pushed  in  too  far,  it 
ma  y  wound  the  plexus  of  veins  on  the  anterior  portion  of  the  dura  mater.. 
The  fluid  flows  out  drop  by  drop,  in  a  gentle  stream  or  in  spurts,  according, 
to  the  pressure.  Suction  is  unnecessary,  and  aspiration  may  cause  sudden, 
reduction  in  pressure  and  unpleasant  symptoms.  Keep  the  child  still,, 
for  movement  may  break  the  needle  or  cause  bleeding.  Remove  the 
needle,  if  the  pulse  fails  or  the  child  turns  faint.  Collect  10-15  c.c.  of  fluid 
in  a  sterile  test  tube  and  plug  with  sterile  wool.  From  a  few  drops  to  4  oz. 
may  be  drawn  off.  It  is  rarely  advisable  to  remove  more  than  2  oz..  at.  a. 
time. 

Make  cultures  on  blood  serum,  serum  agar  and  agar  agar.  Inoculate^ 
guinea  pigs  as  soon  as  possible,  or  fibrin  formation  may  interfere.  Centri- 
f ugalise  the  remainder,  or  stand  it  for  several  hours,  and  make  films  from 
the  deposit.  Stain  and  examine  microscopically.  Estimate  the  quantity 
of  albumin. 

Normal  Fluid  is  clear,  colourless,  faintly  alkaline  and  sterile.  Its. 
specific  gravity  is  1003-1008.  It  is  free  from  morphological  elements,  except 
a  few  lymphocytes  on  centrifugalisation,  and  contains  no  ferment  or 
fibrinogen.  It  contains  chlorides,  traces  of  carbonates,  phosphates,  urea, 
and  cholin,  and  of  a  glucose-like  substance,  which  reduces  Fehling's. 
solution  and  has  been  definitely  shown  by  Halliburton  to  be  sugar.  Serum 
globulin  or  albumin  is  present  in  amounts  of  0-01-0-1  per  cent. 

Abnormal  Fluid  may  be  clear,  turbid,  opalescent,  purulent  or  bloody- 
Blood  is  due  to  injury  of  the  venous  plexus,  Or  to  bleeding  into  the 
ventricles  or  the  subdural  space.  It  may  be  deficient  in  albumin  in  chronic 
hydrocephalus  or  contain  an  excess  in  inflammatory  disease.  As  a  general, 
principle  the  presence  of  a  mere  trace  of  albumin  negatives  acute  inflam- 
mation and  a  distinct  increase  in  the  amount  excludes  simple  hydiocephalus.. 
Coagulation  is  a  sign  of  inflammation.  In  tuberculous  meningitis  the  fluid 
is  clear  or  cloudy,  sometimes  opalescent,  sugar  is  absent  and  a  fibrin  network, 
slowly  forms.  The  albumin  is  0-15-0-2  per  cent.  (Eeiken).  Cells  are 
occasionally  absent.  More  commonly  there  is  a  lymphocytosis,  varying  in. 
degree.    In  a  few  cases  I  have  found  an  excess  of  polymorphs  ;   possibly  a. 


The  Nervous  System.  619- 

sign  of  severity  or  of  secondary  infection.  In  cerebrospinal  meningitis  the 
fluid  may  be  clear  at  first  in  the  meningococcal  type  and  turbid,  containing 
pus,  in  later  stages.  In  other  varieties  it  is  generally  turbid,  opaque,, 
yellow  or  greenish,  perhaps  pure  pus.  Its  characters  may  vary  in  the 
course  of  the  disease.  Sugar  is  diminished  or  absent.  Albumin  reaches 
0-2-0-4  per  cent.  The  percentage  of  polymorphs  reaches  80-90  per  cent. 
In  chronic  meningococcal  cases,  at  the  onset  or  in  the  course  of  the  disease,, 
the  cells  may  be  chiefly  lymphocytes.  Sometimes  only  a  few  are  found. 
Cells  are  absent  in  icterus  neonatorum,  acute  phthisis,  typhoid  fever  and 
dropsical  effusions. 

Bacteriology. — Negative  results  are  of  little  value.  Tubercle  bacilli,, 
streptococcus  pyogenes,  staphylococci,  meningococci,  pneumococci,  b. 
coli  and  b.  typhosus  have  been  found.  On  careful  examination  the  tubercle 
bacillus  will  be  found  in  most  cases  of  tuberculous  meningitis,  by  staining 
the  fine  clot  or  deposit. 

Pressure  can  be  measured  by  Eve's  cerebrospinal  manometer,  but 
there  are  many  sources  of  error  and  the  rate  of  flow  affords  quite  sufficient 
information.  Sometimes  fluid  cannot  be  obtained  for  the  needle  becomes 
blocked.  Or  it  may  be  found  on  one  occasion  and  not  on  another,  the 
foramen  of  Majendie  being  obstructed  and  the  fluid  confined  to  the 
ventricles. 

Therapeutically  lumbar  puncture  is  adopted  for  the  relief  of  pressure,. 
1-4  oz.  being  removed  at  a  time.  In  chronic  hydrocephalus  it  has  proved 
of  temporary  benefit  but  the  fluid  re-collects.  It  may  lessen  headache, 
coma  and  the  other  effects  of  pressure  in  meningitis,  and  possibly  be  of  use 
by  removing  microbes  and  toxins.  It  induces  passive  hypersemia  of  the 
cerebrospinal  vessels,  if  much  is  removed,  and  such  hypersemia  may  be 
beneficial  in  tetany.  Its  curative  value  is  doubtful.  The  injection  of  fluids- 
and  drugs  into  the  vertebral  canal  in  the  treatment  of  disease  is  merely  in 
the  experimental  stage. 

Electrical  Currents  are  used  for  diagnosis,  prognosis  and  treatment ; 
generally  the  Galvanic,  continuous  or  constant  current,  and  the  Faradic, 
induced  or  interrupted  current.  Static  electricity  and  the  sinusoidal 
current  are  of  little  use.  Galvanism  causes  a  single  contraction  when  the 
current  is  suddenly  run  into  or  cut  off  from  the  muscle  ;  i.e.  suddenly 
interrupting  the  current  by  opening  the  circuit,  or  allowing  it  to  flow 
in  by  closing  the  circuit.  A  continuous  current  causes  no  contraction  unless 
the  strength  is  suddenly  changed.  Faradism  causes  continuous  contraction 
for  it  is  equivalent  to  a  constant  make  and  break  of  the  current. 

The  current  is  obtained  from  the  dry  cells  of  Leclanche  or  from  the 
main.  Its  strength  is  measured  in  milliamperes,  the  unit  in  medicine,  by 
a  galvanometer  and  should  not  be  measured  in  terms  of  the  number  of 
cells.  A  rheostat  is  useful  to  regulate  the  strength,  and  an  alternator  to- 
enable  a  combined  faradic  and  galvanic  battery  to  be  employed.    Electrodes- 


«20  Chapter   XL  VIII. 

are  of  various  shape  and  size,  more  or  less  flat,  and  covered  with  chamois 
leather.  The  larger  the  electrode  the  smaller  is  the  resistance  of  the  body. 
This  resistance  is  usually  high  in  children  and  is  chiefly  in  the  epidermis. 
The  conductive  power  of  the  skin  is  increased  by  moisture,  so  the  electrodes 
■are  moistened  with  salt  solution  before  use.  The  anode  or  positive  pole  is 
recognised  by  its  action  on  litmus,  turning  it  blue.  If  the  poles  are  placed 
in  water  more  bubbles  of  hydrogen  appear  round  the  kathode  ;  if  placed 
in  a  solution  of  starch  and  pot.  iod.,  a  deep  blue  colour  will  develop  round 
the  anode.  The  kathode  is  the  more  active  pole  when  applied  to  a  nerve. 
This  is  represented  by  the  formula  K  C  C  >  A  C  C.  A  knowledge  of  motor 
points  is  essential  and  will  be  found  in  works  on  medical  electricity. 

Testing. — Get  the  child  used  to  the  sight  and  noise  of  the  battery,  and 
the  feel  of  the  electrodes,  before  the  current  is  turned  on.  Confidence 
must  be  established.  Use  no  current  stronger  than  necessary  to  cause 
contraction,  so  begin  with  the  weakest  interrupted  current.  Apply  a  large 
flat  electrode  to  the  back  and  the  testing  electrode  to  the  different  motor 
points.  Compare  the  normal  reactions  with  the  abnormal,  and  remember 
that  excitability  varies  in  different  children.  Then  test  with  the  continuous 
current,  beginning  with  the  kathode. 

Normal  Reactions. — A  weak  faradic  current,  applied  to  the  motor  point 
of  a  peripheral  nerve  or  to  a  muscle  directly,  causes  equal  contraction  on 
both  sides.  When  a  weak  galvanic  current,  measured  by  the  galvanometer, 
is  applied  to  the  muscle  it  may  cause  one  or  other  of  the  following  reactions. 
The  contraction  is  short,  sharp  and  quick.  The  first  type  is  the  most 
common. 

1.  KCC>ACC>AOC>KOC. 

2.  KCC>AOC>ACC>KOC. 

3.  KCC>AOC-ACC>KOC. 

The  important  results  are  whether  the  contraction  is  greater  or  less 
with  the  anode  or  the  kathode  on  the  muscle  ;  that  is,  under  which 
conditions  contraction  is  obtained  most  easily. 

The  Reaction  of  Degeneration  (R.D.)  is  more  commonly  partial  than 
•complete  for  many  muscular  fibres  may  be  unaffected.  A  stronger  current 
is  required  and  weaker  contractions  are  produced  than  on  the  sound  side. 
The  reactions  to  galvanism  may  be  the  same  as  in  complete  R.D.  In  the 
■complete  variety  faradic  excitability  is  abolished  in  both  nerve  and  muscle. 
The  response  to  galvanism  of  the  motor  nerve  is  abolished.  The  reaction 
of  the  muscle  to  galvanism  is  exaggerated,  i.e.,  a  contraction  is  caused  by 
a  smaller  current.  The  contraction  is  slow,  sluggish  and  often  delayed  ; 
and  there  is  an  inversion  of  the  normal  formula,  thus  A  CC=or>KCC, 
and  later  KOC  =  or>AOC.  Erb  regards  a  slow  and  prolonged  con- 
traction with  a  weak  current  as  always  present  and  pathognomonic.  The 
presence  of  R.D.  indicates  mischief   in   the  lower  motor  neuron  (cord, 


The   Nervous  System.  621 

nerve  or  end  plate)  but  does  not  enable  us  to  differentiate  all  diseases  of  the- 
spino-neural  system.  It  is  possible  that  the  prognosis  is  worse  in  complete- 
than  in  partial  R.D.,  but  some  regard  both  as  of  equal  importance. 
Electrical  reactions  are  only  of  value  when  considered  relatively  to  other 
physical  signs.  R.D.  is  of  relative  and  not  of  absolute  importance. 
Muscles  may  show  this  reaction  without  any  sign  of  paralysis,  and  they  may 
have  recovered  their  functions  before  there  is  any  improvement  in  their 
electrical  reactions.  The  reactions  on  stimulation  of  the  nerve  in  partial 
R.D.  are  of  more  value  in  prognosis  than  the  condition  of  the  muscle. 

Electro-therapeutics. — Electrical  treatment  is  of  decided  benefit  but  its- 
value  is  greatly  over-rated.  The  good  results  are  partly  due  to  the  mental 
effect,  as  in  various  neuroses,  and  in  part  to  the  direct  influence  on  the 
muscle,  retarding  the  degenerative  processes  and  maintaining  nutrition,, 
while  the  nerve  or  nerve  cells  have  an  opportunity  of  recovery.  It  is- 
employed  in  the  form  of  galvanism  or  faradism,  locally  or  generally.  Both 
poles  are  applied  over  the  affected  area,  or  the  kathode  is  applied  to  this- 
region  and  a  large  flat  anode  to  the  spine.  Begin  with  a  current  of  3  ma. 
for  10-15  minutes  daily  or  on  alternate  days.  An  electric  bath  can  be  used 
for  a  single  limb  or  the  whole  body.  The  bath  is  made  of  porcelain  and  2 
large  flat  copper  electrodes  are  placed  in  it,  or  1  such  electrode  and  a 
small  one  which  is  applied  to  the  affected  parts.  Use  a  galvanic  or  faradio 
current  of  a  strength  of  5-10  ma.  for  10-15  minutes  in  water  at  95°  F. 
The  hip  bath  is  preferable  for  paraplegic  forms  of  infantile  palsy. 

Classification. — It  is  impossible  to  devise  a  classification  based  on 
locality  for  nervous  diseases  are  rarely  localised.  One  group  may  be- 
limited  to  the  Malformations.  Zappert  suggests  a  division  into  Endogenous- 
and  Exogenous  diseases. 

An  Endogenous  or  in-born  affection  is  one  which  is  dependent  on  an 
inherited  weakness,  deficient  resisting  power  or  faulty  development  of  the- 
nerve  cells  or  nerve  tracts.  Gowers  speaks  of  this  as  Abiotrophy.  The 
nervous  tissues  wear  out  unduly  early.  There  is  a  physiological  premature- 
senescence,  slow  and  insidious  in  onset,  inevitable  and  progressive  in 
course,  and  without  retrocession.  The  child  is  doomed  from  the  moment- 
of  conception.  These  diseases  are  independent  of  external  influenees- 
and  are  possibly  dependent  on  consanguinity,  alcoholism  or  various- 
toxaemias  in  the  parents.  They  are  racial  and  familial,  occasionally 
sporadic.  They  are  not  always  identical  in  different  families  and  show 
family  modifications  of  type.  The  changes  are  atrophic  or  aplasic,  without 
inflammation.  Higher  cells  atrophy  and  lower  tissues  hypertrophy.  The 
degeneration  is  localised  in  one  system.  Progressive  bulbar  palsy,  primary 
cerebrospinal  sclerosis,  amaurotic  family  idiocy,  Freidreich's  ataxia,  and 
muscular  dystrophies  are  the  main  members  of  this  group. 

The  Exogenous  diseases  are  those  dependent  on  congenital  syphilis- 
and   possibly  tuberculosis  ;    and  on  post-natal  causes,  such  as  microbial 


•622 


Chapter   XL  VI II. 


infections,  by  the  action  of  toxins  or  mechanical  interference  with  circula- 
tion or  nutrition.  The  organism  may  be  present  in  the  affected  part,  as 
in  meningitis  ;  present  in  other  parts,  as  in  diphtheria  and  tetanus  ;  or 
undiscoverable,  as  in  infantile  palsy.  In  certain  conditions  no  morbid 
■change  or  organism  is  found,  e.g.  tetany,  insanity,  hysteria.  Poisons,  such 
as  lead  and  alcohol,  are  also  causes.  It  is  difficult  to  bring  the  effects  of 
traumatism  and  circulatory  affections,  the  results  of  embolism,  thrombosis 
■or  haemorrhage,  into  this  classification,  except  in  so  far  as  they  are 
■exogenous  in  origin. 


CHAPTER    XL1X. 

MALFORMATIONS    OF    THE    NERVOUS    SYSTEM. 

Cranial   Deformities — Cranial  and  Cerebrospinal  Defects — Spina  Bifida — 
Cerebral  Malformations  —  Macrocephalus  —  Microcephalics  —  Hydro- 
'  cephalus — Porencephalies — Syringomyelia. 

Oxycephalus.  —  Syn.  :  Steeple  or  Tower  Skull  —  Pointed  Head  — 
Thurmkopf. — This  is  a  curious  deformity  of  the  skull  often  associated  with 
other  congenital  defects  and  stigmata  of  degeneration.  The  skull  is  dome- 
shaped  or  the  height  of  the  anterior  part  is  abnormal  and  the  temporal 
regions  bulge.  Occasionally  it  is  scaphocephaly.  The  superior  maxilla  may 
be  deformed.  The  cause  is  obscure.  The  deformity  is  present  at  birth  but 
is  rarely  extreme.  Carpenter  has  reported  cases  in  3  children  of  the 
same  family  with  other  congenital  defects.  Other  children  of  the  same 
mother  were  normal.  It  is  generally  associated  with  exophthalmos, 
proptosis,  divergent  squint,  nystagmus,  ocular  palsy,  and  defective  vision 
•or  blindness  in  one  or  both  eyes.  The  eyes  may  be  dislocated  forward. 
The  ocular  defects  are  due  to  the  deformity.  Optic  neuritis  or  post- 
neuritic atrophy  is  usual  and  begins  comparatively  early  in  life.  It  has  been 
ascribed  to  stenosis  of  the  optic  foramen,  but  this  is  usually  of  normal  size. 
Enslin  found  the  nerve  constricted  in  3  fatal  cases.  Other  possible  causes 
are  pressure  on  the  optic  chiasma  or  optic  tracts,  altered  course  and  kinking 
of  the  nerve,  defect  in  the  occipital  lobe,  premature  synostosis  and 
increased  intracranial  pressure,  pachymeningitis,  foetal  meningitis  and 
osteitis.  Some  of  these  children  are  quite  intelligent.  Others  show  mental 
defect,  convulsions  in  infancy  and  epilepsy  in  later  life.  Death  is  generally 
due  to  intercurrent  disease. 

A  modified  form  shows  defective  development  of  the  back  of  the  skull, 
almost  complete  absence  of  the  occipital  protuberance,  dome-shaped 
forehead,  protrusion  of  the  eye-balls,  blindness  and  other  defects,  though 
the  fundi  are  normal. 

Hyperostosis  Cranii,  or  excessive  thickness  of  the  skull  bones,  has  been 
reported  by  Andrewes  (1902)  in  an  imbecile  boy,  4  years  old.  All  the 
membrane  bones  of  the  skull,  especially  the  frontal  and  parietal,  and  to  a 
Jess  extent  the  lower  jaw,  were  greatly  thickened  and  consisted  of  uniform 
dense  cancellous  bone.  Voelcker  has  seen  a  similar  case  in  a  rachitic 
imbecile. 


624  Chapter  XLIX. 

Abnormal  Sutures  due  to  irregular  ossification  of  the  parietal  bones  are 
of  rare  occurrence.  In  a  boy,  aged  8  months,  the  right  parietal  was  divided 
by  an  oblique  suture  into  2  almost  equal  parts.  The  left  bone  consisted 
of  an  anterior  and  posterior  half,  and  the  posterior  half  was  subdivided 
into  an  upper  and  lower  portion.  It  had  apparently  developed  from  S 
centres  of  ossification.  There  are  records  of  10  similar  cases,  all  unilateral. 
It  gives  rise  to  no  symptoms.  Both  bones  may  be  absent.  The  chief 
importance  of  the  presence  of  irregular  sutures  is  that  they  may  be  mis- 
taken for  fractures  or  for  linear  craniotabes.  Cranial  depressions  have  been 
described  in  the  section  on  injuries  at  birth  (p.  111). 

Meningocele. — A  cranial  meningocele  is  a  protrusion  of  the  membranes- 
of  the  brain,  causing  a  distensile,  translucent,  non-pulsating  tumour  of 
variable  size.  On  coughing  or  straining  the  .tumour  becomes  more  tense 
and  bulging,  except  in  those  rare  cases  in  which  the  communication  with 
the  cranial  cavity  is  closed.  It  is  due  to  a  failure  of  development  of  the 
posterior  part  of  the  skull  in  consequence  of  hydrocephalus  in  foetal  life. 
The  orifice  is  situated  in  the  median  line  of  the  occipital  bone.  If  it  is  very 
near  the  foramen  magnum  it  is  difficult  to  diagnose  from  spina  bifida,  a 
cervical  meningocele.  This  is  a  rare  situation  for  spina  bifida.  A  remark- 
able case  was  that  of  a  boy  who  died  at  the  age  of  18  days.  Labour  was 
difficult  and  instrumental.  A  small  meningocele  protruded  through  the 
frontal  bone,  rather  more  to  the  left  than  the  right  of  the  median  line.  The 
protrusion  was  about  the  size  of  half  a  walnut.  It  could  be  reduced,  and 
became  tense  on  crying.  There  were 'also  present  a  cephalhematoma  over 
the  left  parietal  bone,  haemorrhage  between  the  dura  and  parietals  on 
each  side,  craniotabes  of  the  posterior  parts  of  the  parietals,  a  lumbo- 
sacral myelomeningocele,  double  talipes  and  hydrocephalus,  but  the  central 
canal  of  the  cord  was  not  dilated.  The  arches  of  five  vertebrae  were 
deficient. 

A  meningocele  may  be  treated  by  the  withdrawal  of  a  little  fluid,  and 
liberal  application  of  collodion  to  the  sac  to  induce  contraction.  Operation 
is  justifiable  if  the  communication  is  closed. 

Encephalocele  or  Meningo-encephalocele  is  a  tumour  of  variable  size, 
usually  in  the  median  line,  due  to  the  protrusion  of  brain  and  membrane. 
It  pulsates  and  is  not  translucent.  It  is  most  common  in  the  occipital 
region,  but  less  common  than  meningocele.  It  may  be  situated  anteriorly, 
especially  at  the  root  of  the  nose,  and  may  involve  both  orbit  and  forehead  ; 
and  is  rarely  sagittal.  The  symptoms  vary  with  the  size  and  situation  and 
may  be  absent.  Idiocy,  squint,  nystagmus,  optic  atrophy,  and  other 
deformities  may  be  present.  Like  a  meningocele  it  may  be  so  large  as  to 
cause  the  appearance  of  "  double  head."  It  must  be  diagnosed  from 
simple  tumours  and  dermoid  cysts.  Small  ones  can  sometimes  be  replaced. 
They  are  compatible  with  life  if  small  and  untreated  ;  but  if  large,  death 
results  from  secondary  infection.     Some  cases,  chiefly  nasal  ones,  can  be 


Malformations  of  the   Nervous  System.  625 

cured  by  excision.     The  occipital   lobes    have    been     removed    without 
affecting  vision  or  other  faculties. 

Spina  Bifida  is  much  more  frequent  than  cerebral  protrusion.  It  i;i 
due  to,  or  the  cause  of,  the  failure  of  the  medullary  groove  to  unite.  The 
arrest  of  development  affects  the  mesodermic  layer  only  or  involves  also  tne 
ectoderm  and  endoderm.  Its  slightest  form  is  a  mere  cleft,  usually  lumbo- 
sacral, with  no  protrusion  of  fluid  or  tumour.  This  is  known  as  Spina 
Bifida  Occulta.  It  may  be  overlaid  by  a  hairy  mole  with  hair  several 
inches  long.  It  is  occasionally  associated  with  post-anal  dimple,  sphincter 
trouble,  perineal  anaesthesia  and  club-foot.  A  fibro-muscular  tumour  is 
present  and  can  sometimes  be  felt  in  the  spinal  canal  (Zappert).  Incon- 
tinence of  urine,  perforating  ulcer,  neuralgias  and  palsies  may  develop 
later,  as  a  result  of  mechanical  interference  with  the  growth  of  the  cord 
through  its  adhesion  to  the  skin.  Such  adhesions  must  be  removed.  It 
may  not  be  suspected  until  late  childhood  or  even  adolescence.  The  other 
varieties  depend  upon  their  constituent  structures.  Of  these  the  myelo- 
meningocele is  the  most  common  and  the  myelocystocele  exceedingly  rare. 

A  Myelomeningocele,  meningomyelocele  or  myelocele,  is  a  broad 
based  tumour,  usually  in  the  Jumbo-sacral  region  and  occasionally  cervical 
or  thoracic.  It  is  oval,  dark  red,  vascular,  soft,  fluctuating  and  elastic,  and 
does  not  project  much  above  the  surrounding  skin.  The  surface  may  be 
ulcerated.  Pressure  on  the  tumour  causes  bulging  of  the  fontanelle.  It 
is  due  to  defective  development  of  the  medullary  groove  with  consequent 
formation  of  a  cleft  in  the  vertebrae,  defective  closure  of  the  spine  and 
membranes  which  are  wanting  on  the  dorsal  aspect,  fissure  in  the  cord  and 
sulcus  in  the  skin.  The  bodies  of  the  vertebrae  are  intact.  The  wall  consists 
of  skin  and  dura  mater,  except  for  thin  membrane  at  the  apex,  and  may 
become  covered  with  epidermis  by  proliferation  of  the  surrounding  skin. 
H.  B.  Robinson  reported  a  case  in  which  the  tumour  was  adherent  to  the 
right  side  of  the  spine,  just  below  the  transverse  mesocolon,  and  simulated 
an  abdominal  cyst. 

It  is  often  associated  with  hydrocephalus,  dilated  fourth  ventricle, 
hydromyelia  and  other  defects  such  as  umbilical  hernia,  exomphalos  and 
intestinal  fistula,  club-foot,  absent  reflexes,  and  paralysis  of  the  bladder, 
rectum,  perineal  muscles  and  lower  limbs.  The  paralytic  symptoms  are 
generally  marked  ;  peihaps  limited  to  the  feet  and  sphincters  if  the  tumour 
is  sacral.  The  ilio-psoas  is  unaffected.  Other  signs  are  right-angled 
flexion  of  the  thighs  at  the  hip  joint ;  obliteration  of  anal  folds  or  funnel- 
shaped  protrusion  of  the  anal  region  ;  occasionally  prolapse  of  rectum  and 
uterus ;  and  trophic  ulceration  of  buttocks  and  genito-anal  regions. 
Ulceration  of  the  wall,  rupture,  sepsis,  purulent  meningitis  and  cystitis 
are  likely  to  occur.    Most  cases  die  within  two  weeks. 

A  Myelocystocele  or  syringo-myelocele  differs  from  myelomeningocele 
in  that  the  cord  has  been  enclosed  in  the  spinal  canal.      It  then  protrudes 

2  s 


G26  Chapter  XLIX. 

with  the  membranes  through  a  fissure  in  consequence  of  dilatation  of  the 
central  canal,  and  is  therefore  lined  with  epithelium  like  that  of  the  centra] 
canal.  The  cleft  is  of  limited  size,  frequently  a  little  to  the  side  of  the 
median  line  and  usually  sacral.  The  tumour  consists  of  fluid,  epithelium, 
expanded  cord  tissue,  membranes  and  skin.  At  first  the  skin  is  normal,  but 
later  it  becomes  excoriated  and  ulcerated  from  distension  by  fluid.  The 
ventral  part  of  the  spinal  marrow  is  more  or  less  preserved  and  the  motor 
tracts  are  perhaps  not  interfered  with,  so  there  may  be  no  palsy.  Hydro- 
cephalus, diastasis  of  the  recti  muscles  of  the  abdomen,  extrophy  of  the 
bladder  and  club-foot  are  often  present. 

A  Spinal  Meningocele  is  rarely  seen  as  a  museum  specimen  and  is 
consequently  said  to  be  very  rare  ;  probably  it  is  more  frequent,  less  fatal, 
and  often  gets  well  spontaneously  or  on  treatment. 

It  is  a  hernia]  protrusion,  between  two  arches  or  through  a  cleft  in  the 
vertebral  column,  containing  fluid  and  no  cord  tissue.  The  dura  mater  may 
be  defective.  It  is  almost  always  in  the  lumbo-sacral  region,  rarely  in  the 
cervical  or  dorsal.  It  is  often  pedunculated,  transparent  to  transmitted 
light,  and  covered  by  normal  or  altered  skin,  or  partially  by  a  thin  membrane 
which  readily  ulcerates.  It  is  not  reduced  by  pressure.  Occasionally  it 
bulges  on  crying  or  pressure  on  it  causes  bulging  of  the  fontanelle.  It  may 
be  as  big  as  the  child's  head.  In  the  sacral  region  the  nerves  of  the  cauda 
equina  may  be  present  in  the  wall  of  the  sac.  Usually  there  are  no  symptoms 
and  no  palsy.  Other  defects,  and  occasionally  defective  sensibility  and 
movement,  may  be  present  in  the  lower  part  of  the  body.  A  myelocysto- 
meningocele is  a  combination  of  meningocele  and  myelocystocele  due  to 
fluid  collecting  between  the  pia  and  arachnoid. 

Differential  diagnosis  is  often  difficult.  The  cleft  in  the  vertebrae  is 
broad  in  myelomeningocele.  In  the  other  varieties  the  cleft  is  very  narrow, 
the  skin  is  usually  intact,  and  functional  disturbances  are  infrequent.  The 
skin  over  a  myelocystocele  is  thin.  A  meningocele  is  almost  always  sacral 
and  has  a  small  pedicle.  A  myelocystocele  may  be  present  anywhere. 
If  it  is  low  down,  it  is  lumbo-sacral  and  generally  associated  with  other 
defects.  It  is  rarely  possible  to  be  certain  that  no  part  of  the  cord  or  nerves 
is  included  in  the  sac.  The  general  diagnosis  depends  on  the  presence  of  a 
tumour  at  birth  in  a  certain  situation,  of  a  definite  shape  and  consistence, 
and  causing  pressure  symptoms.  Congenital  sacral  tumours  may  be  der- 
moids, teratoid  mixed  tumours,  or  true  teratomata  arising  from  a  second 
embryo  and  small  in  size  up  to  accessory  limbs. 

Treatment. — Simple  tapping  is  followed  by  re-accumulation  of  fluid. 
It  is  useful  as  a  palliative,  to  allow  an  ulcer  to  heal  before  proceeding  to 
excision.  Repeated  tapping  may  be  followed  by  leakage,  infection  and 
meningitis.  Morton's  fluid,  dr.  1  (iodine  1,  pot.  iod.  6,  glycerine  50  parts)  is 
sometimes  injected  after  allowing  about  two-thirds  of  the  fluid  to  escape. 
It    is   immediately   withdrawn.      The    puncture    is    painted    over    with 


Malformations  of  the   Nervous  System.  627 

'collodion  and  the  whole  tumour  with  collodion  and  iodoform.  It  may  cause 
fatal  collapse  at  the  time  and  usually  produces  severe  constitutional  reaction 
.afterwards.  It  is  probably  only  curative  in  cases  of  meningocele  and  only 
.advisable  in  quite  inoperable  cases.  A  meningocele  may  be  excised.  Nerve 
bundles  in  the  sac  must  be  returned  if  possible  ;  failing  that,  they  must  be 
removed.  The  operation  should  be  deferred,  if  the  child  is  weakly,  until 
the  sixth  month  of  age.  Operation  is  useless  in  myelomeningocele ; 
justifiable  in  myelocystocele,  for  the  cord  entering  the  dorsal  wall  of  the 
tumour  is  functionless  ;  and  may  be  tried  for  myelocystomeningocele. 
Buccheri  (1908)  reported  excellent  results  from  the  treatment  of  19  out  of  21 
cases  by  radical  closure  of  the  orifice.  They  were  classified  as  meningocele  2, 
myelocystocele  18,  myelomeningocele  1  ;  males  9,  females  12  ;  age  2  days 
to  3  years,  the  maj  ority  under  40  days.  Mean  duration  of  treatment  10  days ; 
11  healed  by  first  intention  ;  3  out  of  4  ulcerated  ones  recovered  ;  3  died. 
'The  patients  remained  well  afterwards.  Possibly  the  varieties  were  named 
differently.  Operation  is  contra-indicated  by  hydrocephalus,  a  large  cleft 
.and  insufficient  skin  to  make  good  flaps,  other  grave  defects,  and  marked 
paralysis  of  the  lower  limbs  and  sphincters,  especially  if  associated  with 
talipes.  Hydrocephalus  may  develop  after  successful  operation.  The 
•chief  dangers  are  fatal  shock  and  collapse,  due  to  sudden  escape  of  fluid  or 
manipulation  of  nerves  and  cord,  subsequent  leakage  and  sepsis. 

Sacro-coccygeal  Dimples,  Sinuses  and  Cysts.— In  many  babies  and  fewer 
adults  a  rounded  depression  or  a  longitudinal  furrow  of  variable  depth  is 
.situated  over  the  coccyx  above  the  anus.  A  dimple  or  indentation  is  the 
most  common  form.  In  about  one-tenth  of  the  cases  there  is  an  orifice 
of  a  fistula  or  sinus.  The  skin  around  and  lining  the  depression  is  pinkish, 
more  glossy  and  moister  than  normal,  and  adherent  to  the  deeper  structures. 
The  moisture  may  be  enough  to  damp  the  clothes.  The  size  and  depth 
vary  from  a  faint  indentation  to  a  deep  pit  or  sinus  several  centimetres 
•deep,  with  a  very  fine  orifice  or  one  so  large  as  to  simulate  the  anus.  There 
may  be  an  epidermoid  cyst,  entirely  cut  off  or  possessing  one  or  more 
fistulous  openings.  These  cysts  are  not  always  in  the  middle  line.  They  are 
often  composed  of  several  more  or  less  dilated  tubules,  containing  mucoid 
fluid  and  lined  by  a  single  layer  of  large  columnar  cells. 

These  abnormalities  are  situated  near  the  tip  of  the  coccyx,  in  the 
sacro-coccygeal  region,  over  the  lower  part  of  the  sacrum,  or  between  the 
coccyx  and  sacrum.  They  are  probably  vestigial  remnants.  Epithelium, 
sebaceous  matter  and  hair  are  liable  to  be  shut  up  in  the  cysts  and 'fistula?. 
The  dimples  are  lined  with  true  skin  but  occasionally  the  cysts  are  lined 
with  epithelium,  ciliated  or  like  that  of  the  small  intestine.  No  treatment 
is  necessary.    If  troublesome  a  cyst  or  fistula  can  be  dissected  out. 

Cerebral  Malformations. — The  bead  is  entirely  absent  in  Acephaly. 
In  Anencephaly  there  is  no  calvarium  or  cerebrum,  and  the  cerebellum  is 


628  Chapter   XLIX. 

is  compatible  with  survival  for  some  days,  and  often  associated  with  other 
defects.  In  Cyclops  the  cal varium  is  present  and  the  cerebrum  ill-developed,, 
arrested  or  cystic  ;  and  the  monster  presents  a  single  eye  in  the  median 
line.  The  convolutions  may  be  unduly  large  (macrogyria)  or  small. 
(microgyria).  Fissures  and  commissures  may  be  arranged  abnormally. 
The  corpus  callosum  may  be  absent.  Cerebellar  aplasia  is  a  probable  cause 
of  Hereditary  Ataxia.  Infantile  nuclear  atrophy,  unilateral  or  bilateral, 
may  produce  ptosis,  ophthalmoplegia,  a  lack  of  facial  expression,  and 
paralysis  and  atrophy  of  the  tongue  with  salivation  and  absent  lachrymal, 
secretion,  if  the  hypoglossal  nuclei  are  the  ones  affected.  Agenesis  corticalis 
produces  cerebral  birth  palsy.  The  agenesis  may  affect  the  cells,  coin- 
misures  and  nerve  tracts. 

Macrocephalus,  or  hypertrophy  of  the  brain,  is  a  rare  congenital  con- 
dition. The  ventricles  are  often  obliterated,  occasionally  dilated,  and  the 
convolutions  are  flattened.  The  skull  may  be  enlarged,  and  the  bones, 
thin  and  porous.  A  persistent  thymus  and  aplasia  of  the  adrenals 
have  been  found  in  adults.  There  may  be  no  symptoms  until  after  the 
first  year  of  life  ;  or  convulsions,  deep  coma  and  death.  Intelligence  is. 
defective. 

Microcephalus. — A  small  baby  has  a  small  head.  In  microcephalus. 
the  head  is  unduly  small  in  proportion  to  the  size  and  age  of  the  child.  At 
the  end  of  the  first  year  of  life  its  circumference  is  14-17  ins.  instead  of  the 
normal  18-19  ins.  In  shape  the  head  may  be  normal  ;  or  it  may  be 
dolichocephalic,  the  transverse  measurement  being  shortened  while  the 
antero-posterior  is  normal  or  increased  and  a  prominent  ridge  is  present  in 
the  middle  line.  More  often  it  is  brachycephalic,  the  antero-posterior 
measurement  being  shortened  and  the  occipital  bone  unduly  vertical.  Or 
it  may  taper  towards  the  vertex,  and  be  dome-shaped  or  roughly  triangular 
in  coronal  section.  The  forehead  is  narrow  and  presents  a  median  ridge 
The  fontanelles  and  sutures  are  prematurely  closed.  The  brain  weighs  only 
30-35  oz.  in  the  adult.  It  may  be  microcephalic,  though  the  skull  is  of 
normal  size.  In  one  variety  cerebral  disease  and  non-development  are- 
present  ;   in  another  no  disease  is  found. 

It  has  been  ascribed  to  premature  synostosis  of  the  cranial  bones,  to- 
lack  of  intracranial  pressure,  and  to  imperfect  development  of  the  brain. 
Possibly  more  than  one  factor  are  concerned  in  each  case.  The  bulk  of 
the  cases  are  of  intra-uterine  origin.  In  some  instances  there  is  moie  or 
less  evidence  of  a  past  encephalitis  or  cerebral  sclerosis  in  infancy  which 
has  interfered  with  the  proper  growth  of  the  brain.  It  has  remained  small 
and  consequently  the  sutures  have  closed  early.  Marasmic  states  in 
infancy  may  lead  to  early  closure  of  the  fontanelles  and  sutures  from  delayed 
cerebral  growth.  Sometimes  the  fontanelles  and  sutures  remain  unduly 
open  and  ossification  is  delayed.  Sclerosis,  degenerative  processes,  hydro- 
cephalus  or  porencephalus  may  be  found  after  death. 


Malformations  of  the   Nervous  System.  G29 

The  symptoms  vary  with  the  degree  of  microcephalics,  and  this  depends 
upon  the  degree  of  sclerosis  or  failure  of  the  development  of  the  brain  or 
of  part  of  the  brain.  The  face  is  small,  eyes  prominent  and  expression 
lacking.  If  only  the  anterior  portions  of  the  brain  are  affected,  the  mental 
state  is  that  of  microcephalus  although  the  head  is  little  smaller  than 
normal.  The  child  is  invariably  feeble-minded,  dull  and  apathetic,  or 
cheerful  and  more  or  less  idiotic,  but  liable  to  attacks  of  temper  and 
other  emotional  disturbance.  Many  are  subject  to  fits  or  to  irregular 
movements  of  the  head,  of  the  type  of  "  head  nodding,"  and  exhibit  loss 
of  power  in  the  limbs,  inco-ordination,  frequently  rigidity,  and  sometimes 
general  flaccidity.  Typical  "  mandarin "  movements  of  the  head  are 
rarely  seen  except  in  microcephalus.  The  child  is  long  in  learning  to  walk 
and  talk,  and  may  never  acquire  these  functions  or  only  imperfectly. 
Habits  of  cleanliness  are  acquired  late,  and  in  rare  instances  not  at  all. 
Nystagmus,  squint,  and  impaired  sensibility  are  sometimes  noted.  The 
knee  jerks  are  usually  absent.  In  the  worst  cases  there  may  be  blindness 
or  deafness.  Defective  or  apparently  defective  sight  is  due  to  a  mental 
•condition.  The  fundus  is  rarely  abnormal.  Sometimes  patches  of  choroid- 
itis are  found,  and  must  be  regarded  as  coincident  rather  than  the  cause 
of  the  visual  defect.  The  evidence  is  opposed  to  the  view  that  the 
choroiditis  is  due  to  congenital  syphilis.  Microcephalus  does  not  necessarily 
interfere  with  bodily  development  and  is  compatible  with  prolonged  life. 
Many  children  remain  small,  while  others  grow  well,  are  healthy  and  even 
pretty.     A  certain  amount  of  improvement  takes  place  in  the  less  serious 

•  cases,  and  with  careful  training  the  child  may  be  partially  taught. 

It  is  probable  that  in  the  following  instance  the  affection  was  post- 
natal in  origin.  The  child  had  digestive  disturbance  at  3  months,  enteric 
catarrh  at  5  months,  and  septic  infection  of  a  vaccine  pock  at  9  months 
resulting  in  a  bad  arm  and  illness  for  .3  weeks.  At  11  months  she  began 
•to  have  attacks  of  vacancy  with  pallor,  closed  eyes,  apncea  and  clenched 
hands,  the  attacks  ending  in  a  crow  and  resembling  laryngospasm.  These 
attacks  became  very  frequent  and  associated  with  rapid  breathing  and 
rocking  movements  of  the  head  and  trunk.     At   18  months  they  still 

•  occurred  in  conjunction  with  attacks  of  screaming,  without  any  apparent 

•cause.  The  screaming  might  come  on  after  an  attack  of  vacancy  or 
independently.  Nodding  or  lateral  movements  of  the  head  and  trunk  also 
continued.  At  2  years  all  the  above  symptoms  ceased  ;  and  at  3  years  the 
child  was  definitely  imbecile  and  microcephalic,  the  circumference  of  the 
head  being  the  same  as  that  of    a   younger  sister  18  months  old.     The 

•child  was  tall,  thin  and  walked  well,  but  could  not  talk  and  the  knee  jerks 
were  absent.    In  after  years  she  was  transferred  to  an  asylum.     This  case 

•suggests  that  it  was  the  result  of  frontal  encephalitis  due  to  sepsis. 

Another  child,  5  years  old,  showed  nystagmus,  head  jerking,  inability 
"to  stand  and  marked  loss  of  sensation.    At  9  months  it  was  noted  that  he 


630  Chapter   XLIX. 

did  not  try  to  use  his  hands.  Nystagmus  and  head  jerking  during  sleep 
began  at  18  months.  At  5  years  he  was  excitable,  destructive,  and  only 
fairly  clean  in  his  habits.  He  bit  his  nails  and  had  lost  a  portion  of  the 
terminal  phalanges  of  the  left  thumb  and  first  finger.  The  knees  were 
scarred  by  old  burns.  Sensation  was  blunted,  for  he  did  not  cry  when  burnt 
or  on  biting  his  fingers  sufficiently  to  make  them  bleed.  The  hands  were 
used  in  a  purposive  but  clumsy  fashion.  Partial  flexion  and  rigidity  of  the 
knees,  absent  knee  jerks,  talipes  valgus,  and  inability  to  stand  or  walk 
were  also  present.  He  was  very  nervous,  peculiarly  frightened  by  the  noise 
of  falling  rain,  and  could  talk  a  little.  Probably  this  was  of  congenital 
origin  and  the  deficient  sensation  may  have  been  due  to  syringomyelia. 

Treatment. — Linear  craniectomy  has  been  advocated  and  tried  on  the 
assumption  that  the  condition  is  due  to  premature  synostosis  and  increased 
intracranial  pressure.  There  is  no  proof  of  any  such  increase  in  pressure 
and  the  symptoms  do  not  suggest  it.  A  longitudinal  opening  is  made  by  the 
removal  of  bone  on  one  or  both  sides  of  the  sagittal  suture.  Under  strict 
antiseptic  precautions  the  danger  of  operation  is  slight.  Carl  Beck  of  Chicago 
(1897)  collected  70  cases  of  which  20  were  said  to  have  resulted  in  perfect 
and  lasting  improvement.  Jacobi  collected  33  cases  of  which  13  died,. 
14  showed  little  or  no  improvement,  2  were  more  improved,  and  the 
results  were  indefinite  in  the  others.  It  is  unlikely  that  any  benefit  can  be 
derived  from  operation  in  a  genuine  case  of  microcephalus. 

Craniectomy  has  been  tried  in  the  treatment  of  imbecility,  aphasia,, 
athetosis,  paralysis  and  sensory  defects  which  have  proved  incurable  by 
medicinal  measures.  Decided  benefit  has  ensued  in  some  instances,  but  it- 
would  be  absurd  to  expect  improvement  in  cases  of  gross  defect  or  atrophy 
of  the  brain.  Trephining  is  of  value  for  the  reduction  of  the  frequency  and 
severity  of  epileptic  fits,  and  for  optic  neuritis,  a  trephine  hole  covered  by 
membrane  acting  as  a  safety  valve  for  the  relief  of  sudden  changes  in 
intracranial  pressure. 

Hydrocephalus  oi  "  water  on  the  brain  "  is  congenital  oi  acquired. 
It  is  convenient  to  consider  all  varieties  in  the  present  section,  as  well  as 
certain  of  the  causes  which  give  rise  to  them.  If  the  excess  of  fluid  is  in  the 
cavities  of  the  brain,  the  hydrocephalus  is  called  Internal ;  if  in  the  sub- 
dural and  subarachnoid  spaces,  it  is  named  External.  Both  kinds  may  be 
present  simultaneously.  The  main  effects  are  those  of  increased  intra- 
cranial pressure.  Noimally  the  cerebrospinal  fluid  runs  from  the  vertex 
to  the  theca  spinalis  and  is  apparently  absorbed  at  its  lower  end.  If  the 
fluid  is  poured  out  in  excess  or  cannot  escape  from  the  ventricles,  or  is  not 
re-absorbed  in  sufficient  quantity,  then  the  intracranial  pressure  rises. 
Hydrocephalus  can  occur  without  any  sign  of  increased  pressure  or  enlarge- 
ment of  the  head,  if  we  include  under  the  term  some  of  the  cases  of  the 
congenital  variety  dependent  on  cerebral  malformation. 


Malformations  of  the  Nervous  System.  631 

Congenital  external  hydrocephalus  is  commonly  due  to,  and  com- 
pensatory for,  diminution  in  brain  tissue,  dependent  on  gross  cerebral 
defects  or  atrophy.  It  is  spoken  of  as  hydrocephalus  ex  vacuo,  a  name 
applied  also  to  similar  cases  of  the  acquired  type  and  sometimes  to  the 
enlargement  of  the  ventricles  secondary  to  cerebral  atrophy,  a  true  internal 
hydrocephalus.     The  importance  of  this  type  is  small. 

Congenital  internal  hydrocephalus  is  either  the  result  of  maldevelopment 
or  secondaiy  to  intra-uterine  basal  meningitis.  It  may  occur  in  twins  or 
in  several  children  as  a  family  disease.  Possibly  this  depends  on  a 
syphilitic  taint.  Striking  cases  illustrative  of  maldevelopment  may 
be  quoted.  The  brain  of  a  boy,  4  months  old,  was  found  after  death  to 
consist  of  a  medulla  oblongata,  pons,  crura  cerebri,  optic  thalami  and 
cerebellum,  all  of  which  were  small  and  ill-developed.  The  cerebrum  was 
represented  by  a  membranous  bag,  composed  of  two  dilated  ventricles. 
The  aqueduct  of  Sylvius,  where  the  dilatation  ended,  was  extremely  stenosed 
and  at  one  spot  of  quite  microscopic  dimensions.  The  membrane  was  of  the 
same  thickness  as  the  adult  dura  mater  and  did  not  seem  to  contain  any 
nerve  tissue  elements.  He  came  under  treatment  for  vomiting  of  9  days 
duration,  drowsiness,  occasional  screaming  and  a  variable  amount  of 
rigidity  of  the  limbs.  The  head  was  retracted,  the  circumference  16^  ins., 
and  showed  extreme  craniotabes  of  all  the  membrane  bones,  a  large  bulging 
anterior  fontanelle,  an  open  posterior  one  and  open  sutures.  There  were 
rigidity  of  the  neck  muscles,  general  spastic  rigidity  of  the  limbs,  exag- 
gerated knee  jerks,  and  malnutrition.  The  pupils  were  equal  and  reacted 
to  light.  In  the  course  of  development  the  anterior  cerebral  vesicle  is 
divided  into  two  parts,  from  the  centre  of  which  are  developed  the  cerebral 
hemispheres  with  their  ventricular  hollows,  the  corpora  striata  and  the 
olfactory  lobes.  This  portion  of  the  brain  is  known  as  the  pro-cerebrum  or 
prosencephalon.  In  the  above  case  there  was  probably,  in  early  foetal  life, 
excessive  formation  of  fluid  in  the  prosencephalon  and  interference  with  its 
escape.  Consequently  it  became  gradually  distended  into  a  membranous 
bag  of  fluid  and  the  nervous  elements  did  not  develop. 

In  a  girl,  aged  10  weeks,  born  at  full  time  and  weighing  3|  lbs.,  a  similar 
condition  was  present.  The  head  was  large  at  birth  and  had  increased 
since,  measuring  17  ins.  The  body-weight  had  increased  to  6  lb.  14  oz. 
The  discs  were  quite  white  and  merged  into  the  rest  of  the  fundus.  All  the 
membrane  bones  were  unossified,  except  for  small  isolated  patches  of  bone, 
chiefly  situated  in  the  normal  sites  of  the  centres  of  ossification.  A  third 
child,  a  girl  aged  4  months  at  death,  showed  a  like  condition  of  the  membrane 
bones  of  the  skull.  She  weighed  3|  lbs.  at  birth.  At  3  months  the  head  was 
large  and  top-heavy,  16  ins.  circumference.  The  child  attained  a  weight  of 
10  lbs.  and  a  cranial  measurement  of  18  ins.  before  death.  The  discs  were 
indistinguishable  from  the  surrounding  fundus  and  there  was  extensive  old 
choroiditis.     The  child  cried  much,  seemed  blind  and  unintelligent,  rolled 


£32  Chapter   XLIX. 

the  eyes  during  sleep  and  was  unable  to  support  the  head,  but  there 
was  no  spasticity.  The  cerebral  condition  was  as  in  the  first  cases,  though 
not  quite  so  extreme.  The  cortex  was  almost  membranous,  except  in  the 
occipital  region  where  it  was  about  f  in.  thick.  In  a  fourth  case,  a  boy  aged 
6  months  at  death,  there  was  general  rigidity  of  the  back  and  limbs  and 
retraction  of  the  head,  with  spasmodic  exacerbations.  It  was  said  to  have 
come  on  at  the  age  of  7  weeks.  A  few  pigment  spots  were  present  in  one 
fundus.  The  case  appeared  one  of  spastic  diplegia.  At  the  autopsy  it  was 
found  that  the  frontal  and  parietal  portions  of  the  brain  were  converted 
into  a  bilateral  cystic  formation,  bounded  mesially  by  a  wall  containing  a 
moderate  amount  of  brain  substance.  In  none  of  these  cases  was  there  any 
evidence  of  syphilis  as  the  cause  of  the  error  of  development  in  the 
prosencephalon. 

This  condition  is  sometimes  called  hydromicrocephalus,  hydranen- 
cephalus  and  bilateral  porencephalus.  There  may  be  no  enlargement  of  the 
head,  or  both  the  fluid  and  head  measurements  go  on  increasing  if  the  chiTd 
lives.  The  head  may  remain  small  from  premature  ossification  and  union 
of  the  sutures.  Congenital  hydrocephalus  resulting  from  intra-uterine 
inflammation  is  identical  with  the  acquired  variety. 

Acquired  External  Hydrocephalus  is  a  sequence  of  meningeal  inflam- 
mation or  new  growths.  Possibly  it  is  compensatory  to  the  diminution  of 
brain  substance  in  cerebral  atrophic  states.  It  has  been  found  in  marasmus 
and  pernicious  anaemia.  The  amount  of  fluid  varies  from  a  few  ounces  to  a 
pint,  and  may  cause  enlargement  of  the  head  and  separation  of  the  sutures, 
unless  they  are  already  firmly  united.  The  brain  substance  is  usually 
cedematous.  Symptoms  may  be  absent  or  take  the  form  of  twitchings,  con- 
vulsions and  collapse.  An  interesting  case  was  that  of  a  boy,  7  years  old, 
taken  ill  suddenly  with  severe  headache  and  screaming.  Three  days  later 
he  was  irritable,  drowsy  and  intensely  stupid.  The  head  was  a  little 
retracted  and  the  knee  jerks  exaggerated.  There  was  no  optic  neuritis. 
Three  days  later  he  had  severe  convulsions,  mostly  of  the  right  side,  with 
unconsciousness.  He  was  trephined  over  the  right  Rolandic  area  and  much 
cerebrospinal  fluid  let  out,  after  which  the  brain  began  to  pulsate.  The  fits 
did  not  recur  and,  after  remaining  rather  stationary  for  2  weeks,  he  rapidly 
improved.  In  another  3  weeks  he  had  a  further  attack  of  convulsions  and 
unconsciousness,  remaining  in  this  state  for  3  or  4  days,  when  he  again 
recovered.  Three  months  later  he  was  apparently  well,  but  his  memory  was 
bad  and  he  always  preferred  to  use  the  left  hand. 

Serous  Meningitis  or  Serous  Apoplexy. — The  case  just  described  is 
probably  a  true  instance  of  a  primary  serous  meningitis,  an  inflammation 
of  the  pia-arachnoid  which  may  spread  to  the  ventricles.  This  has  been 
described  by  Quincke  under  the  title  of  meningitis  serosa  ventriculorum, 
and  by  others  as  ventricular  serous  meningitis  or  acute  ependymitis.  In  its 
acute  form  it  may  be  spoken  of  as  "  serous  apoplexy  "  ;  in  its  chronic  type, 


Malformations  of  the  Nervous  System.  633 

us  "  acquired  internal  hydrocephalus."  It  is  doubtful  whether  it  is  ever 
limited  to  the  external  membranes  or  the  cavities  of  the  brain.  If  it  is, 
external  and  internal  hydrocephalus  may  occur  alone  or  conjointly.  The 
fluid  is  clear  and  contains  an  increased  amount  of  albumin,  fibrin  and  cells, 
chiefly  small  lymphocytes. 

Serous  apoplexy  in  infancy  gives  rise  to  convulsions  and  high  fever  ; 
sometimes  hyperpyrexia  and  coma.  The  pupils  are  contracted  and  slight 
rigidity  may  be  present.  It  is  usually  fatal  in  less  than  24  hours.  Coma 
is  the  chief  sign  in  cases  of  gradual  onset.  In  older  children  it  produces 
headache,  fever,  drowsiness,  coma,  teeth-grinding,  conjugate  deviation  of 
the  eyes,  irregular  and  rapid  pulse,  retraction  of  the  abdomen  and  impaired 
muscular  power.  Fever  may  be  absent,  slight  or  inconstant.  The  vision 
is  markedly  affected.  Less  virulent  cases  display  meningeal  symptoms 
and  are  sometimes  described  as  menincjismus.  This  is  a  bad  name,  which 
should  be  discarded,  for  similar  symptoms  may  indicate  vascular  distur- 
bance or  cerebral  toxsemia. 

The  etiology  is  the  same  as  that  of  meningitis.  Post  mortem  examina- 
tion may  show  nothing  except  a  little  increase  in  fluid,  a  granular  state  of  the 
ependyma,  an  oedema  of  the  pia-arachnoid,  or  the  early  acute  stage  of 
purulent  meningitis.  It  is  diagnosed  with  difficulty  from  acute  encephalitis 
and  simple  basal  meningitis,  and  the  diagnosis  may  remain  in  doubt  even 
when  it  has  passed  into  the  stage  of  chronic  hydrocephalus.  Some  cases 
get  well.  Others  become  chronic  and  present  headache,  vertigo,  optic 
neuritis,  vomiting,  ataxia,  mental  changes,  etc.  ;  signs  such  as  are  seen  in 
•cases  of  cerebral  tumour. 

Acute  Ependymitis  may  be  of  the  type  above  described.  In  a  few 
instances  it  is  due  to  a  pneumococcal  or  streptococcal  infection,  and  after 
death  pus  is  found  in  the  ventricles,  without  meningitis.  Turbid  fluid  is 
often  found  in  the  ventricles,  pus  rarely.  It  may  result  from  suppurative 
inflammation  of  a  spina  bifida,  rupture  of  an  intracranial  abscess, 
occasionally  purulent  meningitis,  and  possibly  from  primary  inflammation 
of  the  ependyma.  It  is  rarely  uncomplicated  and  may  be  secondary.  The 
onset  is  acute  with  vomiting,  headache,  and  perhaps  convulsions.  The 
fever  is  persistently  high  and  somewhat  hectic  in  type  ;  the  pulse  and 
breathing  frequent  and  irregular.  Consciousness  is  soon  lost  and  there  is 
peisistent  vomiting,  squint,  bulging  fontanelle,  slight  head  retraction, 
frequent  fits  and  emaciation.  During  life  it  is  difficult  to  distinguish  it 
from  meningitis.  The  chief  diagnostic  features  are  the  bulging  fontanelle, 
exaggerated  knee  jerks,  absent  Kernig's  sign,  and  a  high  temperature. 
Death  results  in  3-6  weeks. 

Acquired  Internal  Hydrocephalus  is  a  sequel  of  ependymitis  or  serous 
meningitis,  and  much  more  frequently  occurs  in  the  course  of  acute 
meningitis  or  as  a  sequel  of  basal  meningitis  of  varied  causation.  Many 
cases,  beginning  in  the  first  few  months  of  life  and  diagnosed  as  congenital, 


634  Chapter   XLIX. 

are  really  a  sequel  of  a  mild  unrecognised  attack  of  basal  meningitis.  It- 
may  be  regarded  as  a  symptom  of  this  disease.  Occasionally  it  is  due  to 
sinus  phlebitis,  sclerosis  or  the  pressure  of  tumours.  Its  frequent  occurrence- 
in  tuberculous  meningitis  has  led  to  this  disease  being  named  acute  hydro- 
cephalus, a  title  which  ought  never  to  be  used,  for  the  effusion  may  be 
due  to  many  other  causes.  Used  without  qualification,  hydrocephalus 
means  the  effusion  of  an  abnormal  amount  of  fluid  into  the  cavities  of 
the  brain,  and  dilatation  of  the  lateral  ventricles,  the  third  and  fourth 
ventricles,  the  iter  a  tertio  ad  quartum  ventriculum,  and  even  the  central 
canal  of  the  bulb  and  upper  part  of  the  cord.  A  few  cases  have  followed 
successful  operation  for  the  cure  of  spina  bifida  or  encephalocele. 

Morbid  Anatomy. — Congenital  cases  may  exhibit  gross  cerebral  defects,, 
spina  bifida  and  other  deformities.  Evidence  of  old  basal  meningitis  is 
exceptional.  It  is  most  common  in  acquired  internal  hydrocephalus.  A 
new  growth  is  found  in  rare  cases.  The  amount  of  fluid  varies  from  a  few 
ounces  to  several  pints.  It  is  greatest  in  the  congenital  cases  and  those 
arising  in  the  first  few  months  of  life,  before  the  sutures  have  ossified.  In 
cases  secondary  to  inflammatory  disease  the  amount  rarely  exceeds  half  a 
pint  in  the  first  4  years  of  life.  Its  composition  is  that  of  normal 
cerebrospinal  fluid.  It  may  be  turbid  and  contain  more  albumin,  if  it  is  of 
inflammatory  origin.  In  rare  instances  it  is  purulent,  sometimes  as  the 
result  of  operative  interference. 

As  the  fluid  accumulates  the  cerebral  tissue  becomes  compressed  and 
thinned,  reduced  to  a  layer  only  a  few  millimetres  thick,  constituting  a  thin 
wall  of  a  vast  cavity.  The  convolutions  are  flattened  and  eventually  all. 
trace  of  them  is  lost.  The  occipital  region  suffers  less  than  other  parts  of 
the  cerebrum.  The  septum  lucidum  is  broken  down  or  reduced  to  a  thin, 
membrane,  and  all  the  communications  between  the  ventricles  are  greatly 
enlarged.  The  brain  substance  left  in  the  cortex,  if  any,  is  pale  and 
homogeneous,  showing  no  differentiation  into  grey  and  white  matter  ;  and 
microscopical  examination  shows  granular  and  broken  down  nerve  cells.. 
In  the  worst  cases  only  the  cerebellum,  pons  and  basal  ganglia  are  left,  and 
even  the  basal  ganglia  may  be  almost  unrecognisable.  In  milder  degrees 
the  ependyma  is  normal,  or  finely  granular  on  the  surface  and  perhaps- 
thickened.  The  choroid  plexuses  vary.  The  external  enlargement  of  the- 
skull  is  conspicuous  for  the  cranium  is  proportionate  to  the  effusion.  The 
bones  are  thin  and  the  sutures  widely  separated,  sometimes  even  those  of 
the  base.  The  gaps  are  filled  in  by  Wormian  bones  in  mild  cases  which, 
recover. 

Pathology. — There  may  be  a  past  or  comparatively  recent  history  of 
symptoms  indicative  of  inflammatory  mischief  at  the  base  of  the  brain. 
The  actual  development  of  the  effusion  can  be  watched  in  certain  cases- 
of  basal  meningitis.  It  is  due  to  : — (1)  Blockage  of  the  foramen  of  Munro,. 
aqueduct  of  Sylvius  and  the  fourth  ventricle  ;   (2)  Blockage  of  the  foramen. 


Malformations  of  the  Nervous  System.  635- 

of  Majendie  and  the  apertura?  laterales  ventriculi  quarti ;  (3)  Thrombosis 
of  the  vense  Galeni.  If  both  veins  are  thrombosed  death  ensues  from 
cerebral  anaemia  before  hydrocephalus  can  develop.  The  foramen  of 
Majendie  is  often  non-existent.  If  no  such  explanation  is  available,  the 
affection  may  be  due  to  ependymitis.  This  is  almost  certainly  the  cause  in 
cases  which  can  be  drained  by  lumbar  puncture.  Idiopathic  effusions  are: 
said  not  to  be  infrequent  in  rickets  but  I  have  been  unable  to  find  any 
evidence  in  support  of  this  statement.  Some  of  the  supposed  acquired  cases, 
are  really  of  congenital  origin,  although  there  may  be  no  signs  of  the 
affection  until  some  months  after  birth. 

The  symptoms  are  practically  identical  in  congenital  and  acquired 
effusion,  except  that  the  former  may  be  conjoined  with  microcephaly. 
The  condition  may  be  suggested  by  headache,  vomiting,  mental  impairment 
and  fits,  but  even  these  may  be  absent  unless  the  fluid  is  actually  increasing, 
and  the  diagnosis  has  to  be  based  on  the  physical  signs. 

Chief  among  them  is  the  alteration  in  the  cranium.  The  earlier  the- 
disease  begins,  the  larger  the  head  becomes.  Its  shape  is  peculiar,  remark* 
ably  globular,  less  often  pyramidal.  It  is  increased  in  height  out  of 
proportion  to  its  length,  and  bulges  more  in  front  than  behind.  The 
forehead  is  large,  high  and  prominent,  and  there  is  a  prominence  at  the 
root  of  the  nose.  The  temporal  and  parietal  bones  are  pushed  outward  and 
diverge  as  they  pass  upward.  The  fontanelles  are  large,  tense,  bulging 
and  fluctuating.  The  sutures  are  separated,  perhaps  as  much  as  2-3  ins. 
The  bones  are  thinned  and  crackle  on  pressure,  or  the  whole  cranium 
may  feel  like  a  membrane,  with  or  without  isolated  patches  of  bone  in 
it,  and  may  even  be  translucent.  The  hair  is  scanty.  The  scalp  is  thin 
and  the  superficial  veins,  dilated  in  an  attempt  to  increase  the  collateral, 
circulation,  show  up  as  dusky  blue  cords  and  feel  as  if  running  in  definite 
grooves  in  the  bone.  If  the  child  is  much  wasted,  the  abnormal  size  of  the- 
head  is  still  more  evident.  It  is  often  so  large  and  heavy  that  the  child 
is  unable  to  support  it,  and  it  may  attain  a  circumference  of  30  ins.  The 
face  is  triangular  and  looks  abnormally  small  in  contrast  to  the  huge- 
cranium. 

The  eyes  protrude,  from  flattening  of  the  upper  wall  of  the  orbit.  The 
sclerotic  above  the  cornea  is  often  exposed,  while  the  pupils  may  be  partly 
covered  by  the  lower  lids.  In  the  early  stages  there  are  no  ocular  changes. 
At  first  the  pupils  are  usually  small  and  equal.  Later  they  may  become- 
dilated  and  immobile.  Squint,  nystagmus,  myopia,  hemianopia  and 
amaurosis  may  develop.  The  blindness  is  due  to  pressure  of  the  dilated 
third  ventricle  on  the  optic  tracts  and  chiasma  ;  and  optic  atrophy  is- 
rarely  preceded  by  papillitis  in  infancy  and  early  childhood.  Hearing 
remains  normal  for  a  long  time.  Alterations  in  the  sense  of  smell  and  taste 
are  difficult  to  estimate. 


636  Chapter   XLIX. 

Other  symptoms  depend  on  the  causation,  the  amount  of  damage 
done  to  the  cerebral  tissues,  the  stationary  or  progressive  character  of  the 
effusion,  and  the  possibility  of  skull  expansion.  In  mild  secondary  cases 
of  small  effusion,  stationary  in  character,  there  may  be  no  signs  beyond  a 
slight  increase  in  the  size  of  the  head.  If  the  fluid  is  effused  slowly,  there 
are  few  cerebral  symptoms  for  the  brain  accommodates  itself,  especially 
if  the  bones  yield  readily.  The  mental  faculties  may  be  normal,  or  even 
above  the  average,  although  there  is  a  considerable  excess  of  fluid,  provided 
the  skull  expands.  More  commonly  the  child  is  placid,  slow,  lethargic,  dull, 
stupid  or  even  completely  imbecile.  Somnolence  is  not  infrequent.  It  is 
extraordinary  how  long  the  mental  faculties  will  remain  unimpaired,  if 
the  fluid  collects  slowly  and  the  head  can  expand,  in  spite  of  the  cortex 
becoming  thinner  and  thinner.  In  some  cases  development  is  retarded 
and  the  child  is  unable  to  support  the  head  until  2-3  years  old.  Walking 
and  standing  are  interfered  with  early.  The  child  often  does  not  learn  to 
walk,  and  the  lower  limbs  remain  small  and  undeveloped.  Paraplegic 
conditions  and  rigidity  of  the  legs,  imperfect  control  over  the  hands  and 
arms,  contractures  of  the  hands,  and  exaggerated  reflexes  are  present  in 
severe  cases.  The  habits  of  cleanliness  are  lost  or  are  not  acquired.  The 
appetite  is  good,  even  voracious,  and  digestion  is  good.  Pulse,  respiration 
and  temperature  are  normal  ;  occasionally  the  temperature  is  persistently 
subnormal. 

Concealed  Hydrocephalus  is  an  effusion  in  older  children  with  un- 
yielding sutures  ;  either  the  persistence  of  a  mild  attack  in  earlier  life 
or  secondary  and  limited  in  degree.  Some  of  these  children  have  acute 
symptoms  ;  headache,  vomiting  and  optic  neuritis.  Intense,  paroxysmal 
headache  may  cause  sudden  death.  Persistent  malnutrition,  retarded 
development,  peculiarities  of  temper,  morals  or  emotions,  incontinence, 
palsies,  convulsions  and  insanity  may  be  noted.  In  others  there  are  fine 
tremors  of  the  tongue,  lips  and  hands  ;  slight  exophthalmos  ;  weakness 
•of  the  lower  limbs  ;  optic  neuritis,  and  fluctuating  facial  or  ocular  palsies. 
Cases  of  this  type,  when  a  sequel  of  effusion  in  earlier  life,  generally  have  an 
enlarged  cranium  and  are  often  called  Chronic  Hydrocephalus. 

Retraction  of  the  head,  partly  from  the  weight  and  partly  from 
basal  irritation,  inability  to  support  the  head,  Vomiting,  irregular  fever, 
twitchings  and  convulsions  may  be  present,  if  the  fluid  is  increasing  or  if 
there  is  continued  basal  irritation.  Sudden  attacks  of  headache,  vomiting 
and  fever  are  due  to  exacerbations  of  the  basal  mischief  or  increased  effusion. 

Diagnosis. — The  prominent  forehead  and  square  head  of  rickets  are  not 
hydrocephalic  although  the  child  is  often  said  to  "  have  a  touch  of  water 
on  the  brain."  The  chief  points  in  diagnosis  are  that  the  head  is  unduly 
large  for  the  age  and  size  of  the  child,  that  the  enlargement  is  progressive 
and  the  sutures  are  separating,  and  that  intelligence  and  motor  functions 
are  becoming  impaired.     Rapidity  of  enlargement  is  of  as  much  value  as 


Malformations  of  the  Nervous  System.  03? 

the  actual  size.  An  increase  in  circumference  of  an  inch  during  a  month 
is  practically  conclusive.  Increased  size  of  the  head  in  infants,  and 
increasing  mental  disturbance  and  fits  in  older  children,  are  signs  of 
increasing  effusion.  The  sutures  may  separate  after  apparent  closure  up 
to  3,  and  possibly  4,  years  of  age.  Active  symptoms  are  due  to  progressive 
basal  meningitis  or  greater  effusion.  Congenital  hydrocephalus  is  difficult 
of  diagnosis,  if  the  cranium  is  not  enlarged,  for  the  mental  incapacity  is 
perhaps  unrecognisable,  unless  profound,  under  1  year  of  age.  Optic 
atrophy  and  spasticity  of  the  limbs  are  valuable  signs,  for  they  indicate 
gross  cerebral  mischief  or  defect.  In  doubtful  cases  the  tenseness  of  the 
fontanelle,  the  occurrence  of  fits,  and  cyrtometric  tracings  at  intervals  of  a 
month  are  of  much  assistance. 

Course  and  Prognosis. — The  effusion  may  remain  stationary  in  the 
acquired  variety  and  the  signs  thereof  improve.  In  a  mild  case  the  child 
may  develop  physically  and  mentally,  and  grow  up  with  merely  an  unusually 
large  head.  Others  exhibit  motor  weakness,  blindness  and  permanent, 
mental  deficiency  (paralytic  idiocy).  Congenital  cases  generally  die  in  the 
first  few  months  from  marasmus,  convulsions  or  coma  ;  few  live  beyond 
4-5  years.  The  duration  of  life  depends  on  the  amount  of  effusion  and  the. 
amount  of  care  devoted  to  the  child.  Some  are  stillborn,  or  it  maybe  neces- 
sary to  puncture  the  head  to  facilitate  delivery.  The  head  is  rarely  large 
at  birth,  and  the  increasing  size  does  not  attract  attention  for  1-3  months. 
The  prognosis  is  hopeless,  if  the  effusion  is  progressive  or  due  to  a  tumour.. 
Spontaneous  discharge  of  the  fluid  through  the  nose  or  into  the  pharynx 
has  occurred  and  ended  in  recovery  ;  or  the  rapid  evacuation  may  prove 
fatal.  Death  results  from  marasmus,  convulsions,  intercurrent  disease,  and 
exceptionally  rupture  of  the  head.  It  may  be  ushered  in  by  hebetude,, 
flaccid  palsy,  absent  reflexes,  and  loss  of  sphincter  control.  These  children 
are  liable  to  sudden  death,  headache  and  vomiting. 

Treatment. — It  is  useless  to  attempt  to  prevent  effusion  by  diuretics,, 
purgatives,  or  moderate  pressure  with  a  rubber  bandage,  applied  for  a 
week  at  a  time  at  intervals  of  a  week.  The  treatment  during  this  period 
is  that  of  the  meningitis  which  is  the  exciting  cause.  Mercurial  inunctions 
may  be  beneficial.  Operative  measures  are  the  only  means  available  for 
the  removal  of  fluid  and  even  then  it  rapidly  re-accumulates.  It  is  useless 
and  dangerous  to  tap  the  ventricle  with  a  trocar  and  cannula,  inserted  in 
the  anterior  fontanelle  f-l|  in.  from  the  median  line.  Fluid  has  been 
withdrawn  by  this  means  and  sterilised  air  introduced  through  another 
cannula  at  the  same  time,  to  avoid  the  results  of  sudden  reduction  of 
intracranial  pressure.  The  child  died.  Sourma  (1888)  recommended 
exposure  of  the  head  to  the  direct  rays  of  the  sun  daily  for  a  month,. 
15-50  minutes  at  a  time.  It  is  unlikely  to  do  harm.  Lumbar  puncture  is. 
the  best  means  of  removing  fluid,  if  there  is  a  free  communication  between 
the  ventricles  and  the  theca  spinalis.    From  1-3  oz.  should  be  removed  once. 


-638  Chapter   XLIX. 

•or  twice  a  week,  if  there  are  signs  that  the  fluid  is  increasing.  The  sudden 
removal  of  large  quantities  of  fluid  may  cause  fits  or  fatal  collapse.  In  my 
•experience  this  treatment  is  only  of  temporary  benefit,  merely  delaying  the 
progress  of  the  case.  It  was  adopted  for  effusion  in  a  girl,  aged  8  months, 
with  drowsiness,  retraction  of  the  head  and  malnutrition  ;  the  sequel  of 
basal  meningitis  (?)  3  months  previously.  She  was  tapped  17  times  in 
'20  weeks,  35  oz.  being  removed  in  all.  During  this  period  she  gained  124  oz. 
in  weight.  In  spite  of  the  fontanelle  being  no  longer  tense,  the  head 
•continued  to  increase  slowly  in  size  and  the  child  was  apparently  blind  and 
unintelligent.  Other  cases  have  also  failed.  Yet  the  treatment  might  be 
beneficial  and  even  curative,  if  adopted  in  the  early  stages,  for  at  times  the 
•effusion  may  become  stationary  and  it  seems  to  have  a  better  chance  of 
doing  so  if  the  general  nutrition  of  the  patient  improves.  Other  surgical 
measures  are  trephining  through  the  occipital  bone  and  draining  the 
fourth  ventricle,  or  making  a  permanent  communication  between  the 
ventricles  and  the  subarachnoid  space.  Mercury,  as  an  inunction  to  the 
■scalp,  and  iodides  are  the  only  drugs  likely  to  be  of  the  least  benefit.  Con- 
vulsions are  treated  by  the  usual  measures.  Up  to  the  present  the  results  of 
treatment  are  disappointing.  It  is  important  to  maintain  the  general 
nutrition. 

Porencephalus. — Under  the  name  of  porencephalus  may  be  included 
all  those  pathological  holes,  cavities,  hollows  or  depressions  which  extend 
from  the  cortex  towards  the  centre  of  the  brain  and  often  communicate 
with  the  lateral  ventricle.  The  name  was  given  by  Heschl  (1859)  to  that 
deformity  of  the  brain  in  which  there  is  a  communication  between  the  surface 
and  the  lateral  ventricle.  It  was  restricted  by  Audry  (1888)  to  cases  in 
which  there  is  actual  destruction  of  brain  substance  ;  but  the  condition 
may  arise  from  non-development.  Cavities  filled  with  pus  or  blood,  tumour 
or  parasitic  formations,  and  anencephalic  monsters  must  be  excluded. 
Ireland  (1896)  divided  it  into  2  varieties  : — (1)  True  or  Congenital  ; 
the  deformity  dating  from  the  fifth  to  the  seventh  month  of  foetal  life  ; 
(2)  False  or  Acquired  ;  due  to  the  giving  way  of  the  wall  of  the  ventricle 
after  birth,  owing  to  a  destructive  lesion  of  the  cerebral  tissue  between  the 
ventricle  and  the  surface  of  the  hemisphere.  Such  a  lesion  might  occur 
■during  foetal  life,  so  it  would  perhaps  be  better  to  divide  the  cases  into  those 
of  developmental  and  those  of  secondary  origin. 

Morbid  Anatomy. — Some  cavities  are  cyst-like,  limited  by  the  pia  and 
the  ependyma  ;  some  are  limited  by  the  pia  and  open  into  the  ventricle  ; 
and  others  open  into  the  ventricle  and  subarachnoid  space.  A  typical 
cavity  is  funnel-shaped,  lined  by  pia  mater  and  contains  fluid.  The  fluid 
varies  in  quantity  and  may  be  so  abundant  as  to  amount  to  hydrocephalus. 
It  is  usually  as  clear  as  water,  or  of  a  tint  from  yellow  to  brown.  Occasion- 
ally the  sides  of  the  cavity  are  opposed  and  there  is  no  fluid.  The  cavity  is 
«commonly  situated  in  the  portion  of  the  brain  supplied  by  the  middle 


Malformations  of  the  Nervous  System.  639 

■cerebral  artery,  viz.,  the  third  and  ascending  frontal,  the  ascending  parietal, 
the  supramarginal  and  first  temporo-sphenoidal  convolutions.  Less  often 
it  is  in  the  part  supplied  by  the  anterior  or  posterior  cerebral  artery.  Audry 
collected  103  cases  and  found  that  in  32  out  of  96,  in  which  a  good 
description  of  the  lesion  was  given,  it  was  in  both  hemispheres  and  often 
symmetrical.  In  18  almost  the  whole  of  both  hemispheres  had  disappeared. 
The  surrounding  convolutions  may  appear  normal,  may  radiate  from  the 
cavity  outward,  and  may  exhibit  a  more  or  less  cicatricial  change.  The 
basal  ganglia  are  often  smaller  on  the  affected  side.  Secondary  degeneration 
may  follow  on  the  acquired  form  and  failure  of  development  of  the  pyra- 
midal tracts  may  result  from  the  congenital  variety.  A  congenital  cerebral 
palsy  can  occur  although  the  pyramidal  tracts  are  undeveloped  at  birth. 
Sometimes  there  is  marked  asymmetry  or  arrested  development  of  the 
crania]  bones. 

Etiology. — About  two-thirds  of  the  cases  are  of  foetal  origin.  Others 
develop  during  the  first  2  years  of  life  and  more  rarely  later.  It  has  been 
ascribed  to  obliteration  of  fcetal  vessels  (Klebs),  to  anaemia  of  the  middle 
cerebral  artery  (Kundrat),  and  to  non-development.  Kundrat  put  forward 
the  view  that  the  loss  of  substance  affected  definite  vascular  territories, 
but  the  majority  of  cases  anatomically  contradict  this.  The  acquired  form 
may  be  due  to  embolism,  thrombosis,  haemorrhage,  encephalitis  or  external 
injury.  Softening  of  the  cortex  and  underlying  parts  can  result  from 
embolism  or  thrombosis  of  a  cerebral  artery,  and  lead  to  the  formation 
of  a  communication  between  the  lateral  ventricle  and  the  surface  of  the 
brain.  There  is  very  seldom  positive  evidence  of  change  in  the  arteries 
supplying  the  affected  part  of  the  brain.  It  is  most  frequent  in  the  region 
of  the  Sylvian  fissure.  Congenital  syphilis,  obstetrical  causes  and  marasmus 
in  the  newborn  are  suggested  factors  with  no  evidence  in  their  favour. 

The  symptoms  vary  with  the  size  and  situation  of  the  cavity  or  cavities. 
When  both  hemispheres  are  involved  there  are  usually  idiocy,  often  deaf- 
mutism,  convulsions,  paralyses,  diplegia,  rigidity,  contractures  and  cranial 
deformity.  The  palsy  is  of  the  cerebral  spastic  type.  A  small  unilateral 
cavity  may  cause  no  symptoms.  More  often  it  is  fairly  large,  affects  the 
motor  region,  and  produces  partial  or  complete  hemiplegia  of  the  opposite 
side.  The  intelligence  in  these  cases  may  be  unimpaired  or  merely  backward. 
Convulsions  are  not  infrequent  in  extensive  lesions.  Aphasia  is  rare,  except 
in  congenital  cases  with  large  cavities.  Sensation  may  be  unimpaired,  but 
it  cannot  be  accurately  tested  when  the  intellectual  faculties  are  affected. 

Thrombosis  of  the  posterior  cerebral  artery  was  the  assigned  cause  in 
an  epileptic  girl,  aged  22,  who  developed  left  hemiplegia  and  convulsions 
at  3  days  of  age  (Gibson  &  Turner,  1898).  The  autopsy  showed  much 
atrophy  of  the  right  hemisphere,  with  a  large  cyst  in  the  posterior  portion, 
and  atrophy  of  the  convolutions  and  the  left  cerebellar  hemisphere. 
Thrombosis  of  the  middle  cerebral  arterv  in  the  later  months  of  fcetal  life 


640  Chapter   XLIX. 

was  the  explanation  put  forward  in  the  case  of  a  patient,  76  years  old,  who 
died  fiom  pneumonia  during  dementia  of  16  years  duration  (D.  A.  Shirres, 
1902).  He  was  born  at  full  time,  though  the  mother  nearly  aborted  after 
a  severe  fright  in  the  seventh  month  of  pregnancy.  Stiffness  of  the  right 
arm  and  fingers  were  noted  at  1  week.  He  was  rather  backwaid  intellec- 
tually, did  not  walk  until  the  third  year,  nor  talk  until  the  fourth  year,  and 
his  right  foot  was  always  inclined  to  drag.  He  had  no  fits.  He  learnt  to 
write  with  the  left  hand,  married  twice,  had  no  children,  and  his  mental 
faculties  failed  at  60  years  of  age.  The  left  hemisphere  showed  extensive 
porencephalus,  a  sausage-shaped  area  of  destruction,  the  brain  substance 
being  replaced  by  a  membranous  sac  containing  clear  fluid.  The  right 
hemisphere  weighed  560  gms.,  the  left  302  gms.  There  was  also  atrophy  of 
the  optic  thalamus,  the  posterior  limb  of  the  internal  capsule,  the  corpora 
quadrigemina  and  optic  tract,  and  degenerated  pyramidal  fibres  in  the 
cerebral  peduncle,  pons  and  fillet.  Possibly  the  cases  described  (p.  631) 
as  non-development  of  the  prosencephalon  or  congenital  hydrocephalus 
might  be  termed  bilateral  porencephalus. 

Prognosis. — The  affection  is  often  incompatible  with  life.  Only  3  out 
of  18  congenital  cases  lived  beyond  infancy  (Kundrat).  Of  95  cases,  16  lived 
less  than  a  month,  14  died  under  2  years,  32  died  in  the  second  period  of 
infancy  or  in  adolescence,  and  33  lived  to  adult  age  (Audry).  The  outlook 
depends  on  the  extent  of  the  cavitation.  If  the  cavity  is  single,  small  and 
unilateral,  there  is  no  inherent  reason  why  life  should  be  shortened.  If  the 
cavities  are  large  and  bilateral,  the  child  is  practically  certain  to  be  a 
hopeless  idiot  and  to  die  in  infancy.  The  degree  of  diplegic  spasticity  is  a 
measure  of  the  extent  of  the  lesion.  About  one-sixth  of  these  children  die 
from  phthisis. 

Syringomyelia. — In  this  affection  one  or  more  cavities  are  found  in  the 
spinal  cord,  most  often  in  the  cervical  region.  The  cavity  may  be  merely  a 
dilatation  of  the  central  canal,  or  a  space  in  communication  therewith, 
congenital  in  origin,  lined  by  the  same  kind  of  epithelium,  and  surrounded 
by  sclerotic  tissue.  Or  there  may  be  excavation,  the  result  of  softening  and 
liquefaction  of  a  gliomatous  or  sarcomatous  growth  which  infiltrates  the 
cord  and  greatly  increases  its  bulk.  The  first  type  is  the  one  which  chiefly 
occurs  in  children.  Bramann  (1899)  reported  cases  of  symmetrical  gangrene 
of  the  fingers  and  toes  in  3  brothers,  aged  7-13  years  ;  and  Bruns  (1903) 
an  instance  of  familial  syringomyelia  in  4  out  of  5  children,  which  began 
in  each  at  17  years  of  age  with  perforating  ulcers  of  the  balls  of  the  great 
toes.  The  symptoms  vary  with  the  site  and  extent  of  the  excavation,  and 
are  muscular,  sensory  and  trophic.  Other  congenital  defects  of  the  nervous 
system  may  be  present. 

The  intrinsic  muscles  of  the  hand  waste  and  the  hand  becomes  claw- 
like, the  shoulder  muscles  waste  and  lateral  curvature  is  not  uncommon. 
If    the   bulb    is    involved,   there    may   be   hemiatrophy    of   the   tongue. 


Malformations  of  the  Nervous  System.  611 

Extension  of  the  affection  upward  causes  nystagmus,  ocular  palsies,  and 
difficulties  in  articulation  and  deglutition.  Signs  of  sclerosis  and  pressure 
on  the  motor  tracts  may  arise,  e.g.  spasticity.  The  characteristic  sensory 
change  is  loss  of  sensation  to  heat  and  cold,  usually  combined  with 
analgesia.  Heat  may  be  felt  as  cold  and  cold  as  heat.  Tactile  sensation 
may  be  normal  or  completely  abolished.  These  patients  are  very  liable  to 
burn  themselves.  Excessive  redness  and  sweating,  of  a  limb  or  generalised, 
result  from  vasomotor  and  secretory  disturbance.  Arthritic  changes  of  the 
type  of  Charcot's  joint,  perforating  ulcer,  atrophy  of  bone,  acromegaly 
or  cheiromegaly  may  arise.  Morvari's  Disease,  described  by  him  as  occur- 
ring only  in  the  upper  limb,  is  a  variety  characterised  by  multiple  painless 
whitlows,  secondary  loss  of  portions  of  the  extremities,  vasomotor  symptoms 
and  muscular  atrophy.  The  symptoms  of  syringomyelia  are  rare  before 
15  years  of  age.  If  of  congenital  origin,  the  disease  may  remain  stationary. 
It  is  progressive  when  due  to  new  growth,  and  liable  to  neoplastic  formations 
in  the  congenital  variety.  Death  is  often  due  to  intercurrent  disease. 
Treatment  is  general  and  symptomatic. 


Purulent- 


CHAPTER    L. 

MENINGITIS. 

Cerebrospinal ;      Epidemic    and    Sporadic — Post-basic- 
cnlous — Syphilitic — Pachymeningitis . 


Tuber- 


Meningitis  or  leptomeningitis  is  a  genera]  inflammation  of  the  pia- 
arachnoid.  There  are  probably  as  many  varieties  as  there  are  microbes 
which  attack  the  meninges.  All  cases  are  cerebrospinal,  but  the  extent 
of  the  spinal  inflammation  is  variable  and  may  be  trivial.  Careful  examina- 
tion always  reveals  extension  to  the  brain,  so  the  affection  is  strictly  a 
meningo-encephalitis.  The  infective  organism  reaches  the  meninges  through 
the  blood  or  lymph,  or  by  direct  extension  from  adjacent  structures. 
Predisposing  causes  are  lowered  vitality,  injury  and  heat-stroke.  The 
symptoms  vary  little  with  the  type,  and  may  be  absent  throughout  or 
obscured  by  those  of  the  primary  disease.  The  main  features  are  headache, 
intracranial  pressure,  tense  fontanelle,  psychical  changes,  cerebral  mal- 
nutrition and  irritation,  and  generally  fever.  The  age-incidence  of  the 
most  frequent  varieties  is  shown  in  the  following  table,  based  on  a  series 
of  125  cases  ;    males  66,  females  59. 

The   Age- Incidence  of  Meningitis. 


Months  Months 
0-6         6-12 

Year 
1-2 

Year 
2-3 

Year 
3-4 

Year 
4-5 

Total 

Over 

5 
Years 

Cerebrospinal 

15             11 

4 

3 

2 

0 

35 

1 

Pneumococcal 

5 

3 

2 

0 

1 

0 

11 

0 

Tuberculous... 

3 

7 

16 

13 

10 

5 

54 

17 

Total     ... 

1 

23 

21 

22 

16 

13 

5 

100 

18 

Of  these  125  cases  111  were  fatal  and  88  were  examined  after  death.  Of 
71  tuberculous  cases  58  were  verified  after  death  and  54  were  under  5  years 
of  age.  All  the  pneumococcal  ones  were  fatal  and  verified  post  mortem  ; 
the  youngest  was  only  3  days  old.  Out  of  36  sporadic  or  post-basic 
cerebrospinal  cases  35  were  under  4  years  of  age.     The  diagnosis  was  verified 


Meningitis.  643 

after  death  in  20  out  of  24  which  were  fatal  and  by  lumbar  puncture  during 
life  in  some  of  the  remainder.  Only  5  were  ascribed  to  ear  disease  and 
2  to  injury.  Other  cases  ending  in  recovery  have  been  omitted  because  of 
an  element  of  doubt  in  the  diagnosis. 

Classification. — The  division  into  primary  and  secondary  meningitis, 
according  to  the  discovery  or  not  of  a  primary  source  of  infection,  is 
valueless.  The  division  into  meningitis  of  the  convexity  and  that  of  the 
base  is  of  little  use,  for  both  are  frequently  involved.  The  most  useful 
■classification  is  the  following  : — 

(1)  Septic,  Suppurative  or  Purulent. — This  is  an  acute  secondary 
meningitis  due  to  many  organisms  and  divisible  according  to  its 
bacteriology  into  : — 

(a)  Pneumococcal,  secondary  to  pneumonia  or  direct  infection  from  the 
nose  ;    sometimes  primary. 

(6)  Influenzal,  secondary  to  affections  of  the  naso-pharynx,  adjoining 
sinuses,  and  otitis  media  ;  often  a  mixed  infection.  The  organism 
has  been  found  in  the  cerebrospinal  fluid  during  life  and  in  the 
exudate  after  death. 

(c)  Typhoidal. 

(d)  Pyogenic,  commonly  streptococcal  or  staphylococcal  ;  secondary 
to  injury,  bone  disease,  and  scarlet  fever. 

(e)  B.   Coli  Infections. 

Purulent  meningitis  cannot  be  differentiated  absolutely  by  clinical, 
pathological  or  bacterial  evidence  from  the  next  group,  and  is  sometimes 
included  in  one  group  named  "  Acute  Meningitis." 

(2)  Cerebrospinal  Meningitis. — This  is  an  acute  primary  meningitis, 
■due  to  the  diplococcus  intracellulars  meningitidis  or  meningococcus,  and 
sometimes  to  the  pneumococcus.  It  may  be  epidemic  or  sporadic  in 
•occurrence.     Post-basic  meningitis  is  also  of  this  type. 

(3)  Tuberculous  Meningitis. 

(4)  Syphilitic  Meningitis. 

(5)  Pachymeningitis. 

All  forms  of  meningitis  are  anatomically  much  alike.  Every  organism 
produces  more  or  less  the  same  kind  of  exudation.  In  the  epidemic  type  the 
.amount  of  exudate  is  considerable  and  often  greater  in  the  membranes  of 
the  cord  than  in  those  of  the  brain.  It  consists  of  polymorphs  in  a  sero- 
•alburninous  fluid.     The  meningococci  are  found  in  the  protoplasm  of  the 

I  neutrophilic  leucocytes.  Lymphocytes  and  mononuclear  cells  are  present 
in  much  smaller  numbers.     In  later  stages  these  cells  may  predominate 


644  Chapter  L. 

richer  in  fibrin  and  that  of  streptococcal  meningitis  is  almost  the  same  in 
character  ;  the  polymorphs  far  outnumber  the  mononuclear  cells.  In  the 
tuberculous  disease  mononuclear  cells  are  predominant.  Fibrin  is  abundant 
in  the  exudate  of  acute  cases  but  in  the  more  chronic  forms  it  is  scanty  or 
absent. 

Purulent  Meningitis. — Syn.  :  Septic  or  Suppurative  Meningitis — 
Acute  Meningitis  or  Meningo-encephalitis. — This  variety  includes  all  those 
acute  attacks  which  are  not  due  to  the  meningococcus.  It  is  characterised 
by  the  effusion  of  pus  or  purulent  lymph,  and  generally,  but  by  no  means, 
always,  affects  the  convexity  of  the  brain.  Its  localisation  depends  mainly 
upon  the  primary  cause.  It  may  occur  at  any  age,  even  in  the  newborn. 
Of  12  recent  cases,  11  were  under  4  years  of  age.  The  exciting  causes  were 
a  blow  on  the  head  by  a  cricket  ball,  purulent  pleurisy  2,  otitis  media  2y 
and  epiphysitis  1  ;  and  the  other  6  were  probably  meningococcal.  The 
usual  causes  are  blows  on  the  head,  heat-stroke,  extension  of  septic 
inflammation  from  the  scalp  or  bones,  extension  of  inflammation  from  the- 
nose,  ear  or  orbit,  rupture  of  an  intracranial  abscess,  specific  fevers,, 
erysipelas,  pyemic  conditions,  and  infective  endocarditis,  influenza,  puru- 
lent pleurisy  and  pneumonia.  It  is  stated  that  the  middle  ear  is  by  far  the 
most  frequent  source  of  infection  ;  but  much  too  great  importance  has. 
been  attached  to  otitis  media.  This  is  a  common  terminal  affection  in 
children  dying  from  all  causes,  and  in  meningitis  is  quite  as  likely  to  be 
secondary  as  primary.  It  is  generally  stated  that  young  infants  are 
particularly  liable  to  extension  of  inflammation  from  the  middle  ear  to  the 
meninges,  along  the  connective  tissue  passing  from  the  tympanic  mucosa 
and  mastoid  cells  through  the  petro-squamous  fissure  to  the  dura  mater. 
Possibly  infection  may  be  carried  along  the  sheaths  of  arteries,  veins  or 
lymphatics.  If  the  inflammation  is  confined  to  the  tympanum  and  does, 
not  involve  the  labyrinth  there  is  little  danger,  but  the  labyrinth  may  be 
affected  in  infants.  On  naked  eye  examination  there  is  often  no  evidence  of 
direct  communication.  The  otitis  media  of  measles  and  scarlet  fever- 
generally  causes  sinus  thrombosis  before  it  sets  up  meningitis.  The 
tympanum  so  often  contains  sero-pus  in  infants  dying  from  other  diseases,, 
that  it  seems  unlikely  to  be  the  source  of  infection.  Were  it  so,  one  would 
expect  meningitis  to  be  a  much  more  common  disease.  Possibly  the. 
infective  organism  gets  in  through  the  naso-pharyngeal  mucosa  or  other- 
channels.  Extension  from  the  nasal  cavity  takes  place  through  the 
cribriform  plate  of  the  ethmoid.  The  disease  has  followed  operative  treat- 
ment of  the  naso-pharynx,  e.g.  removal  of  tonsils,  adenoids  and  polypi. 

Bacteriology. — In  25  cases,  Netter  found  the  pneumococcus  18, 
streptococcus  4,  meningococcus  2,  and  other  organisms  in  3.  These  results, 
coincide  with  general  experience.  The  pneumococcus  is  far  the  most 
common  organism  and  may  cause  epidemics.  In  cases  associated  with  ear 
disease,  the  latter  is  often  pneumococcal.     This  variety  of  meningitis  mav 


Meningitis.  G45 

complicate  any  inflammatory  pleural  or  lung  affection.  Primary  pneu- 
mococcal meningitis  has  been  recorded  in  a  few  cases.  The  next  most 
■common  organism  is  the  streptococcus,  secondary  to  a  general  or  local 
infection.  The  other  organisms  that  have  been  found  are  the  influenza 
bacillus,  typhoid,  paratyphoid,  B.  coli,  B.  pyocyaneus,  Friedlander's 
bacillus,  various  staphylococci,  the  gonococcus  and  even  bacillus  lactis 
iaerogenes. 

Morbid  Anatomy. — Slight  inflammation  is  limited  to  hypersemia  of 
the  pia,  which  is  infiltrated  with  streaks  and  dots  of  purulent  lymph 
•due  to  effusion  into  the  subarachnoid  space,  and  therefore  adherent. 
If  more  pronounced  there  may  be  extensive  thickening  and  matting  of  the 
membrane,  and  much  lymph  and  pus.  Purulent  effusions  extend  to  the 
subdural  space  and  form  a  layer  on  the  surface  of  the  brain  which  can  often 
be  peeled  or  washed  off.  Pneumococcal  cases  generally  show  a  thick  layer 
•of  greenish  yellow  pus  over  the  convexity  in  24-48  hours.  It  is  often  most 
marked  on  the  posterior  half  of  the  base  of  the  brain  and  thus  simulates 
post-basic  meningitis.  In  influenzal  meningitis  thick  greenish  pus  may  be 
found  over  the  vertex  and  base,  and  may  extend  in  a  thick  layer  round  the 
spinal  cord,  especially  posteriorly  and  laterally.  When  caused  by  disease 
•of  the  nose  or  ear,  the  inflammation  is  most  marked  at  the  base  and  sides 
•of  the  brain.  In  other  varieties  it  mainly  affects  the  vertex.  The  con- 
volutions are  flattened  by  pressure  from  within.  The  inflammation  affects 
the  choroid  plexus  and  the  ependyma  so  much  as  to  deserve  the  name  of 
'"  ependymitis."  This  produces  an  increase  in  the  intra-ventricular  fluid 
which  is  clear,  turbid,  sero-purulent  or  purulent.  Thrombosis  may  be 
present  in  the  cerebral  sinuses  or  the  superficial  veins  of  the  cortex.  In 
very  chronic  cases  the  membranes  are  thickened  and  adherent ;  and  the 
•cortex  undergoes  more  or  less  atrophy  and  sclerosis. 

Symptoms. — The  onset  is  gradual  or  sudden.  It  is  usually  sudden,  if 
the  child  is  well  previously  or  if  due  to  rupture  of  an  intracerebral  abscess. 
It  is  ushered  in  with  headache,  vomiting,  rigors,  delirium  and  high  fever  ; 
or  with  fever,  rapid  pulse,  furred  tongue,  anorexia,  vomiting,  restlessness 
and  drowsiness.  More  frequently  the  symptoms  develop  gradually  ;  an 
irritative  stage  being  followed  by  coma  and  paralysis,  and  preceded  by  head- 
ache, general  or  localised,  and  sometimes  intermittent.  Prodromal  signs 
.aie  those  of  the  antecedent  disease,  and  sometimes  may  be  entirely  absent 
or  such  as  can  be  ascribed  to  the  disease. 

Retraction  of  the  head,  rigidity  of  the  neck  and  opisthotonos  may 
occur  quite  early,  but  are  much  less  common  than  in  tuberculous  and 
meningococcal  meningitis.  Kernig's  sign,  retraction  of  the  abdomen,  and 
general  rigidity  may  be  present.  These  symptoms  depend  upon  tonic 
muscular  spasm  or  hypertonia.  Convulsions  are  fairly  common  and 
generalised.  They  may  be  unilateral,  or  begin  on  one  side  or  in  one  limb 
and  quickly  involve  the  whole  body.    Muscular  twitchings  and  spasmodic 


646  Chapter  L. 

or  continuous  rigidity  are  also  common.  The  fontanelle  bulges.  Paralysis, 
usually  more  or  less  completely  hemiplegic,  may  be  present  after  the  fits, 
or  may  arise  independently.  Convulsions  and  rapidly  increasing  coma  may 
be  the  only  symptoms.  The  mental  condition  varies.  Often  the  child  lies- 
in  a  condition  of  stupor  or  semi-coma  ;  or  delirium  is  present  and  soon 
lapses  into  coma.  Teeth-grinding,  champing  of  the  jaws  and  trismus  develop 
in  the  course  of  the  disease. 

Irregular  squints  and  movements  of  the  eyes,  nystagmus,  conjugate 
deviation  and  paralysis  of  the  sixth  nerve  are  often  present.  The  pupils  are 
generally  dilated,  frequently  rigid  and  unequal.  Optic  neuritis  may  be 
absent  throughout  or  develop  in  late  stages. 

The  fever  is  high,  103-105°  F.  ;  lowest  in  the  influenzal  type.  The 
pulse  is  frequent,  sometimes  infrequent,  and  is  not  irregular.  It  becomes 
abnormally  rapid  before  death.  Respiration  is  frequent  or  irregular.  The 
reflexes  are  very  variable  and  alter  in  the  course  of  the  disease.  In  pneu- 
mococcal and  streptococcal  forms  the  organism  can  almost  always  be 
recovered  by  culture  from  the  blood  and  cerebrospinal  fluid. 

In  the  mildest  cases  the  symptoms  may  be  limited  to  headache,  sleep- 
lessness, mental  disturbance,  slight  retraction  of  the  head  and  moderate 
fever.  These  cases  are  difficult  to  diagnose  from  otitis  media  and  from 
encephalitis.  Sometimes  the  disease  is  "  latent,''''  that  is  it  gives  rise  to  no 
distinctive  features,  when  it  occurs  as  a  terminal  event  in  the  course  of  an 
acute  disease,  and  is  only  discovered  at  the  autopsy.  Consciousness  may  be 
present  till  a  few  hours  before  death,  or  there  may  be  marked  somnolence 
with  a  tense  pulseless  fontanelle  in  infants. 

Primary  pneumococcal  meningitis  is  usually  severe  and  rapidly  fatal, 
but  it  may  be  mild.  It  can  only  be  diagnosed  by  lumbar  puncture.  A  boy, 
9  months  old,  developed  fever,  vomiting,  head  retraction,  and  diarrhoea 
with  offensive  stools  at  the  onset,  followed  by  constipation.  The  fontanelle 
was  tense,  temperature  range  103-105°  F.,  knee  jerks  active,  and  Kernig's 
sign  present.  The  breathing  was  rapid  and  the  course  like  that  of  pneu- 
monia, the  temperature  falling  on  the  tenth  day.  The  child  never  seemed 
very  ill  and  recovered.  The  pneumococcus  was  found  in  the  cerebrospinal 
fluid. 

Course  and  Prognosis. — The  outlook  depends  Upon  the  cause  and  the 
acuteness  of  the  symptoms.  It  is  best  in  pneumococcal  cases  and  those 
secondary  to  heat-stroke.  Under  other  conditions  the  prospect  is  bad. 
The  influenzal  type,  though  purulent,  is  not  always  fatal.  The  duration 
averages  8  or  9  days,  and  death  is  due  to  convulsions,  or  cardiac  or 
respiratory  failure.  Even  if  recovery  takes  place  it  is  common  for  some- 
mental  defect  to  remain  or  motor  defects  to  ensue. 

Diagnosis  depends  upon  the  conjunction  of  symptoms  of  acute 
meningitis  with  some  cause  likely  to  induce  a  suppurative  form  of  disease. 
The  child  must  be  carefully  examined  and  the  history  inquired  into  for 


Meningitis.  647 

evidence  of  one  or  other  of  the  etiological  factors  above  mentioned.  It  is 
chiefly  likely  to  be  mistaken  for  tuberculous  or  cerebrospinal  meningitis, 
encephalitis,  acute  otitis  media,  and  enteric  fever.  If  the  process  is  limited 
to  the  convexity  of  the  brain,  cerebral  symptoms  may  be  absent  or  masked 
by  those  of  the  primary  disease.  Deafness  is  generally  associated  with  facial 
paralysis,  whereas  in  otitis  media  it  occurs  independently  and  may  be 
unilateral.  The  examination  of  the  fluid  obtained  by  lumbar  puncture  is 
essential  to  accurate  diagnosis  (p.  618). 

The  treatment  will  be  considered  in  connection  with  other  forms 
of  meningitis. 

Cerebrospinal  Meningitis. — Syn.  :  Cerebrospinal  Fever — Spotted  Fever 
— Malignant  Purpuric  Fever — Stiff-neck  Fever  of  America —  Acute  General 
Lepto-meningitis. — The  epidemic  type  of  cerebrospinal  fever  should  strictly 
be  grouped  with  the  specific  fevers,  but  on  account  of  the  preponderance 
of  cerebral  symptoms,  it  is  better  included  with  the  other  forms  of  menin- 
gitis. Sporadic  cases  and  the  post-basic  meningitis  of  infants  are  due  to  a 
similar  microbial  infection,  and  their  course  and  symptoms  are  usually 
typical  of  a  meningitis.     It  is  due  to  a  systemic  infection  of  microbial  origin. 

The  disease  was  recognised  as  a  distinct  entity  in  Geneva  by  Yieusseaux 
in  1805,  and  it  spread  in  epidemic  form  in  America  from  1806  onwards. 
Since  then  numerous  epidemics  have  been  reported  in  many  parts  of  the 
world.  A  big  outbreak  occurred  in  the  State  of  New  York  in  1904-1905, 
and  a  still  bigger  one  in  Silesia.  Since  1906  outbreaks  have  occurred  in 
Glasgow,  Edinburgh  and  Leith,  Falkirk  and  Grangemouth,  Belfast,  Cork 
and  Dublin,  various  parts  of  America,  Hamburg,  Copenhagen,  Naples  and 
Gibraltar.  This  distribution  is  interesting,  for  the  outbreaks  are  most  of 
them  in  relation  to  seaport  centres  in  connection  with  each  other. 

Bacteriology. — Micrococci  were  found  in  the  blood  and  exudate  by 
Gaucher  (1881)  ;  in  the  exudate  by  Leyden  and  Ughetti  (1883)  ;  in  the 
blood,  exudate  and  protoplasm  of  the  cells  by  Marchiafava  and  Celli  (1884), 
The  organism  was  cultivated  and  described  by  Weichselbaum  (1887). 
He  found  it  in  the  ventricular  fluid  in  the  polynuclear  cells  and  named  it  the 
diplococcus  intracellularis  meningitidis.  These  results  have  been  confirmed 
by  numerous  other  observers. 

The  organism  occurs  in  single  cocci,  pairs,  tetrads  or  groups,  and  is 
markedly  intra-cellular.  It  is  aerobic  and  grows  beston  nutrose ascitic  agar 
or  "  nasgar,"  and  forms  in  24  hours  at  37°  C.  smooth,  moist,  grey,  trans- 
lucent, circular  and  oval  colonies  with  regular  outline  ;  it  will  not  grow  on 
nasgar  below  25°  C.  Its  vitality  is  low,  and  it  is  rapidly  killed  by  drying 
and  sunlight.  Microscopically  it  is  indistinguishable  from  the  gonococcus 
and,  like  this  organism  and  the  micrococcus  catarrhalis,  it  is  Gram-negative. 
It  does  not  clot  milk.  It  produces  an  acid  reaction  in  dextrose  and  maltose 
media.      The   micrococcus   catarrhalis  is   smaller,    and   produces  no   acid 


648  Chapter  L. 

reaction  in  these  media.     The  organism  produces  indol  but  no  gas.     Its 
pathogenic  virulence  is  variable,  and  the  poison  is  an  endotoxin. 

It  was  found  by  lumbar  puncture  in  82  per  cent,  of  810  cases  in  New 
York  in  1901.  Elser  (1905)  isolated  it  in  109  out  of  130  cases.  It  may  be 
found  in  the  blood  and  is  then  a  sign  of  severity.  It  is  not  always  present 
in  pure  culture  and  may  be  mixed  with  pneumococci,  staphylococci,  strepto- 
cocci, B.  coli,  B.  typhosus,  the  influenza  bacillus,  the  diplococcus  crassus 
and  even  the  tubercle  bacillus.  It  may  be  crowded  out  by  these  other 
organisms.  A  Gram-positive  coccus,  in  other  respects  the  same  as  the 
meningococcus,  has  also  been  found.  Thus  the  bacteriological  evidence  is 
strongly  in  favour  of  the  disease  being  due  to  a  general  blood  infection,  by 
the  meningococcus,  producing  local  manifestations  and  meningitis. 

Morbid  Anatomy. — In  early  cases  nothing  is  found  beyond  intense 
hyperemia  of  the  pia-arachnoid,  perhaps  localised,  acute  congestion  of 
the  brain  and  engorgement  of  the  sinuses.  Later  on  the  effusion  of  serum 
and  lymph  leads  to  the  brain,  sometimes  within  24  hours,  being  covered 
with  greenish-yellow  pus.  The  exudation  is  serous,  fibrinous  or  purulent. 
It  is  chiefly  situated  over  and  around  the  optic  commissure,  cerebellum,  pons, 
bulb,  and  along  the  Sylvian  fissure.  It  may  extend  up  the  sides  and  appear 
in  patches  on  the  coitex,  or  cover  the  whole  brain.  The  brain  shows  bright 
red  spots  on  section,  the  "  puncta  vasculosa,"  due  to  dilatation  of  the 
vessels.  The  cortex  is  cedematous  and  shows  cell  infiltration  of  the  super- 
ficial layers.  It  may  be  softened  locally  (focal  encephalitis)  or  generally. 
The  fluid  in  the  ventricles  varies  in  amount,  and  in  character  from  mere 
turbidity  to  pure  pus.  The  cord  exhibits  similar  hyperaeinia  of  the 
membranes  and  exudations  of  variable  character,  chiefly  on  the  posterior 
surface.  Occasionally  the  whole  cord  is  covered  with  thick  purulent  lymph. 
The  lungs  and  pleura  may  show  bronchitis,  broncho-pneumonia,  atelectasis, 
hypostatic  congestion,  pleurisy  and  pleural  petechia?.  Petechia?  may  be 
found  over  the  heart  and  pericardium  ;  and  serous,  hemorrhagic  or  purulent 
pericarditis  may  be  present.  An  enlarged  spleen  is  found  in  about  half 
the  cases.  The  mesenteric  glands  are  enlaiged  and  congested  ;  the  solitary 
follicles  enlarged  and  bright  red  ;  and  the  small  intestine  engorged.  This 
lymphatism  was  specially  noted  by  Wettenhoffer  in  the  Silesian  epidemic, 
and  is  said  to  follow  intraspinal  inoculation  in  monkeys.  Other  anatomical 
changes  are  due  to  complications, viz.,  eye  and  ear  disease,  purulent  arthritis, 
endocarditis,  enteritis  and  nephritis.  Patients,  who  have  recovered  and 
died  subsequently  from  other  disease,  usually  show  thickening  and  adhesion 
of  the  pia  to  the  brain,  local  opacities  and  thickenings,  and  occasionally 
areas  of  sclerosis  and  hydrocephalus. 

Mode  of  Infection. — There  is  a  certain  amount  of  evidence  that  the 
nose  is  the  chief  channel  of  infection,  for  the  organism  has  been  found  in 
the  nasal  discharge  in  25-50  per  cent,  of  the  cases,  and  even  in  the  unaffected. 
Possibly  the  infection  is  conveyed,  via  the  adenoid  tissue  in  the  naso- 


Meningitis.  GI9 

pharynx,  through  the  lymphatics  and  blood  vessels.  On  the  other  hand  it  is 
very  rare  for  inflammation  of  the  meninges  to  develop  by  continuity  from 
the  ethmoid  cells,  and  it  is  uncommon  to  find  meningitis  over  the  inferior 
part  of  the  frontal  lobe.  Perhaps  the  nasal  cavities  are  infected  from  the 
meninges.  A  possible  source  of  infection  is  through  the  conjunctiva,  for 
■conjunctivitis  is  a  frequent  early  sign.  Wettenhoffer  (1906)  regards  the 
tonsils  as  the  probable  source  of  entry,  and  states  that  the  risk  of  infection 
varies  directly  as  the  size  of  the  tonsils.  The  throat  is  often  found  injected. 
There  is  no  reliable  evidence  that  the  disease  is  conveyed  by  contacts,  and 
meningococci  were  not  found  in  the  throat  in  such  cases  in  the  Belfast 
•epidemic.  Another  argument  against  nasal  infection  is  the  fact  that  the 
lesions  in  the  spinal  cord  are  of  older  standing  than  those  of  the  brain. 
Brain  symptoms  may  be  slight,  though  pus  is  found  in  the  canal.  The  early 
loss  of  abdominal  reflexes  also  suggests  a  cord  infection.  Another  view  is 
that  it  is  spread  by  infected  dust,  for  outbreaks  may  occur  in  the  same 
house  after  long  intervals.  Possibly  it  is  a  form  of  food  infection  for  it 
rarely  occurs  in  the  breast-fed.  It  is  most  frequent  among  the  poor  in 
whom  the  liability  to  food  infection  is  great.  It  is  especially  common  in 
•children,  who  may  acquire  the  infection  through  crawling  about  floors, 
playing  in  dusty  streets,  and  putting  various  objects  in  their  mouths. 
Further  support  of  the  hypothesis  of  intestinal  infection  is  found  in  the 
marked  abdominal  lesions.  The  intestines  are  engorged,  and  the  solitary 
•and  mesenteric  glands  enlarged. 

Etiology. — Epidemics  are  due  to  increased  virulence  of  the  organism 
■and  an  associated  depressant  factor.  Outbreaks  are  frequent  in  barracks 
and  under  all  conditions  of  overcrowding  and  bad  hygiene.  School  epidemics 
are  rare,  and  the  disease  is  not  common  among  the  better  classes.  Lower 
animals,  especially  horses,  are  liable  to  it,  but  there  is  no  evidence  of  the 
■communicability  of  the  disease  from  animal  to  man.  In  the  occurrence  of 
house  epidemics  and  other  outbreaks  it  is  paralleled  by  similar  outbreaks 
•of  pneumonia  and  typhus.  It  was  probably  spread  by  coughing  and 
sneezing  in  the  few  cases  of  direct  infection  on  record.  There  is  no  reliable 
■evidence  that  it  is  spread  by  contacts.  Isolated  sporadic  cases  are  not 
infrequent  in  various  districts  and  at  different  times  of  the  year,  but 
they  do  not  act  as  foci  for  the  spread  of  the  disease.  It  is  therefore 
■only  mildly  contagious.  Those  outbreaks  which  occur  as  a  complication 
or  sequel  of  infectious  fever,  pneumonia  or  epidemic  dianhcea,  are  possibly 
•due  to  other  organisms.  The  disease  is  most  common  in  winter  and  spring, 
perhaps  on  account  of  the  liability  to  nasal  catarrh,  exposure  to  cold,  and 
the  lack  of  sunlight. 

Both  sexes  are  equally  liable,  especially  in  childhood,  but  in  later  life 
it  is  much  more  prevalent  in  males.  Children  with  a  tendency  to  lympha- 
tism,  e.g.  adenoids  and  enlarged  tonsils,  are  particularly  susceptible.  It  is 
most  frequent  under  the  age  of  5  years  ;   after  10  years  it  is  distinctly  less 


650  Chapter  L. 

common,  and  after  30  decidedly  rare.  It  has  been  recorded  as  early  as- 
3  weeks  of  life.  From  70-90  per  cent,  of  the  fatal  cases  are  under  15  years  of 
age.  In  New  York  67  per  cent,  of  2180  cases  were  under  10  years  and  of 
these  15  per  cent,  were  under  1  year. 

Symptoms. — The  incubation  period  is  uncertain,  probably  from  1-4 
days.  There  are  two  main  types  of  the  disease  : — (1)  Toxaemic,  malignant 
or  fulminating,  with  profound  blood  poisoning ;  and  (2)  Meningitic. 
The  onset  is  sudden  in  about  90  per  cent.  It  may  be  extremely  gradual,  no- 
symptoms  being  noted  before  hydrocephalus  has  begun.  For  a  few  hours 
or  days  there  may  be  premonitory  symptoms  such  as  headache,  languor, 
anorexia,  chilliness,  pain  in  the  back  and  limbs,  stiffness  of  the  neck  muscles,. 
a  full  and  strong  pulse,  and  temperature  101-102°  F.  In  an  acute  toxaemic- 
sporadic  case  in  an  infant,  18  months  old,  the  first  symptom  was  pain  in 
the  ankle  of  a  few  hours  duration  ;  this  was  followed  by  convulsions  for 
24  hours,  temperature  105°  F.,  dyspnoea,  very  frequent  pulse,  uncon- 
sciousness and  other  signs  of  a  profound  toxaemia,  suggestive  of  a  pneumo- 
coccal infection.  Definite  meningitic  symptoms  developed  in  a  few  days.. 
The  usual  onset  is  in  the  latter  half  of  the  day  with  vomiting,  stiffness  of  the 
neck  or  retraction  of  the  head,  severe  occipital  headache,  high  fever,  rigors 
or  chilliness  and  convulsions.  Headache  is  less  marked  in  children  than 
in  adults  and  convulsions  are  more  common.  The  child  rapidly  passes  into' 
a  state  of  stupor  or  delirium  ;  and  coma  may  come  on  in  a  few  hours.  In 
the  toxaemic,  malignant  or  fulminating  cases  are  found  great  depression,, 
muscular  spasms  and  purpuric  rash,  with  moderate  fever  and  perhaps  a 
pulse  rate  as  low  as  50.  Thus  a  4-month  old,  well-nourished  baby  had 
a  little  abdominal  pain  and  in  a  few  hours  was  distinctly  drowsy  ;  a  few 
bright  red  purpuric  spots  were  found  ;  the  pulse  rate  and  respirations 
became  very  frequent,  pupils  small  and  unequal,  and  death  occurred  within 
36  hours,  preceded  by  a  discharge  of  turbid  fluid  from  the  nose,  mouth 
and  left  ear.  Many  more  spots  had  come  out  on  the  upper  part  of  the 
back,  and  large  patches  of  purplish  discoloration  on  the  back  and  thighs. 
Pain  in  the  limbs  and  trunk  are  often  present,  sometimes  temporarily  ; 
and  giddiness  or  vertigo  is  not  uncommon.  Inflammatory  conditions  of  the 
tonsils,  fauces,  pharynx  and  posterior  nares  have  been  noted  at  the  onset 
in  many  acute  cases,  especially  in  the  Silesian  epidemic. 

In  a  typical  case  the  child  lies  on  the  side  with  the  head  retracted,  spine 
arched  forward  and  the  limbs  flexed  ;  the  neck  muscles  are  very  rigid  and 
resist  forward  flexion  of  the  head.  It  is  restless,  screams  from  pain,  and 
exhibits  general  hyperaesthesia,  sometimes  tenderness  over  the  cervical 
vertebrae.  The  headache  may  be  referred  to  any  part  of  the  skull  and  is 
severe.  Pain  continues  duiing  the  acute  stages  and,  besides  being  felt  in  the 
head,  is  also  referred  to  the  back  of  the  neck  and  spine  and  almost  any  part 
of  the  body  ;  the  slightest  movement  may  cause  most  severe  pain.  It 
usually  diminishes  during  the  second  week. 


Meningitis.  651 

Muscular  contractures  result  from  the  irritation  and  give  rise  to  the 
stiffness  of  the  muscles  of  the  neck  and  back,  retraction  of  the  head, 
opisthotonos  and  flexion  of  the  limbs.  It  comes  on  in  the  course  of  2  or  3 
days,  may  persist  for  some  weeks,  and  disappears  slowly.  The  rigidity 
of  the  neck  may  vary  from  day  to  day  and  is  usually  the  last  sign  to 
disappear.  Teeth  grinding,  twitching  of  the  mouth  angles,  twitching  of  the 
hands  and  arms,  rolling  of  the  eyes  and  squint  are  frequently  piesent. 

Hyper£esthesia  is  more  marked  in  this  than  in  any  other  form  of 
meningitis.  It  may  even  be  detected  when  the  child  is  almost  comatose. 
There  is  marked  sensitiveness  to  cold.  The  skin  may  exhibit  the  tache 
cerebrale.  In  bad  cases  a  dusky  mottling  is  seen  during  the  first  2  weeks, 
and  in  the  worst  the  skin  is  covered  with  subcutaneous  haemorrhages, 
varying  from  minute  red  dots  to  bluish  spots  and  larger  patches  like  bruises. 
This  purpuric  eruption  gave  rise  to  the  name  of  "  spotted  fever,"  but  it 
is  quite  uncommon  nowadays.  The  rash  may  come  out  in  crops  and  is 
sometimes  like  that  of  typhoid.  Towards  the  end  in  fatal  cases  are  found 
fine  punctate  haemorrhages  over  the  abdomen,  and  even  larger  subcutaneous 
bruises  are  not  uncommon.  A  rash  occurs  at  some  period  in  about  20  per 
cent.  Herpetic  eruptions  about  the  lips  and  angles  of  the  mouth,  and 
occasionally  on  the  other  parts  supplied  by  branches  of  the  fifth  nerve, 
occur  in  about  10  per  cent.  Erythematous  and  roseolous  rashes,  suggestive 
of  scarlet  fever  or  measles,  have  also  been  noted. 

Reflex  action  is  often  abolished  early.  The  knee  jerks  are  sometimes 
exaggerated  at  the  onset,  and  almost  always  absent  later  ;  occasionally  they 
are  variable.  The  abdominal  reflex  is  lost  early.  There  is  no  ankleclonus 
and  no  Babinski  sign.  Kernig's  sign  is  more  often  present  than  absent. 
It  is  frequently  difficult  to  elicit  under  the  age  of  2,  and  usually  present 
after  that  age. 

The  tongue  is  moist  and  slightly  furred  ;  appetite  impaired  or  lost ; 
and  thirst  and  constipation  may  be  present.  Swallowing  may  be  difficult 
because  of  the  retraction  of  the  head  or  paralysis  of  the  muscles  of  degluti- 
tion. There  is  no  special  tendency  to  constipation,  and  diarrhoea  is  by  no 
means  an  infrequent  complication.  Retraction  of  the  abdomen  is  not  a 
notable  symptom.  Vomiting  is  common  at  the  onset  and  during  the  course 
of  the  disease,  reappearing  with  exacerbations  of  the  morbid  process.  It 
is  sometimes  frequent  in  protracted  cases  and  relieved  by  lumbar  puncture. 
It  is  of  the  cerebral  type,  unaccompanied  by  nausea,  and  sometimes  ex- 
plosive or  projectile.  In  later  stages  it  is  due  to  hydrocephalus.  Loss  of 
flesh  and  strength  is  lapid  and  severe,  much  more  so  than  in  tuberculous 
meningitis.  The  spleen  is  sometimes  enlarged  and  the  glands  are  often  hard 
and  shotty. 

The  pulse  is  increased  in  frequency  in  proportion  to  the  severity  of  the 
attack,  but  it  may  be  slow  and  fall  in  severe  cases.  It  becomes  less  frequent 
and  irregular  from  coma  due  to  intra-ventricular  effusion.    It  often  varies 


652  Chapter    L. 

greatly  in  frequency  at  different  periods  of  the  day,  but  it  rarely  presents 
the  intermissions  and  characteristic  irregularity  of  tuberculous  meningitis. 
The  ratio  of  pulse  and  respiration  is  irregular.  Towards  the  end  the  pulse 
becomes  uncountable.  Marked  leucocytosis,  with  diminution  or  absence 
of  eosinophils,  is  found  on  examination  of  the  blood  in  bad  cases.  Myo- 
carditis was  noted  as  common  and  a  frequent  cause  of  death  in  the  Lisbon 
epidemic. 

The  respiration  is  increased  in  frequency,  occasionally  sighing  or 
irregular,  sometimes  of  the  Cheyne-Stokes  type.  Cyanosis  may  be  present 
in  malignant  cases  apart  from  any  cause  in  the  heart  or  lungs. 

The  temperature  is  variable,  generally  proportionate  in  height  to  the 
severity  of  the  attack,  but  it  may  be  low  or  subnormal  in  bad  cases.  As  a 
rule  it  rises  to  103°-105°  F.  and  becomes  hyperpyrexia!  towards  the  end. 
In  malignant  cases  hyperpyrexia  may  be  present  at  the  onset.  Great 
variations  in  the  height  of  the  fever  may. be  noted  in  the  course  of  a  few 
hours.  The  usual  range  is  100-105°  F.,  and  it  is  often  higher  in  the  morning 
than  the  evening.  Sometimes  the  fever  is  of  the  continued  type  at  the 
onset  and  after  that  markedly  hectic.  Its  duration  varies.  Frequently  it 
lasts  4-6  weeks,  and  often  much  longer. 

The  urine  is  normal  in  amount  or  increased.  Blood  and  casts  have  been 
found  in  it ;  but  haeruorrhagic  nephritis  and  paralysis  of  the  bladder  are 
rare  complications.  Retention  is  apt  to  be  overlooked.  Incontinence  of 
urine  and  faeces  is  a  frequent  symptom. 

The  mental  condition  shows  every  grade  of  disturbance  from  simple 
apathy  to  coma  or  acute  delirium.  Usually  the  initial  irritability  and 
resentment  of  disturbance  are  quickly  followed  by  stupor  and  coma. 
Except  when  comatose  the  child  is  restless  from  pain  and  delirium.  If  the 
delirium  in  early  stages  is  violent,  it  is  short  and  soon  passes  into  coma. 
Taste  and  smell  are  difficult  to  test  and  are  rarely  affected.  Otitis  media  or 
interna  may  cause  permanent  deafness,  but  such  deafness  can  arise  quite 
independently  from  cerebral  causes  and  prove  permanent. 

The  eyes  show  a  great  variety  of  changes.  At  the  onset  they  are 
suffused  from  slight  conjunctivitis  ;  photophobia  and  squint  are  common, 
and  the  pupils  small.  Conjunctivitis  is  often  present  and  may  be  intense. 
Retraction  of  the  eyelids  may  be  noted  as  early  as  the  fourth  day,  but  is 
more  frequent  in  chronic  cases.  The  motor  symptoms  include  palsy  of  the 
third,  fourth  and  sixth  nerves  giving  rise  to  ptosis,  squint  and  diplopia. 
External  squint  is  frequent  and  variable  during  the  acute  stages.  It  is 
commonly  due  to  nerve  irritation  and  rarely  permanent  from  nerve  palsy. 
Conjugate  deviation  is  caused  by  cortical  inflammation  or  lesion  of  the 
nucleus  of  the  sixth  nerve.  Paralysis  of  the  ophthalmic  division  of  the 
fifth  nerve  and  anaesthesia  of  the  cornea  are  probably  antecedent  causes  of 
corneal  ulcer.  In  later  stages  the  pupils  are  dilated,  sometimes  unequal, 
and  in  bad  cases  respond  feebly  to  light.     Optic  neuritis  is  infrequent  and 


Meningitis.  653 

late  in  development,  and  may  be  followed  by  atrophy.  Blindness  may  be- 
present  from  no  obvious  cause  and  possibly  due  to  affection  of  the  occipital 
cortex.  A  plastic  and  suppurative  choroiditis,  with  iritis  and  occasionally 
pus  in  the  anterior  chamber,  may  occur  early  or  late  in  the  illness.  It  is. 
sometimes  called  panophthalmitis,  metastatic  choroiditis,  or  pseudoglioma. 
In  one  acute  case  it  commenced  in  the  first  week  and  in  another  chronic 
case  it  was  treated  in  the  eye  department  for  some  2  or  3  weeks  before 
meningitis  was  suspected.    Panophthalmitis  is  rare. 

Convulsions,  local  or  general,  may  occur  at  the  onset  or  termination 
and  less  often  in  the  course  of  the  illness.  Other  complications  are  hydro- 
cephalus, aphasia,  hemiplegia,  paralysis  of  the  muscles  of  deglutition,  and 
choreiform  movements  ;  acute  multiple  arthritis  ;  pneumonia,  broncho- 
pneumonia and  pericarditis  ;  and  acute  catarrh  of  the  nasal  fossae  and 
accessory  sinuses  in  the  nose. 

Varieties. — An  ambulatory  type  is  very  rare.  Abortive  attacks  are: 
common  in  some  epidemics.  The  onset  is  severe  but  the  symptoms  subside 
in  a  day  or  two,  and  convalescence  is  rapid  and  complete.  An  intermittent 
type  is  characterised  by  alternate  irregular  intermissions.  Chronic  cases 
last  for  months  with  recurrences.  On  grounds  of  severity  they  can  be 
divided  into  acute  fulminant,  ordinary,  mild,  abortive  and  chronic  cases. 

Isolated  or  sporadic  cases  differ  little  from  those  in  epidemics.  As  a 
rule  they  are  milder  in  type  and  gradual  in  onset,  though  sometimes  ushered 
in  with  vomiting  or  fits.  The  meningitic  symptoms  may  be  well  marked  or 
limited  to  headache,  vomiting,  retraction  of  the  head,  pain  in  the  neck, 
and  fever.  Rashes  are  infrequent  but  herpetic  eruptions  are  more 
common.  It  is  almost  impossible  to  diagnose  the  disease  from  suppurative 
meningitis  due  to  other  causes,  except  by  bacteriological  examination  of 
the  fluid  obtained  by  lumbar  puncture. 

Post-Basic  Meningitis. — Syn.  :  The  Cervical  Opisthotonos  of  Infants — 
Simple  Post-basal  Meningitis — Posterior-basal  Meningitis — Chronic  Basilar 
Meningitis — Occlusive  Lepto-meningitis. — This  disease  is  called  "  posterior 
basal  "  because  it  affects  chiefly  the  posterior  fossa  of  the  skull,  the  inflam- 
matory products  accumulating  in  the  basal  arachnoid  systems  of  Key  and 
Retzius.  Clinically  it  is  a  variety  of  cerebrospinal  meningitis,  often  very 
chronic,  and  may  end  in  recovery. 

Bacteriology. — A  diplococcus  was  found  by  Still  in  7  out  of  8  cases,, 
and  by  Thursfield  in  8  out  of  9,  no  other  organism  being  present.  It  is. 
probably  identical  with  that  of  Weichselbaum,  merely  differing  in  virulence. 
It  is  aerobic,  grows  well  on  agar  and  in  broth  at  37°  C,  but  does  not  grow 
at  20°  C.  ;  does  not  grow  on  potato  or  curdle  milk.  It  is  Gram-negative, 
closely  resembles  the  gonococcus,  and  as  a  rule  is  smaller  than  the  pneumo- 
coccus.  It  presents  no  lanceolate  forms,  and  its  opposed  surfaces  are  more 
or  less  flattened  and  not  always  equal.  It  grows  more  freely  in  broth  and 
has  greater  vitality  than  Weichselbaum's  organism.    Nevertheless  Jaeger  of 


-654  Chapter  L. 

■Stuttgart  has  kept  the  latter  organism  alive  in  broth  for  14-17  days  ;  and 
Netter  (1903)  states  that  he  has  kept  it  alive  for  more  than  4  years  by 
subculture  in  broth. 

Agglutination  tests  seem  to  indicate  a  difference  between  these 
organisms.  In  the  Belfast  epidemic  the  blood  agglutinated  its  own 
meningococci,  but  not  those  of  simple  basal  cases  ;  and  the  blood  of  basal 
•cases  reacted  to  cocci  of  their  own  type  but  not  to  those  of  the  epidemic  type. 
The  organism  is  seldom  present  in  great  numbers.  It  may  be  associated 
with  the  pneumococcus,  staphylococcus,  and  the  influenza  or  tubercle 
bacillus,  but  is  usually  found  in  pure  culture.  It  has  not  been  found  in 
the  blood.  Cultures  should  be  made  from  the  sub-pial  exudation  at  the 
base  of  the  brain,  the  intra-ventricular  fluid  or  that  obtained  by  lumbar 
puncture. 

Morbid  Anatomy. — The  inflammation  is  limited  to  the  base  of  the 
brain,  chiefly  the  interpeduncular  space  and  the  region  between  the  bulb 
and  cerebellum,  the  ventricles  and  the  upper  part  of  the  cord.  The  under 
surface  of  the  cerebellum  and  the  apices  of  the  temporo-sphenoidal  lobes 
are  often  involved.  It  may  extend  all  over  the  base  of  the  brain,  right  down 
the  cord,  and  rarely  on  to  the  vertex.  The  pia-arachnoid  is  thickened  and 
injected,  adherent  and  covered  with  greenish-yellow  lymph.  Usually  the 
inflammation  begins  over  the  fourth  ventricle.  The  intra-ventricular  and 
sub-arachnoid  fluid  is  increased,  turbid,  and  contains  flakes  of  lymph.  The 
foramina  of  Majendie  and  Luschka  may  be  blocked.  The  viscera  are 
unaffected.  Peri-arthritis  has  been  noted,  with  the  exudation  of  thick 
adhesive  lymph  round  the  tendon  sheaths  of  the  joints  and  even  pus  in  the 
joints,  the  specific  organism  being  isolated  therefrom. 

Etiology. — Heredity  is  unimportant  and  there  is  no  special  sex 
incidence.  The  disease  is  common  under  1  year  of  age,  and  rare  after  the 
-second  year  (p.  642).  From  50-75  per  cent,  occur  in  the  first  year  of  life. 
In  the  epidemic  disease  50  per  cent,  are  under  10  years.  The  seasonal  pre- 
valence varies,  but  it  is  always  prevalent  though  not  common.  The  cases 
-are  more  or  less  equally  distributed  throughout  the  year.  Sometimes  it  is 
more  frequent  in  hot  weather,  at  other  times  when  it  is  cold.  Occasionally 
the  number  and  distribution  of  the  cases  suggest  an  epidemic  character. 

The  predisposing  causes  are  catarrhal  affections,  infective  disorders, 
general  debility,  otorrhcea,  injury,  and  alimentary  infection.  Yet  it  occurs 
in  the  strong,  breast-fed  and  healthy.  The  little  evidence  there  is  of  the 
channel  of  infection  is  in  favour  of  spread  from  the  naso-pharynx  via  the 
Eustachian  tube,  middle  ear,  and  petro-squamosal  suture.  Catarrh  of  the 
naso-pharynx  is  a  frequent  antecedent.  Otitis  media  is  uncommon,  and 
if  present  may  be  secondary. 

Symptoms. — The  onset  is  usually  sudden  with  vomiting,  convulsions 
■or  head  retraction,  bulging  fontanelle,  screaming  and  fever.  These  symp- 
toms are  more  or  less  associated  or  follow  each  other  quickly.    Mild  cases 


Meningitis.  655 

may  start  quite  insidiously,  and  attract  little  attention  until  there  is 
■evidence  of  hydrocephalus.  In  others  there  are  irregular  fever,  headache, 
vomiting,  head  retraction,  bulging  fontanelle,  somnolence  and  rapid  pulse. 
Languor  and  irritability  quickly  supervene  on  an  acute  onset.  The  intellect 
is  dull,  and  the  child  lies  quiet  and  unobservant.  Drowsiness,  coma  and 
delirium  are  occasionally  present  in  acute  cases,  or  as  the  result  of 
hydrocephalus. 

Retraction  of  the  head  is  a  cardinal  sign  in  young  infants  but  may  be 
absent  in  older  children,  though  usually  rigidity  of  the  neck  muscles  is 
present.  It  is  probably  the  position  in  which  the  meninges  are  most 
Telaxed  and  kept  at  rest.  It  may  be  associated  with  opisthotonos,  coming  on 
spasmodically  and  so  severely  that  the  occiput  and  sacrum  or  heels  are 
approximated,  or  the  child  rests  on  the  head  and  heels.  In  its  extreme  form 
it  is  rarely  persistent  but  it  never  quite  disappears,  and  a  certain  amount  of 
rigidity  of  the  neck  muscles  and  retraction  of  the  head  is  always  present. 
Later,  the  head  may  fall  back  on  account  of  paresis  of  the  neck  muscles. 
Retraction  of  the  head,  vomiting,  wasting,  and  a  variable  degree  of  fever 
may  be  the  only  signs  present  throughout.  The  retraction  is  commonly 
associated  with  general  tonic  rigidity  of  the  Jimbs,  most  marked  in  the 
legs,  which  are  fully  extended,  often  crossed,  with  the  feet  arched  and  the 
toes  pointed  or  flexed.  The  arms  are  extended,  adducted  and  over- 
pronated.  This  rigidity  may  be  replaced  by  intermissions  of  flaccidity. 
Tonic  spasms  may  alternate  with  clonic  ones,  and  general  convulsions  are 
not  uncommon  though  less  so  than  in  other  types  of  meningitis.  The  knee 
jerks  are  exaggerated.  A  mask-like  rigidity  of  the  face,  retraction  of  the 
angles  of  the  mouth,  teeth  grinding,  champing  movements  of  the  tongue 
and  jaws,  and  sucking  movements  of  the  lips  are  sometimes  noted. 

Vomiting  is  frequent  and  explosive.  It  may  be  the  most  marked 
symptom,  or  slight  and  comparatively  unimportant.  Anorexia  is  common  ; 
and  severe  head  retraction  may  interfere  with  swallowing.  Emaciation  is 
great  and  rapid,  especially  if  there  is  much  vomiting  or  enteric  disturbance. 
Constipation  is  rare,  and  enteric  catarrh  or  simple  diarrhoea  not  infrequent. 
The  abdomen  presents  no  special  feature  unless  there  is  flatulent  distension 
from  enteric  trouble,  or  retraction  from  emptiness  due  to  continued  vomiting. 
The  tache  cerebrale  is  frequently  absent. 

Ocular  symptoms  are  often  absent  or  present  in  variable  degrees. 
Retraction  of  the  upper  lids  is  common.  The  eyes  are  wide  open  and 
staring ;  a  marked  contrast  to  the  photophobia  and  closed  eyes  of 
tuberculous  meningitis.  Squint  is  variable  and  transient,  ocular  palsy  rare, 
and  nystagmus,  pseudo-nystagmus  or  an  oscillation  of  the  eyes  common. 
These  signs  are  due  to  the  spasmodic  rigidity.  The  pupils  are  usually 
normal ;  may  be  unequal,  dilated,  and  oscillatory  ;  or  pin-point  in  early 
stages  and  dilate  as  hydrocephalus  develops.  A  transient  amaurosis,  the 
"  fleeting  amaurosis  "  of    S.  Stephenson  or  "  acute  cerebral  amaurosis  of 


656 


Chapter  L. 


infancy  "  of  Gay,  has  been  described.  It  occurs  in  about  one-third  of  the 
cases,  or  even  more  frequently,  being  present  at  some  period  of  the  illness, 
sometimes  not  until  1  month  after  the  onset.  It  begins  insidiously,  occasion- 
ally suddenly.  It  lasts  for  3-6  or  more  weeks,  even  for  years,  and  probably 
is  never  permanent.  Vision  returns  gradually.  It  is  not  due  to  hydro- 
cephalus, for  it  may  disappear  though  the  latter  progresses.  The  pupils 
are  slightly  enlarged  and  react  little  if  at  all  to  light.  There  are  no  fundus 
changes.  It  is  due  to  inhibition  of  lower  visual  centres  in  the  biain.  Optic- 
neuritis  is  relatively  rare,  occurring  in  perhaps  15-20  per  cent.  Primary 
atrophy  may  result  from  hydrocephalus.  Pseudo-glioma  is  an  occasional 
complication. 

Labyrinthitis  may  occur  early  in  severe  cases,  but  is  more  common  in 
mild  ones.  It  is  often  associated  with  otitis  media  and  is  generally  bilateral. 
In  older  children  it  gives  rise  to  giddiness. 

The  head  does  not  alter  unless  hydrocephalus  develops.  The  fontanelle 
bulges,  and  the  superficial  veins  of  the  scalp  are  prominent.  Later,  the 
sutures  may  separate.  The  circumference  of  the  head  must  be  measured 
weekly. 

The  pulse  rate  is  increased.  Leucocytosis  is  considerable  in  early  stages. 
Vasomotor  disturbance  is  uncommon.  The  respiration  may  be  accelerated. 
Breathing  is  sometimes  sighing,  and  yawning  may  be  present.  In  late 
stages  "  cyclic  "  or  "  cerebral  grouped  breathing,"  a  pause  following  groups 
of  3-6  respirations  of  equal  depth,  is  present  but  is  of  no  prognostic  value. 
True  Cheyne-Stokes  breathing  is  rare  and  a  bad  sign. 

The  temperature  is  most  variable.  As  a  rule  it  is  of  the  irregular  hectic 
type.  Sometimes  there  is  little  or  no  fever  ;  or  a  continuous  high  fever  at 
the  onset ;  or  periodical  large  oscillations  of  a  hectic  type  and  at  varying 
times  of  the  day.  The  temperature  may  rise  6°  or  7°  in  a  few  hours,  and 
fall  again  in  another  few  hours  or  not  for  half  a  day.  Such  paroxysms  may 
occur  daily,  or  at  irregular  intervals,  and  are  generally  accompanied  by 
headache,  chilliness,  and  increase  in  the  symptoms. 

Course  and  Prognosis. — Gradually  the  child  loses  flesh  and  strength, 
develops  hydrocephalus,  and  dies  from  asthenia,  marasmus  or  terminal 
convulsions.  In  a  few  cases  the  cerebrospinal  fluid  has  been  discharged 
through  the  nose.  Erythematous  rashes  are  not  infrequent.  Arthritis  is  a 
rare  complication.  Recovery  may  be  complete  or  various  sequelae  may  be 
left,  notably  hydrocephalus,  deaf-mutism,  various  degrees  of  imbecility 
and  general  rigidity.  The  prognosis  improves  with  the  age  of  the  child. 
Few  under  1  year  recover,  and  few  over  3  years  die.  The  mortality  of  cases 
admitted  into  hospital  is  about  70  per  cent.  Probably  many  mild  cases 
are  not  diagnosed  and  the  real  mortality  is  not  over  50  per  cent.  Relapses 
and  intermissions  are  frequent.  The  average  duration  of  fatal  cases  is 
6-8  weeks,  but  the  disease  may  prove  fatal  in  1  week  or  may  last  for  3  months. 


Meningitis.  657 

Some   infants   die   subsequently   from   hydrocephalus,    and    even     quite 
suddenly  after  apparently  perfect  recovery. 

The  diagnosis  depends  on  the  age  of  the  child,  the  marked  retraction  of 
the  head,  rigidity,  retraction  of  the  upper  eyelids,  amaurosis  without 
fundus  changes,  the  absence  of  constipation,  the  slight  degree  of  psychic 
disturbance,  and  the  prolonged  indefinite  course.  It  cannot  always  be 
diagnosed  from  the  tuberculous  variety  in  early  life,  except  on  careful 
examination  of  the  fluid  obtained  by  lumbar  puncture.  Sometimes  it  is 
difficult  to  differentiate  the  retraction  from  the  reflex  opisthotonos  due  to 
otitis  media,  hydrocephalus,  teething,  gastro-intestinal  causes,  cerebral 
tumour,  typhoid  fever,  and  chronic  tetanus. 

Diagnosis  of  Meningitis. — Cerebral  symptoms  are  so  common  in  acute 
febrile  diseases,  especially  lobar  pneumonia,  that  meningitis  is  frequently 
diagnosed  when  it  does  not  exist.  Cases  of  sudden  onset,  with  vomiting  and 
high  fever,  simulate  scarlet  fever.  Sporadic  cases  and  those  of  mild  type 
are  apt  to  be  ascribed  to  digestive  disturbances  or  teething.  It  is  often 
difficult  to  exclude  reflex  causes  of  head  retraction.  Internal  hydro- 
cephalus may  be  the  only  sign,  and  it  is  impossible,  in  the  absence  of  a 
definite  history  of  an  acute  onset,  to  decide  whether  it  is  of  primary  origin 
or  secondary  to  basal  meningitis.  The  epidemic  is  almost  identical  with  the 
suppurative  form.  In  the  former  a  sudden  onset,  marked  hyperesthesia 
and  pain,  and  retraction  of  the  head,  are  more  likely  to  be  present ;  in  the 
latter  the  history  of  a  cause,  or  the  presence  of  a  primary  affection  likely  to 
give  rise  to  it,  is  often  of  assistance.  Tuberculous  meningitis  is  generally 
of  more  gradual  onset  with  less  fever  and  prostration,  less  pain  and  general 
hyperaesthesia.  The  examination  of  the  cerebrospinal  fluid  yields  valuable 
evidence.  The  epidemic  type  may  have  to  be  diagnosed  from  typhus 
fever,  malignant  exanthems,  influenza,  cerebral  pneumonia,  sunstroke, 
the  hyperpyrexia  of  acute  rheumatism,  gastro-enteritis,  and  broncho- 
pneumonia. Outbreaks  due  to  the  pneumococcus  can  only  be  distinguished 
from  those  due  to  the  meningococcus  by  bacteriology.  Meningococci  may 
not  be  found  at  first  and  are  sometimes  not  present  until  the  twentieth  day. 
The  serum  does  not  develop  agglutinating  properties  for  some  days  ;  a 
fresh  strain  of  cocci  must  be  employed. 

Prognosis. — Pneumococcal  and  streptococcal  cases  are  almost  always 
fatal.  The  mortality  in  the  meningococcal  epidemics  is  varied  and  may 
reach  92  per  cent.  In  some  mild  epidemics  it  is  extremely  small.  As  a 
rule  about  half  the  cases  die;  and  the  mortality  is  higher  at  the  beginning 
than  at  the  end  of  an  epidemic.  The  initial  convulsions  may  prove  fatal. 
In  the  New  York  epidemic  7  per  cent,  died  on  the  first  day  ;  31  per  cent,  in 
the  first  5  days.  Fatal  cases  usually  terminate  in  a  week.  The  milder 
sporadic  cases  and  post-basic  ones  in  infants  are  often  very  protracted. 
An  acute  sporadic  case  in  a  4-month  old,  breast-fed,  fat  child  ended  fatally 
within  36  hours.     Another  one,  even  more  severe  at  the  onset,  ended  in 

2   u 


658  Chapter  L. 

recovery  after  several  weeks  of  severe  illness.  In  acute  attacks  the  prospect 
of  recovery  is  increased  if  the  first  fortnight  elapses  without  any  serious 
complication.  Convulsions,  high  fever,  delirium  or  coma,  dyspnoea  and  an 
unduly  frequent  pulse  are  unfavourable  signs. 

Bad  symptoms  may  subside  and  the  child  seem  well  on  the  road  to 
recovery  when  a  relapse  or  recrudescence  occurs  and  ends  fatally.  Relapses 
usually  last  3-4  days  and  occur  at  intervals  of  4-8  days.  The  illness  may  be 
prolonged  even  for  months  and  yet  the  child  may  make  a  perfect  recovery. 
Lung  complications,  especially  in  infants,  increase  the  gravity.  Sub- 
cutaneous haemorrhages  and  nephritis  indicate  severe  blood  infection  with 
probably  a  fatal  issue.  Death  may  be  due  to  the  disease,  complications  or 
sequels. 

The  prognosis  as  regards  the  ultimate  effect  on  the  nervous  system 
must  be  guarded.  Mental  impairment,  from  mild  forms  of  irritability, 
temper  and  headache,  up  to  complete  imbecility  and  all  grades  of  mental 
disturbance  and  insanity,  may  ensue.  Other  sequels  are  peculiarities  of 
temper,  morals  and  emotions  ;  deafness  or  blindness  ;  convulsions  and 
epilepsy  ;  nystagmus  and  ataxia  ;  monoplegia  or  hemiplegia  ;  secondary 
contractures,  temporary  or  permanent ;  and  hydrocephalus  which  may 
be  stationary  or  progressive. 

Treatment. — Prophylaxis  is  of  little  importance,  beyond  the  general 
measures  for  the  maintenance  of  health.  In  epidemics  the  use  of  the 
nasal  douche  and  formamint  lozenges,  the  isolation  of  "  contacts  "  and 
■"  intermediaries,"  and  the  thorough  disinfection  of  houses  and  the 
destruction  of  possibly  infected  food  should  be  adopted. 

In  the  early  stages  an  attempt  must  be  made  to  reduce  the  cerebral 
hyperaemia  by  cold  or  ice  to  the  head  and  nape  of  the  neck,  and  in  very  bad 
attacks  to  the  dorsal  and  lumbar  spine,  keeping  the  extremities  warm. 
Keep  the  room  dark  and  cool.  Quiet  is  essential,  the  patient  must  not  even 
be  moved  from  one  room  to  another.  The  eyes  may  be  bandaged  and  the 
ears  stuffed  with  cotton  wool.  Opium  relieves  restlessness,  pain  and 
irritability.  Hydrotherapeutic  measures  include  "  steaming,"  hot  packs 
or  baths  for  15-20  minutes  twice  a  day,  with  ice  bag  to  the  head.  They 
relieve  headache  and  irritability,  promote  sleep,  leduce  delirium  and  the 
tendency  to  convulsions,  lessen  rigidity  and  allay  rigors.  Tepid  sponging 
is  sufficient  in  milder  cases.  The  cold  pack  may  be  needed  to  reduce 
high  fever.  Counter-irritants  to  the  spine  are  of  doubtful  advantage. 
Bleeding  is  apt  to  prove  injurious.  The  local  application  of  1-3  leeches  to 
the  temples  or  mastoids  may  possibly  relieve  headache  and  prevent  coma  or 
convulsions  in  children. 

The  chief  hope  consists  in  maintaining  the  strength  by  careful  nursing 
and  judicious  feeding.  The  diet  should  be  simple,  nutritious  and  easily 
digested.    Nasal  feeding  may  be  required.     The  child  should  be  fed  as  well 


Meningitis.  659 

.•as  possible  without  upsetting  its  digestion.  Wasting  is  often  extreme  and 
gain  in  weight  is  a  favourable  sign. 

Drugs  are  of  little  use  except  for  the  relief  of  symptoms.  Bromides 
.are  given  to  diminish  the  irritability  of  the  brain  and  cord,  and  promote 
rest.  For  headache  apply  ice  locally  and  give  bromide,  phenacetin, 
phenazone,  chloral,  codeia,  morphia,  and  hot  baths.  For  severe  vomiting 
■order  cracked  ice,  ice  to  the  epigastrium,  temporary  starvation,  careful 
feeding  on  small  amounts  of  peptonised  milk,  bismuth,  dilute  hydrochloric 
acid  before  food,  lumbar  puncture  and  morphia  sub  cutem.  Calomel 
■or  saline  cathartics  should  be  given  for  constipation  ;  chloral  and  bromides 
ior  pain  and  restlessness  ;  caffeine  for  pulmonary  cedema  and  respiratory 
paralysis  ;  stimulants  for  collapse  and  a  typhoid  state  ;  morphia  injection 
for  severe  pain  ;  and  for  convulsions,  chloral  by  mouth  or  rectum,  opium, 
•chloroform  inhalations,  morphia  sub  cutem,  lumbar  puncture  and  hot  baths. 
Ergot,  quinine  in  large  doses,  calcium  sulphide,  pot.  iod.,  and  inunctions  of 
mercury  and  iodoform  have  been  recommended  in  the  early  stages  of  an 
acute  attack.  Strychnia  should  be  avoided  throughout ;  so  too  alcohol 
■during  acute  stages,  unless  absolutely  essential  ;  and  the  coal  tar  derivatives 
.are  rarely  advisable  because  of  their  depressant  action. 

Lumbar  puncture  and  the  removal  of  fluid  reduces  intracranial 
pressure  and  withdraws  toxic  products.  It  can  be  repeated  every  2-4  days, 
if  the  fontanelle  is  tense  and  the  signs  of  pressure  marked.  In  the  Lisbon 
■epidemic  the  removal  of  fluid  was  followed  by  injections  of  9-12  c.c.  of 
1  per  cent,  solution  of  oxycyanide  of  mercury. 

Anti-diphtheritic  serum  kills  pure  cultures  of  the  meningococcus  but 
has  not  proved  of  value.  Of  the  various  serums  in  the  market,  namely 
those  made  by  Kolle  and  Wassermann,  Jochmann,  Ruppel,  Dopter,  and 
Flexner  and  Jobling,  the  last  two  appear  the  most  useful.  A  lumbar  punc- 
ture is  done  and  some  of  the  cerebrospinal  fluid  permitted  to  escape.  If  it  is 
very  thick,  normal  saline  fluid  is  injected  and  allowed  to  flow  away.  After 
that  30  c.c.  of  the  serum  is  injected  into  the  canal.  The  signs  of  improve- 
ment are  a  fall  in  temperature,  diminished  leucocytosis,  less  severe  nervous 
■symptoms,  perhaps  return  of  consciousness,  and  fewer  and  weaker  cocci. 
The  injection  is  repeated  in  12  hours,  if  there  is  no  improvement,  and  daily 
until  the  temperature  falls.  Good  results  may  follow  the  injection  of 
.serum  although  no  cerebrospinal  fluid  is  first  removed. 

Normal  serum  possesses  distinct  bactericidal  power.  Repeated  lumbar 
puncture  and  withdrawal  of  fluid  is  of  value,  for  it  causes  the  exudation 
•of  fresh  antitoxic  fluid  to  replace  the  worn-out  fluid  removed.  The  organism 
grows  well  in  cerebrospinal  fluid  and  its  virulence  is  due  to  endotoxins 
liberated  after  its  death.  It  is  therefore  important  to  remove  the  fluid 
•containing  the  toxin,  replacing  it  by  fresh  fluid  secreted  by  the  patient  or 
by  the  injection  of  an  anti-serum  which,  in  order  to  be  beneficial,  should  be 
•used  at  the  onset.    Vaccines  prepared  from  the  patient's  cocci  have  been 


660  Chapter  L. 

used  and  followed  by  recovery  but  the  treatment  is  still  on  its  trial.  Red- 
mann  injected  the  patient's  cerebrospinal  fluid,  obtained  by  lumbar 
puncture,  subcutaneously  in  two  cases.  In  one  the  fever  subsided  in  3  days 
and  the  other  also  recovered.  It  is  extremely  difficult  to  estimate  the 
value  of  such  lines  of  treatment.  Meningococcal  cases  vary  greatly  in 
severity  and  even  the  most  virulent  ones  will  sometimes  recover  quite 
rapidly  under  the  simplest  measures. 

Tuberculous  Meningitis. — By  far  the  most  frequent  variety  of  menin- 
gitis in  children  is  the  basal  meningitis  due  to  the  tubercle  bacillus.  Out  of 
a  series  of  125  cases  under  10  years  of  age,  71  were  diagnosed  as  tuberculous, 
and  the  diagnosis  was  verified  in  58  after  death.  Strictly  speaking  the 
disease  is  rarely  primary  or  localised.  It  is  either  secondary  to  tuberculosis- 
else  where  or  part  of  a  general  infection.  In  children  the  meningeal  symp- 
toms may  be  the  only  ones  present  and  a  positive  diagnosis  of  meningitis 
can  be  made,  whereas  the  presence  of  a  local  focus  or  a  general  tuberculosis- 
can  only  be  inferred.  It  is,  however,  extremely  rare  to  find  no  local  evidence- 
of  disease  elsewhere  after  death. 

Cases  may  be  grouped  into  3  classes.  In  the  first  are  those  rare 
instances  in  which  the  disease  is  limited  to  the  brain  and  no  local  focus  can 
be  found.  Out  of  58  post  mortem  examinations  5,  ranging  from  2-9  years- 
of  age,  were  of  this  nature.  One  of  them  showed  some  caries  of  the  ethmoid 
but  it  was  doubtful  whether  this  was  tuberculous.  Possibly  in  every  case  of 
primary  tuberculous  meningitis  there  is  some  local  focus,  e.g.  in  the  ears 
or  naso-pharynx,  overlooked  at  the  autopsy.  In  the  second  group  are 
those  cases  in  which  the  child  dies  from  meningitis  secondary  to  a  localised 
tuberculosis  with  little  dissemination.  The  primary  focus  is  generally  a. 
tuberculous  gland  in  the  mediastinum  or  mesentery,  and  occasionally 
tuberculous-  disease  of  skin,  bones,  joints,  lungs,  intestines,  nose,  middle 
ear,  etc.  In  the  third  group  are  all  those  cases  in  which  the  meningeal 
affection  is  part  of  a  general  tuberculosis  and  bears  a  comparatively  unim- 
portant relationship  to  the  disease. 

Etiology. — The  general  etiology  is  the  same  as  that  of  tuberculosis 
elsewhere.  The  age-incidence  is  of  considerable  importance.  Out  of  58  cases- 
verified  post  mortem,  46  occurred  during  the  first  5  years  of  life  and  12  in 
the  second  5  years.  Including  other  cases  not  verified  after  death,  54  out 
of  71  were  under  5  years  of  age.  This  may  indicate  that  a  child  susceptible 
to  tuberculosis  usually  develops  it  during  the  early  years  of  life.  Ten 
proved  cases  were  under  1  year  and,  of  these,  3  were  under  6  months,  the 
youngest  being  3  months  of  age.  There  were  16  in  the  second,  13  in  the 
third,  10  in  the  fourth  and  6  in  the  fifth  year  of  life.  Of  26  cases  under 
2  years  of  age,  16  were  12-18  months  old.  Thus  it  is  far  from  rare  in  infancy- 
There  is  no  special  preponderance  of  either  sex,  possibly  a  few  more 
cases  occur  in  boys,  e.g.  38  boys  to  33  girls.  The  seasonal  incidence  of 
66  cases  showed  that  19  began  in  June  and  Julv.    In  22  cases  there  was  no- 


Meningitis.  661 

tuberculous  family  history.  Isolated  cases  occur  in  many  families  without 
any  tuberculous  heredity.  On  the  other  hand  many  cases  of  tuberculosis 
in  the  first  year  of  life  are  strongly  suggestive  of  direct  infection  from  a 
tuberculous  relative  or  nurse.  Reich  (1878)  reported  10  fatal  cases  within 
14  months  in  infants  who  all  had  the  same  phthisical  midwife  and  were 
children  of  healthy  parentage.  Probably  they  were  infected  at  or  shortly 
after  birth.    Seven  of  the  10  died  in  the  fourth  month  of  life. 

Injury  is  a  doubtful  cause.  In  1  patient  aged  2  years,  who  had  had  a 
fall  3  weeks  before  the  illness,  both  her  father  and  sister  were  "  consumptive  " 
and  the  presence  of  pleuritic  adhesions  at  the  apex  of  one  lung  suggested 
former  tuberculosis.  The  possibility  of  injury  being  an  exciting  cause  is  of 
great  importance  in  the  case  of  school  children.  If  the  child  receives  a  box 
on  the  ear,  or  a  blow  on  the  head,  at  the  hands  of  the  teacher  and  subse- 
quently dies  from  tuberculous  meningitis,  the  unfortunate  teacher  may  be 
hauled  up  before  the  Coroner's  Court  and  censured  by  a  typical  British 
jury.  The  common  explanation  is  that  the  child  is  punished  for  stupidity 
or  inattention,  the  state  of  mind  so  likely  to  be  present  during  the  early 
stages  of  the  disease.  Careful  examination  may  reveal  a  primary  focus. 
On  the  other  hand  it  is  possible  that  injury  to  the  brain  or  meninges  may 
cause  local  congestion  or  damage  of  such  a  nature  as  to  render  the  affected 
parts  a  suitable  soil  for  the  growth  of  the  bacillus,  which  under  less  ad- 
vantageous conditions  might  have  perished.  An  interval  of  2-3  weeks  must 
necessarily  elapse  between  the  blow  and  onset  of  symptoms  to  allow  for 
the  development  of  the  organism. 

Infection  by  food  is  incredible  apart  from  the  intervention  of  a  local 
tuberculous  process.  The  development  of  the  disease  in  young  infants  and 
•children  who  have  always  appeared  healthy  and  have  not,  as  far  as  is 
known,  been  exposed  to  infection,  can  be  explained  by  the  wide  dissemina- 
tion of  the  tubercle  bacillus  and  the  latency  of  chronic  tuberculous  processes. 
In  many  instances  there  is  a  definite  history  of  a  lung  affection  liable  to 
produce  congestion  and  hyperplasia  of  the  mediastinal  glands,  rendering 
them  particularly  susceptible  to  tuberculous  infection  or  stimulating  a 
latent  focus  into  activity.  Measles  and  whooping  cough  have  a  very  evil 
reputation  in  this  respect.  Or  there  may  be  definite  evidence  of  active  or 
quiescent  tuberculosis  in  some  part  of  the  body.  Occasionally  dissemination 
is  set  up  by  interference  with  tuberculous  disease  of  glands,  bones  or 
joints  by  bonesetters  or  surgeons. 

Morbid  Anatomy. — The  anatomical  changes  may  be  summed  up  as 
basal  meningitis  with  tubercles,  granular  ependymitis,  hydrocephalus,  and 
nutritional  disturbance  of  the  brain.  The  inflammation  of  the  pia-arachnoid, 
mainly  at  the  base  of  the  brain,  is  set  up  by  the  deposition  of  tubercle  bacilli 
and  the  formation  of  miliary  tubercles.  At  first  the  tubercles  may  be 
unassociated  with  inflammation.  They  are  small,  greyish  white  or  trans- 
lucent granules,  situated  along  the  blood  vessels  of  the  pia  mater  and  the 


662  Chapter  L. 

arteries  extending  into  the  brain,  especially  the  branches  of  the  Sylvian 
artery.  Gee  showed  that  by  washing  away  the  brain  substance  the  tubercles- 
could  be  demonstrated  along  the  whole  length  of  the  cerebral  arteries.  The 
bacilli  spread  by  the  blood  or  the  lymphatics  in  the  vessel  walls. 

Even  the  tubercles  may  be  absent,  and  the  meningitic  symptoms  due 
to  bacillary  infiltration  or  to  toxins.  Microscopically  such  a  case  shows- 
diffuse  leucocytic  infiltration  of  the  meninges  and  superficial  brain  substance ; 
the  cells  being  in  some  places  aggregated  into  little  nodules.  The  affection 
is  predominantly  perivascular,  and  a  large  number  of  tubercle  bacilli  are- 
found  wherever  there  is  this  infiltration,  especially  in  the  neighbourhood 
of  vessels. 

The  amount  of  apparent  disease  present  in  some  cases  after  death 
is  marvellously  small,  although  the  symptoms  have  been  well  marked. 
It  may  be  limited  to  thickening  and  matting  together  of  the  membranes- 
at  the  base  of  the  brain,  chiefly  in  the  interpeduncular  space,  and  a  few 
scattered  tubercles.  Sometimes  the  membranes  at  the  base  are  remarkably 
thick  and  opaque  or  gelatinous,  obscuring  the  underlying  structures.  Or 
there  may  be  more  or  less  fibrino-purulent  exudation  and  yellowish  or 
greenish  yellow  lymph.  Purulent  exudations  are  possibly  due  to  mixed 
infections,  and  are  never  so  great  or  extensive  as  those  seen  in  non- 
tuberculous  meningitis.  The  inflammatory  products  are  most  marked  at- 
the  base  over  the  optic  chiasma,  interpeduncular  space,  pons,  and  between 
the  medulla  and  cerebellum.  Frequently  they  extend  up  the  Sylvian 
fissures,  or  may  be  limited  to  this  region,  and  occasionally  extend  on  to  the- 
surface  of  the  brain.  Tubercles  may  be  found  in  patches  on  the  convexity 
of  the  brain,  between  the  two  hemispheres,  and  on  the  folds  of  the  choroid 
plexus. 

The  amount  of  fluid  in  the  pia-arachnoid  space  varies  from  normal 
up  to  4  oz.  It  is  usually  clear,  or  slightly  turbid  from  flakes  of  lymph,  and 
exceptionally  is  sero-purulent.  The  brain  becomes  intensely  congested 
from  extension  of  inflammation  and  a  true  meningo-encephalitis  results. 
This  leads  to  thrombosis  of  small  arteries,  veins  and  cerebral  sinuses,, 
deficient  blood  supply,  increased  venous  pressure,  effusions,  cell  degeneration, 
softening  and  necrosis.  Even  in  acute  cases  the  brain  substance  may 
remain  firm.  More  often  it  is  oedematous,  especially  at  the  base,  and  is 
universally  softened  or  almost  diffluent.  The  softening  may  be  marked, 
although  there  is  no  excess  of  intra-ventricular  fluid.  It  is  due  to  impaired 
nutrition  in  consequence  of  circulatory  and  lymphatic  obstruction,  rather 
than  to  hydrocephalus. 

The  amount  of  effusion  into  the  ventricles  varies.  As  a  rule  it  is  greater 
if  the  illness  is  prolonged.  It  is  partly  dependent  on  obstruction  at  the 
foramen  of  Majendie  and  partly  on  ependyniitis,  for  the  ependyma  is  often 
inflamed,  thickened,  fed  and  granular.  The  fluid  is  clear,  or  slightly  turbid 
from  particles  of  lymph  and  pus. 


Meningitis.  663 

If  the  ventricles  are  much  distended  the  convolutions  are  flattened. 
This  flattening  and  an  excess  of  fluid  are  the  first  points  noted  on  opening 
the  skull.  If  the  sutures  are  un-united  they  may  separate  and  thus  modify 
the  effects  of  pressure.  The  superior  longitudinal  sinus  is  often  more  or 
less  thrombosed  ;  the  cerebral  sinuses  much  distended  with  dark  fluid 
blood  ;  the  superficial  cerebral  veins  similarly  distended  ;  and  the  vense 
Galeni  blocked  by  matting  of  the  velum  interpositum. 

Section  of  the  brain  shows  softening,  punctahsemorrhagica,  and  perhaps 
one  or  more  scattered  tuberculous  nodules,  varying  in  size  from  a  minute 
pea  to  a  good  sized  tumour,  situated  in  any  part  of  the  brain  and  sometimes 
attached  to  the  meninges.  The  cortical  brain  cells  are  globular  or  swollen, 
the  nuclei  contracted  and  the  protoplasm  "  dusty  "  in  appearance. 

Sometimes  the  inflammatory  process  and  a  few  tubercles  extend  down 
the  spinal  cord.  Caseating  meningitis  is  rare.  It  causes  symptoms  like 
Jacksonian  epilepsy  and  is  of  rather  longer  duration  than  ordinary  cases. 
A  diffuse  caseation  of  the  meninges,  principally  of  the  vertex  along  the 
longitudinal  fissure,  and  a  greenish  deposit  extending  into  the  sulci  are  found 
after  death. 

In  23  out  of  27  cases  the  mediastinal  glands  were  tuberculous  ;  in  2 
the  lungs  were  very  tuberculous  but  the  state  of  the  glands  was  not  noted; 
in  the  remaining  2  the  only  anatomical  changes  outside  the  cranium  were 
caries  of  the  ethmoid  in  1  and  localised  apical  pleurisy  in  the  other.  The 
gland  generally  affected,  often  the  only  one,  was  that  situated  at  the 
bifurcation  of  the  trachea  and  sometimes  called  the  "  pretracheal  " 
gland.  In  4  of  the  23  cases  the  mesenteric  glands  were  also  tuberculous. 
In  one  of  these  the  peritoneal  surface  of  the  diaphragm  was  covered  with 
miliary  tubercles,  but  there  was  no  macioscopic  evidence  of  the  disease  in  the 
lungs.  In  another  there  were  tuberculous  nodules  in  the  skin  and  brain,  and 
general  lung  dissemination,  especially  at  the  right  apex.  In  the  remaining 
two,  in  which  both  sets  of  glands  were  caseous,  one  had  tuberculous 
vomica?  in  botb  lungs  and  two  small  ulcers  in  the  intestines,  and  the  other 
had  an  old  caseating  and  calcifying  nodule  in  the  lung.  No  less  than 
12  cases  showed  extensive  pulmonary  disease  of  long  duration. 

Pathology. — As  a  result  of  predisposing  conditions  due  to  inflammatory 
affections  of  the  lung,  or  from  direct  infection,  one  or  more  of  the  mediastinal 
glands  becomes  congested,  infected  with  the  tubercle  bacillus,  and  undergoes 
caseation.  Such  a  gland  may  remain  quiescent,  calcify,  or  break  down  by 
fatty  necrosis.  On  softening,  the  tuberculous  infection  is  carried  by  the 
blood  vessels  throughout  the  body  and  sets  up  general  miliary  tuberculosis. 
The  result  may  be  a  meningitis  to  which  the  patient  succumbs  without  the 
bacilli  having  acquired  much  of  a  hold  elsewhere.  Occasionally  there  is 
general  miliary  tuberculosis  and  the  pia  is  unaffected.  In  other  instances 
infection  may  be  carried  from  tuberculous  glands  elsewhere  or  from 
tuberculous  disease  in  any  organ  without  the  intervention  of  breaking  down 


664  Chapter  L. 

glands.  The  disease  is  spread  through  the  circulation,  rather  than  by- 
extension  or  through  the  lymphatics. 

The  primary  effect  on  the  brain  is  the  formation  of  minute  tubeicles 
in  the  walls  of  the  smallest  arteries.  An  inflammatory  process  is  set  up, 
inducing  an  obliterative  peri- arteritis  and  arteritis,  or  obstruction  to  the 
circulation  of  blood  and  lymph  by  inflammatory  products  at  the  base  of  the 
brain.  The  nutrition  of  the  brain  is  interfered  with  and  softening  results. 
Ventricular  effusion  is  partly  mechanical  and  partly  due  to  inflammation 
of  the  choroid  plexuses  and  ependyma. 

Death  ensues  from  the  nutritional  disturbance  rather  than  from  the 
actual  mechanical  effects  of  retained  or  effused  intra- ventricular  fluid. 
In  only  about  two-thirds  of  the  cases,  which  I  have  examined  post  mortem, 
was  there  an  excess  of  fluid  in  the  ventricles  and  sometimes  the  quantity 
was  little  increased.  Many  children  died  comatose  although  there  was  no 
evidence  of  increased  intracranial  pressure  after  death.  Nor  does  the 
amount  of  softening  depend  upon  the  amount  of  fluid  in  the  ventricles. 
It  may  be  marked  in  the  absence  of  excess  of  fluid,  but  as  a  rule  the  greater 
the  amount  of  fluid  the  greater  is  the  softening.  Both  may  depend  upon  the 
same  cause. 

Symptoms. — The  onset  is  rapid  in  cases  of  prolonged  tuberculosis  ; 
gradual  and  insidious  when  secondary  to  latent  local  disease.  In  the  latter 
class  of  case  it  is  usual  to  divide  the  course  of  the  disease  into  : — (1)  a 
prodromal  stage  passing  into  the  stage  of  invasion;  (2)  a  stage  of  irritation; 
and  (3)  a  stage  of  convulsions  and  coma.  These  stages  pass  more  or  less 
gradually  into  each  other  and  are  not  always  clearly  defined.  In  infants, 
and  occasionally  in  older  children,  the  onset  is  often  sudden  with  con- 
vulsions. The  prodromal  stage  is  sometimes  absent  and  the  child  is 
seized  with  vomiting,  convulsions  and  delirium,  and  soon  dies. 

During  the  prodromal  period,  between  the  infection  of  the  meninges 
and  the  definite  onset  of  symptoms,  the  child  may  show  signs  of  not  being 
quite  in  its  usual  health.  The  mental  attributes  are  altered  and  he  becomes 
peevish  and  irritable,  dull  and  listless,  and  disinclined  to  talk  or  play. 
He  mopes  and  cries  without  provocation,  and  is  easily  tired  or  unusually 
drowsy.  Mental  perversity  and  hysterical  symptoms  may  be  present  about 
puberty.  The  appetite  may  be  impaired,  the  tongue  coated,  and  vomiting 
of  the  cerebral  type  may  result  from  apparently  very  trivial  causes.  _  Perhaps 
there  is  a  little  fever.  Constipation  is  often  marked  ;  one  child,  who  came 
under  my  notice,  had  been  vigorously  treated  for  constipation  for  a  fortnight 
and  even  then  showed  very  slight  symptoms  for  meningitis.  Diarrhoea 
is  not  uncommon  in  infants.  Headache,  usually  frontal,  increased  by 
mental  or  physical  exertion  and  less  frequent  in  the  very  young,  restless 
and  disturbed  sleep,  teeth  grinding,  bad  dreams,  pavor  and  enuresis  are 
sometimes  present.  The  duration  of  this  stage  varies  from  a  few  days  to 
2  or  3  weeks.     Occasionally  there  is  no  definite  prodromal  stage,  the  initial 


Meningitis.  665 

convulsions  passing  rapidly  into  coma.  One  child  vomited  during  the 
day  and  became  unconscious  at  night.  Sometimes  the  stage  is  a  prolonged 
one  of  ill-health,  dependent  on  the  predisposing  tuberculous  disease  and 
incapable  of  being  sharply  denned  from  the  onset  of  the  meningeal  infection. 

Towards  the  end  of  this  stage  the  pulse  is  generally  irregular  in 
rhythm  and  volume,  especially  on  change  of  position  and  exertion.  It  is 
infrequent,  60-80 per  min.  in  children,  80-100ininfants.  Bradycardia  is  often 
absent  in  infants  under  1  year  of  age.  Sighing  respiration,  dryness  and  loss 
of  elasticity  of  the  skin,  and  the  tache  cerebrale  are  often  present.  Less 
frequent  symptoms  are  sucking  and  champing  movements,  teeth  grinding, 
a,bdominal  pain  with  vomiting  and  fever,  and  slight  delirium  at  night. 
In  the  very  young  speechlessness  is  not  uncommon,  delirium  rare. 

Gradually  the  child  passes  into  the  stage  of  cerebral  irritation  with 
hyperesthesia  of  the  general  and  special  senses.  It  dislikes  being  touched, 
moved  or  disturbed  in  any  way  ;  objects  to  light  and  noise  ;  does  not  talk  ; 
may  complain  of  the  head,  crying  out  "  Oh  my  head,"  or  if  unable  to  talk 
■occasionally  gives  a  sharp  piercing  cry,  the  hydrocephalic  cry,  and  is 
unnaturally  drowsy.  It  lies  in  bed  with  the  legs  tucked  up,  the  abdomen 
retracted  and  the  trunk  flexed  ;  and  will  sometimes  pluck  at  the  bed 
•clothes  when  they  are  drawn  off.  The  head  is  slightly  retracted,  or  the 
muscles  at  the  back  of  the  neck  are  more  or  less  rigid,  and  the  head  cannot 
be  bent  forward  without  causing  pain.  Sometimes  it  cannot  be  moved  from 
side  to  side.  Rigidity  of  the  neck  muscles  and  retraction  of  the  head  are 
rarely  entirely  absent.  Coarse  tremor  of  the  hands  and  temporary  squint 
may  be  present.  The  appetite  is  bad,  constipation  persists  and  is  an 
almost  constant  symptom,  and  cerebral  vomiting  is  often  present.  Sleep 
is  not  sound  and  the  eyes  are  half  closed  (ocular  catalepsy).  Lethargy 
deepens,  headache  gets  worse,  vomiting  more  frequent,  and  sometimes  there 
are  convulsions.  The  pulse  and  respiration  are  still  irregular,  and  sighing 
respiration  is  not  uncommon.  Fever  is  irregular  and  rarely  high.  There 
is  incontinence  of  urine  and  fa3ces. 

Gradually  the  child  gets  worse  and  worse.  The  cornea  becomes  less 
sensitive  and  blinking  is  diminished,  leading  to  lack  of  polish  and  slight 
opalescence  of  the  cornea.  Intra-ocular  tension  is  diminished.  Variable 
squint,  ptosis,  rarely  nystagmus,  more  often  conjugate  deviation  of  the 
•eyes  and  corresponding  deviation  of  the  head,  may  be  present.  The  pupils 
-are  often  contracted  in  early  stages  and  later  become  irregular  and  unequal, 
usually  dilated  and  reacting  feebly  to  light  and  eventually  immobile. 
Choked  disc  is  generally  present  at  the  end  of  the  first  week,  often  in  one 
•eye  before  the  other,  and  later  on  optic  neuritis.  Carpenter  and  Stephenson 
found  choroid  tubercles  in  21  out  of  42  cases  of  acute  miliary  tuberculosis 
•and  tuberculous  meningitis  ;  in  8  of  the  cases  in  both  eyes.  They  state 
that  these  are  usually  unilateral,  small,  single,  in  the  form  of  round,  oval 
•or  reniform  areas  of  a  fawn,  grey  or  paper-white  colour,  in  diameter  from 


666  Chapter  L. 

1-3  mm.  They  are  found  in  the  vicinity  of  the  optic  disc  and  macula  lutea.. 
Similar  tubercles  may  be  found  in  chronic  tuberculosis,  even  if  quiescent.. 
They  may  be  present  some  weeks  before  the  onset  of  meningitis,  may  be 
quite  independent  of  it,  and  may  become  obsolescent.  They  are  evidence 
of  tuberculosis  but  not  of  meningitis,  and  it  does  not  follow  that  every  case 
of  meningitis  in  a  tuberculous  subject  is  due  to  the  tubercle  bacillus.. 
Choroid  tubercles  or  optic  neuritis  were  present  in  35  out  of  52  cases 
(Koplik). 

The  irritability  lessens  and  the  child  passes  through  a  stage  of  stupor,, 
during  which  it  can  be  roused  with  difficulty  and  appears  rational,  into- 
deep  coma.  Active  delirium  is  rare  ;  coma-vigil  is  sometimes  noted.  He 
no  longer  speaks  or  shows  a  glimmer  of  intelligence ;  and  frowns  little  or  not 
at  all.  The  corneal  reflex  is  abolished,  and  the  pupils  are  widely  dilated 
or  immobile  (the  far-off  look).  The  fontanelle  in  infants  is  tense  and 
bulging. 

The  limbs  become  rigid,  legs  extended  and  the  arms  flexed  or  extended. 
Head  retraction  is  rarely  very  marked.  Spasmodic  convulsions  set  in. 
They  may  consist  of  slight  twitchings  of  the  facial  or  limb  muscles,  affect 
one  limb  only,  or  be  hemiplegic  in  type  or  geneial.  They  may  be  more 
marked  on  one  side  than  the  other,  and  the  distribution  may  vary  during  the- 
course  of  the  illness,  suggesting  that  they  depend  on  circulatory  dis- 
turbance. If  they  are  limited  to  the  same  regions  throughout,  an 
explanatory  patch  of  intensely  distended  or  thrombosed  superficial  cortical 
vessels,  of  tubercles,  or  of  inflammatory  exudation  in  the  corresponding, 
cortical  region  may  be  found  after  death.  They  may  occur  at  any  stage 
throughout  the  illness.  Temporary  palsy  of  the  face  or  limbs  is  left  after- 
convulsions.  Occasionally  retraction  of  the  head  and  opisthotonos  become 
extreme  and  sometimes  there  is  emprosthotonos. 

During  this  stage  the  child  rarely  swallows  and  has  to  be  fed  by  nasal 
tube.  The  lips  and  teeth  are  covered  with  sordes.  Vomiting  often  ceases- 
when  the  child  is  fed  nasally.  Constipation  persists  and  wasting  is  pro- 
gressive. The  abdomen  is  often  retracted  at  first,  but  later  on,  and  even 
from  the  onset  in  infants,  it  becomes  distended  from  flatulence  and  intestinal 
paralysis.  The  hydrocephalic  cry  may  persist  at  intervals  during  the 
early  stage  of  coma.  More  commonly  it  is  absent  and  the  child  merely 
utters  an  occasional  low  moan. 

The  pulse  rate  does  not  vary  directly  with  the  temperature  ;  it  becomes 
more  frequent,  smaller,  and  probably  more  regular.  Towards  the  end  it  is 
very  frequent,  very  small  and  soft,  and  perhaps  uncountable  ;  due  to  vagus 
palsy.  Vasomotor  disturbances  appear  in  the  form  of  brilliant,  irregular 
flushing  of  the  cheeks,  sometimes  unilateral  and  perhaps  associated  with 
profuse  sweating  which  is  also  at  times  limited  to  one  side.  The  breathing 
becomes  shallow  and  irregular  ;  noisy  and  rattling,  due  to  accumulation  of 
mucus  in  the  dorsal  posture  ;    and  often  assumes  the  Cheyne-Stokes  type 


Meningitis.  667 

during  the  last  few  days.  This  type  of  breathing  usually  indicates  a  fatal 
issue  within  2  days  but  I  have  known  it  occur  as  long  as  14  days  before 
death.  It  may  subside  and  recur.  Periodic  grouped  breathing  with 
intervening  pauses,  but  without  the  gradual  rise  and  fall  in  depth,  also 
occurs.  During  the  pause  the  pupils  are  normal  or  a  little  contracted  ; 
they  then  slowly  and  widely  dilate,  rapidly  subsiding  with  the  next  pause 
in  breathing.  This  dilatation  is  not  affected  by  light.  Retention  of  urine 
may  be  due  to  coma  or  dulness  of  the  senses,  rarely  to  spinal  involvement. 

The  superficial  reflexes  are  retained  until  the  onset  of  coma.  The  knee 
jerks  and  plantar  reflexes  may  be  normal,  absent  or  exaggerated.  At  the 
onset  they  are  often  exaggerated.  In  the  stage  of  coma  they  are  abolished. 
Kernig's  sign  occurs  in  about  60  per  cent.,  less  frequently  than  in  other 
types  of  meningitis.  Babinski's  sign  is  commonly  absent,  but  it  may  be 
present  after  convulsions  of  the  leg  and  in  rigidity.  According  to  Koplik 
it  is  more  common  than  Kernig's  sign  and  exceptional  in  cerebrospinal 
fever.     There  is  no  ankleclonus. 

The  fever  is  mild  and  irregular  in  type  throughout  the  early  stages. 
The  temperature  rarely  exceeds  100-101°  F.  and  is  often  about  the  normal 
level.  It  is  liable  to  be  modified  by  active  tuberculous  disease  in  the  lung 
or  elsewhere,  mixed  infection  or  general  tuberculosis.  It  may  fall,  if 
previously  high  from  general  tuberculosis.  From  48-12  hours  before  death 
it  frequently  begins  to  rise  steadily  and  rapidly,  and  may  go  on  rising  after 
death  even  up  to  109°  F.  in  the  rectum.  Sometimes  death  is  preceded  by  a 
subnormal  temperature.  Occasional  symptoms  are  attacks  of  partial 
syncope  and  clonic  spasms  of  the  jaw  and  tongue. 

Death  takes  place  quietly  from  syncope  in  the  stage  of  coma,  sometimes 
during  the  act  of  feeding  the  child,  or  during  convulsions.  Coma  may 
precede  death  by  a  few  hours  or  several  weeks,  and  frequently  the  child 
lives  for  3  or  4  days  although  death  is  expected  at  any  moment. 

Varieties  in  Infancy. — Three  special  kinds  can  be  differentiated.  In 
the  convulsive  type  convulsions  are  followed  by  fever  and  rigidity  of  the 
neck,  with  more  or  less  hemiplegia  or  paraplegia,  and  then  fits  ending 
fatally  in  2  or  3  days.  A  hemiplegic  type  simulates  unilateral  brain  disease. 
The  paralysis  may  develop  suddenly  without  loss  of  consciousness  or 
convulsions.  Usually  slight  fever  is  followed  by  hemiplegia  and  then 
convulsions ;  andlater  on  by  rigidity  of  the  neck  muscles,  bulging fontanelle, 
exaggerated  reflexes,  coma  and  death.  No  explanation  of  the  paralysis  is 
found  in  the  brain  or  meninges.  The  somnolent  type  begins  with  malaise 
and  vomiting  for  7-14  days,  and  progressive  sleepiness  which  at  first  is 
ascribed  to  fatigue.  The  child  remains  drowsy  for  hours  at  a  time,  with  the 
eyes  half  open.  This  ocular  catalepsy,  a  fixity  of  gaze  due  to  absence  of 
winking,  depends  upon  amblyopia  and  loss  of  conjunctival  reflex.  The 
pulse   is   irregular,    emaciation   gradual    and   progressive,    and    vomiting, 


668  Chapter  L. 

diarrhoea  and  tympanites  may  occur.     The  drowsiness  passes  into  torpor, 
coma,  and  death  in  4-8  days  after  full  development. 

Course  and  Duration  depend  very  largely  on  the  presence  of  lung 
disease  or  general  tuberculosis.  Some  cases  are  much  more  acute  than 
others.  Sometimes  we  find  periods  of  remission  or  temporary  amelioration 
of  the  symptoms.  They  occur  in  the  second  stage  of  the  disease  and  last 
for  a  few  days  up  to  2  weeks.  The  child  may  regain  consciousness  and 
recognise  its  surroundings,  creating  false  hopes  in  the  minds  of  the  parents 
and  possibly  even  of  the  doctor,  who  at  any  rate  hopes  that  he  has  made 
a  mistake  in  diagnosis.  Prolonged  remissions  for  months  or  years  have 
been  noted  ;  20  cases  since  1894  (A.  E.  Martin,  1909).  The  symptoms 
completely  disappear.  The  diagnosis  must  be  confirmed  by  tubercles  in 
the  choroid,  or  bacilli  in  the  cerebrospinal  fluid  and  the  production  of 
inoculation  tuberculosis  in  guinea  pigs.  Choroidal  tubercles  are  not 
absolute  proof  that  the  meningitis  is  tuberculous.  During  the  remission 
the  nervous  system  shows  traces  of  cerebral  irritation,  indicating  that  the 
disease  is  only  dormant.  Such  cases  must  be  local  at  first.  Ordinarily  the 
progress  is  slowly  but  definitely  onward  to  a  fatal  issue.  An  analysis  of 
65  cases  showed  that  4  died  in  the  first,  27  in  the  second,  21  in  the  third, 
10  in  the  fourth,  and  3  in  the  fifth  week  of  the  attack.  Almost  all  died  in 
9-19  days,  usually  about  the  fourteenth  day.  Breast-fed  infants  live  longer 
than  the  bottle-fed  for  nutrition  is  better  maintained.  Infants  live  longer 
than  children  because  the  skull  is  yielding.  Acute  cases  secondary  to  tuber- 
culosis of  the  lungs  often  end  in  a  few  days  ;  convulsions,  stupor  and  coma 
following  each  other  in  rapid  succession.  Mild  cases  may  last  as  long  as 
6-8  weeks.  A  prolonged  period  of  drowsiness,  opisthotonos,  rigidity  and 
contracted  pupils,  may  be  due  to  intra-ventricular  effusion. 

Diagnosis. — During  the  prodromal  stage  the  slight  symptoms  present 
may  be  overlooked  or  ascribed  to  some  trivial  cause  such  as  indigestion, 
constipation,  teething  or  worms.  This  is  especially  true  in  infants,  for 
dyspepsia  and  constipation  can  produce  most  of  the  premonitory  symptoms. 
Much  stress  must  be  laid  upon  irregularity  of  the  pulse  combined  with 
infrequency,  irregular  breathing,  constipation,  vomiting  without  apparent 
cause,  drowsiness,  retraction  of  the  head  and  convulsions.  The  main 
difficulty  is  in  differentiating  it  during  the  first  two  years  of  life  from  simple 
basal  meningitis,  but  in  this  the  symptoms  are  fewer  and  milder  in  type, 
irregularity  and  infrequency  of  the  pulse  uncommon,  constipation  often 
absent,  and  the  fever  higher.  The  age-incidence  is  of  some  assistance.  In 
many  instances  diagnosis  is  impossible  without  lumbar  puncture.  It  is 
also  difficult  to  differentiate  it  from  acute  otitis  in  infancy.  An  aural 
examination  is  necessary.  Pneumonia  may  produce  somewhat  similar 
cerebral  symptoms  but  is  more  suggestive  of  cerebrospinal  or  suppurative 
meningitis.  Other  causes  of  retraction  of  the  head,  such  as  described  under 
basal  meningitis,  must  be  excluded.  The  chief  error  consists  in  ascribing  the 
onset  of  the  disease  to  a  gastric  attack. 


Meningitis.  669 

Prognosis. — It  is  possible  but  very  improbable  that  recovery  can  take 
place,  for  the  disease  is  rarely  limited  to  the  brain  and  is  usually  part  of  a 
general  tuberculosis.  No  case  can  be  accepted  as  one  of  undoubted 
recovery  unless  tubercle  bacilli  have  been  found  in  the  cerebrospinal  fluid. 
Reliance  upon  clinical  symptoms  for  accurate  diagnosis  is  unsafe.  Henckel 
(1900)  reported  a  case  of  recovery  after  a  long  and  tedious  illness,  bacilli 
having  been  found  in  the  cerebrospinal  fluid.  The  cases  of  prolonged 
remission  are  also  in  favour  of  the  possibility  of  recovery,  provided  that 
the  disease  is  limited  to  a  local  affection  of  the  meninges.  The  signs  of 
approaching  death  are  increasing  frequency  of  the  pulse,  vasomotor 
paralysis,  Cheyne-Stokes  breathing,  and  a  rapidly  rising  temperature. 

Treatment. — It  is  of  the  utmost  importance  to  protect  children  during 
the  first  5  years  of  life  from  exposure  to  infection.  This  is  particularly 
necessary  after  attacks  of  measles,  whooping  cough  or  any  lung  affection. 
Once  the  meninges  are  attacked  we  are  practically  helpless  to  arrest  the 
disease.  The  child  must  be  carefully  fed,  by  nasal  tube  if  necessary.  Ice 
or  cold  by  means  of  Leiter's  tubes  can  be  applied  to  the  head,  and  phena- 
cetin  given,  to  relieve  headache.  Leeches  to  the  nostrils  and  mastoids, 
counter-irritants  behind  the  ears,  inunctions  of  mercury,  and  many  other 
remedies  being  tried  in  vain.  Blistering  the  nape  of  the  neck  only  inflicts 
increased  suffering ;  shaving  the  head  merely  disfigures  the  child. 
Bromides  and  chloral  control  the  convulsions.  Small  frequent  doses  of 
calomel  and  iodide  of  potassium  can  be  given. 

The  general  measures  of  treatment  are  devoted  to  the  relief  of  symptoms 
and  are  such  as  are  above  recommended  in  other  forms  of  meningitis  (p.  658). 
The  main  dependence  must  be  on  mercurials  and  bromides,  or  chloral, 
combined  with  diet,  complete  rest,  and  careful  nursing. 

Operative  treatment  has  been  tried.  It  consists  of  drainage  of  the 
subarachnoid  space  either  by  trephining  the  skull  in  the  occipital  region  or 
by  lumbar  puncture.  It  is  indicated  as  a  means  of  relieving  pressure  and 
on  the  assumption  that  the  child  is  dying  from  coma  due  to  pressure.  Such 
is  by  no  means  always  the  case,  for  many  of  these  patients  die  comatose  and 
no  increased  intracranial  pressure  is  found  after  death.  The  coma  is 
chiefly  due  to  the  impaired  nutrition  of  the  brain,  which  may  or  may  not  be 
associated  with  excess  of  fluid  in  the  ventricles.  Moreover,  except  in  very 
young  infants  with  un-united  sutures,  we  cannot  ascertain  in  any  particular 
case  whether  there  is  an  excess  of  fluid  in  the  ventricles  or  how  much,  if  any, 
of  the  coma  is  due  to  such  excess.  Operative  treatment  must  be  regarded 
as  experimental  rather  than  curative.  The  removal  of  fluid  by  lumbar 
puncture  can  do  no  harm  and  may  relieve  some  of  the  symptoms. 

Syphilitic  Meningitis. — The  few  instances  of  supposed  syphilitic 
meningitis  are  usually  of  the  same  type  as  post-basic  meningitis,  with  much 
thickening  and  matting  together  of  the  membranes  at  the  base  of  the  brain. 
At  an  early  age  it  is  impossible  of  diagnosis  from  this  variety  and  it  is 


^70  Chapter  L. 

probable  that  there  is  no  true  syphilitic  meningitis  in  infancy,  and  that  the 
supposed  cases  are  simply  post-basic  meningitis  in  syphilitic  infants. 
A  baby,  4  months  old,  had  retraction  of  the  head,  moderate  fever,  wasting 
.and  occasional  vomiting.  There  was  a  family  history  of  syphilis  and 
■evidence  of  the  disease  in  the  shape  of  typical  squamous  patches  on  the 
buttocks  and  thighs.  In  spite  of  specific  treatment  death  occurred  in 
7  weeks,  during  which  retraction  of  the  head  and  opisthotonos  became 
•extreme,  moderate  hydrocephalus  developed,  and  vomiting  and  wasting 
persisted.  A  simple  basal  meningitis  was  found  at  the  autopsy,  with  no 
indication  that  it  was  specific. 

In  congenital  syphilis  local  white  thickenings  of  the  meninges  and 
adhesions  may  be  found  at  the  vertex  and  base,  thickening  and  scarring  of 
the  ependyma,  and  often  hydrocephalus.  Cortical  lesions  are  a  cause  of 
.Jacksonian  epilepsy.  Cerebral  syphilis  of  the  acquired  type  may  occur 
about  the  age  of  puberty  in  the  same  forms  as  in  adults. 

Pachymeningitis  is  iare.  It  generally  depends  on  contiguous  bone 
disease,  e.g.  necrosis  of  cranial  bones,  disease  of  the  nose  or  middle  ear.  It 
is  usually  infective.  Pus  collects  between  the  dura  mater  and  bone,  perhaps 
in  sufficient  amount  to  give  rise  to  symptoms  of  intracranial  abscess. 
Lspto-meningitis  and  sinus  thrombosis  are  secondary  effects.  Some  cases 
are  syphilitic,  even  as  early  as  4  years  of  age,  and  associated  with  gummata 
or  cerebral  sclerosis.  This  variety  maybe  hsernorrhagic,  diffuse  or  basal, 
or  localised,  chronic  and  gummatous.  Pachymeningitis  of  the  cord  is  usually 
•due  to  tuberculous  caries. 

Internal  hemorrhagic  pachymeningitis  is  occasionally  found  under  3 
generally  under  1  year  of  age.  It  is  due  to  cachexia,  infective  diseases, 
injury,  syphilis  and  heemorrhagic  affections.  Sometimes  it  begins  as  a 
serous  external  meningitis  (p.  632)  and  the  haemorrhage  takes  place  into  the 
effusion  secondarily.  In  cachexia  there  are  no  symptoms.  Other  cases 
show  increased  intracranial  pressure,  bulging  fontanelle,  headache,  vomiting, 
myosis,  papillitis,  retinal  haemorrhage,  pulse  anomalies,  twitchings  and 
-convulsions.  The  signs  are  similar  to  those  of  serous  apoplexy  and  the 
diagnosis  is  based  on  the  results  of  lumbar  puncture.  Some  cases  are 
recurrent.     It  is  usually  fatal. 

Hematoma  of  the  dura  mater  is  a  variety  of  pachymeningitis  haemor- 

rhagica.    It  is  the  result  of  similar  causes,  and  most  frequently  due  to  injury 

-at  birth.    The  common  site  is  the  convexity,  on  one  or  both  sides  ;   and  the 

•size  is  variable.    Symptoms  vary  with  the  size  and  locality.    They  may  be 

absent,  localised  to  one  side,  or  general  and  like  those  of  the  last  variety. 

It   may  simulate  sinus  thrombosis.     Cases  due  to  injury  may  recover 

•  completely.    Occasionally  a  subdural  cyst  is  left  as  a  sequel.    The  treatment 

of  these  affections  is  that  of  the  primary  disease  and  directed  to  the  relief 

-of  symptoms. 


CHAPTER    LI. 

CEREBEAL  AND  CEREBELLAR  DEGENERATIONS. 

Agenesis  Corticalis  —  Cerebral  Spastic  Paralysis  —  Infantile  Cerebral 
Degeneration — Amaurotic  Family  Idiocy — General  Paralysis — Cere- 
bellar Ataxia —  Auto-intoxications. 

The  cerebral  and  cerebellar  scleroses  occupy  an  intermediate  position. 
Some  of  them  are  endogenous  in  origin,  due  to  abiotrophy.  Others  are 
•exogenous,  secondary  to  encephalitis,  congenital  syphilis,  vascular  mischief 
and  other  causes.  The  sclerosis  may  be  limited  to  the  cerebellum  or  the 
cerebrum,  in  whole  or  in  part,  or  quite  localised.  The  brain  substance  is 
.shrivelled,  brownish  and  thickened  ;  and  shows  atrophy  and  degeneration 
■of  the  nerve  cells  and  fibres,  proportionate  to  the  degree  of  sclerosis,  pro- 
liferation of  the  perivascular  tissues  and  thickening  of  the  vessel  walls,  and 
proliferation  of  the  neuroglia,  especially  in  the  septa.  The  initial  symptoms 
are  those  of  the  primary  disease  at  first,  and  subsequently  depend  on  the 
•distribution  and  extent  of  the  sclerosis.  The  various  affections  in  which 
there  is  sclerosis  may  be  classified  according  to  the  date  of  their  origin 
into  : — 

I.  Pre-natal  Group,  due  to  causes  in  action  before  birth. 

(1)  Gross    cerebral     defects,     e.g.     anencephaly,    porencephalus, 

hydrocephalus,     non-development     of    the    prosencephalon 
and  other  malformations. 

(2)  Agenesis  corticalis,  a  backward  or  arrested  development  of  the 

nerve  cells  in  the  cortex. 

(3)  Infantile  cerebral  degeneration,  i.e.  degeneration  of  the  cells 

in  the  cortex  endogenous  in  origin. 

(4)  Delayed  development  of  the  motor  tract,  perhaps  dependent 

on  agenesis  corticalis. 

(5)  Diffuse  or  focal  encephalitis  or  meningo-encephalitis,  due  to 

infection  or  toxaemia  of  maternal  origin. 

{6)   Syphilitic  endarteritis  and  thrombosis. 


672  Chapter  LI. 

II.  Natal  Group,  due  to  causes  in  action    during  birth  and  almost 
invariably  traumatic. 

(1)  Meningeal  haemorrhage. 

(2)  Encephalitis,  secondary  to  injury  or  primary. 

III.  Post-natal  Group  ;  cases  arising  from  causes  set  in  action  subse- 
quent to  birth. 

(1)  Arterial    disease,    endarteritis ;     embolism,    thrombosis    and 

haemorrhage. 

(2)  Encephalitis     or     meningo-encephalitis,     due     to     infection, 

toxsemia  or  injury. 

(3)  Head  injury  and  (?)  heat-stroke. 

(4)  Secondary  porencephalus,  cysts  and  tumours. 

Agenesis  Corticalis. — A  considerable  number  of  cases  of  diplegic 
spasticity  occur  in  infants  at  whose  birth  there  was  no  difficulty,  no  injury 
from  forceps,  and  no  asphyxia.  Most  of  these  children  are  small,  delicate 
or  premature.  Probably  there  is  an  imperfect,  incomplete,  delayed  or 
arrested  development  of  the  motor  cells  in  the  cortex  of  the  brain  or  of  the 
motor  tract.  If  this  is  the  explanation,  it  matters  little  whether  labour  was 
difficult  or  easy.  A  possible  cause  is  congenital  syphilis  but  in  many  cases 
it  can  be  excluded  with  certainty.  It  is  difficult  to  separate  agenesis  cor- 
ticalis from  failure  of  development  of  the  pyramidal  tracts,  and  probably 
the  two  affections  are  combined.  If  the  cause  is  in  the  cortex  it  is  likely 
to  be  generalised  and  not  limited  to  the  motor  regions.  The  mental  capacity 
will  be  considerably  affected.  A  mere  delay  in  development  of  the  pyramidal 
tracts  will  not  affect  the  mental  state. 

The  pyramidal  tract  is  developed  in  the  fifth  to  the  seventh  month 
of  foetal  life,  and  in  premature  infants  is  almost  wholly  non-medullated  and 
therefore  function! ess,  for  the  myelin  sheaths  of  this  tract  develop  at  the 
end  of  the  ninth  month  and  the  tract  is  not  fully  developed  until  later.  There 
is  the  further  possibility  that,  because  of  the  incompleteness  of  its  develop- 
ment and  lack  of  protective  myelin  sheaths,  it  is  more  liable  to  injury  during 
labour.  In  its  downward  growth  during  infancy  the  lowest  fibres  of  this 
tract  receive  their  myelin  sheaths  last  and  may  never  acquire  them.  For 
this  reason  the  spastic  paralysis  is  most  common  and  most  permanent 
in  the  lower  limbs. 

Cerebral  Spastic  Paralysis. — Syn.  :  Little's  Disease — Congenital  Spastic 
Rigidity  of  Limbs — Congenital  Birth  Palsy — Spastic  Paraplegia — Infantile 
Spasmodic  Paraplegia — Primary  Spastic  Paraplegia — Cerebral  Diplegia — 
Paraplegia  Spastica  Cerebralis — Spasmodic  Spinal  Paralysis — Spasmodic 
Tabes  Dorsalis. — Heine  described  this  disease  in  1840.  Little  fully 
investigated  it  during  the  years  1846-1870,  and  in  1862  published  a  paper 


Cerebral  and   Cerebellar  Degenerations.  673 

"  On  the  influence  of  abnormal  parturition,  difficult  labour,  premature  birth 
and  asphyxia  neonatorum  on  the  mental  and  physical  condition  of  the 
child,  especially  in  relation  to  deformities."  He  first  suggested  the  relation 
of  the  symptoms  to  injury  of  the  brain  at  birth.  The  affection  Little 
described  was  spastic  paraplegia  due  to  meningeal  haemorrhage.  Since  then 
the  name  "  Little's  Disease  "  has  been  confined  to  cases  occurring  in  infants 
born  before  term  or  at  term  with  instrumental  assistance.  In  a  wider 
sense  "  cerebral  spastic  paralysis  "  includes  cases  in  which  there  is  evidence 
of  an  affection  of  both  cerebral  hemispheres,  and  those  of  spastic  palsy  and 
rigidity  due  to  a  unilateral  cerebral  lesion.  The  characteristics  of  these 
diseases  are  similar  but  their  localisation  varies.  Post-natal  cases  are  more 
likely  to  be  unilateral  than  ante-natal  and  natal  ones.  Eigidity  is  the  chief 
feature,  with  or  without  associated  symptoms.  According  to  their  dis- 
tribution and  characters  they  are  divisible  into  : — 

(1)  Hemiplegia.     Monoplegia    with    contracture.      Spasmodic    facial 

palsy. 

(2)  Cerebral  diplegia  or  bilateral  spastic  (spasmodic)  hemiplegia. 

(3)  Affections  in  which  rigidity  is  slight  ;    viz.  bilateral  and  unilateral 

athetosis,  athetotic  diplegia,  congenital  spastic  chorea. 

(4)  General    spastic    (spasmodic)    rigidity    with    varying    degrees    of 

idiocy.  Atypical  forms  occur  in  which  the  mental  changes  are 
associated  with  slight  general  rigidity,  the  mischief  being  mainly 
in  the  frontal  region. 

(5)  Paraplegic  rigidity  or  Little's  disease.     Paraplegic  paralysis  is  a 

rare  sub-variety. 

(6)  Familial  spasmodic  affections. 

In  all  these  affections  we  find  persistent  rigidity,  an  intact  reflex  arc,  and 
alterations  in  the  pyramidal  tract  which  are  generally  cerebral,  occasionally 
spinal,  in  origin. 

The  motor  residua  of  cerebral  palsies  are  of  several  kinds.  In  some 
instances  they  are  so  marked  that  the  disease  is  named  in  accordance  with 
the  preponderance  of  a  special  residuum,  as  is  seen  in  the  following  table  of 
the  different  varieties  : — 

(1)  Contractures. 

(a)  Spasms  : — clonic,  tonic,  or  intermittent. 

(b)  Muscular  rigidity. 

(c)  Early  contractures  : — paralytic,  passive  and  temporary. 

(d)  Late  contractures  : — constant,  continuous  and  fixed. 

2   x 


674  Chapter  LI. 

(2)  Exaggerated  tendon  reflexes. 

(3)  Associated  movements. 

(4)  Tremors  : — (a)    Simple,  like  those    of    paralysis    agitans    or    of 

disseminated  sclerosis  ;    (6)  Keflex  clonus. 

(5)  Hemichorea,  simple  and  constant. 

(6)  Hemi-ataxia,  a  disturbance  of  co-ordination  on  intended  movements. 

(7)  Athetosis. 

Out  of  859  collected  cases  (R.  Jones,  1906)  the  percentages  of  the 
different  kinds  of  paralysis  were  hemiplegia  60,  diplegia  18,  paraplegia  16, 
monoplegia  4. 

Pathology. — The  causation  of  these  affections  is  illustrated  in  the 
classification  of  the  various  groups.  Maternal  illness,  eclampsia,  and  injury 
during  pregnancy  may  have  some  predisposing  influence.  Of  natal  cases 
the  majority  are  due  to  meningeal  haemorrhage  from  injury  by  too  narrow 
a  pelvic  outlet,  forceps,  or  asphyxia  due  to  constriction  of  the  neck.  The 
child  may  be  born  black  in  the  face,  have  convulsions  during  the  first  weeks 
of  life,  and  be  mentally  deficient.  When  forceps  are  used  the  damage  is 
probably  due  to  the  defective  mechanism  of  labour,  e.g.  a  large  head  and 
small  pelvis,  which  necessitates  their  use,  rather  than  to  actual  injury  by 
the  instrument.  Some  cases  are  due  to  violent  precipitate  labour.  In  view 
of  the  position  of  the  motor  areas  it  is  easy  to  understand  that  haemorrhage 
on  the  surface  of  the  brain  may  occur  in  such  a  position  as  to  affect  the  leg 
centres  only.  According  to  the  extent  and  the  direction  in  which  extension 
takes  place,  it  is  obvious  why  in  some  instances  one  or  both  arms,  and  even 
the  face,  are  also  involved.  If  it  extends  forward  on  to  the  frontal  region, 
the  mental  faculties  will  be  impaired.  The  larger  the  haemorrhage  the 
wider  is  the  distribution  of  the  spastic  paralysis  and  the  greater  the  pro- 
bability of  mental  impairment.  If  it  spreads  to  the  occipital  region  it  may 
cause  squint  and  hemianopia.  The  haemorrhage  is  usually  under  the  arach- 
noid on  the  convexity  of  the  cerebrum,  generally  bilateral,  and  diminishes 
in  extent  from  the  median  line  outward.  Less  frequently  it  is  between  the 
arachnoid  and  the  dura  mater,  and  occasionally  subdural.  It  is  due  to 
compression  of  the  superior  longitudinal  sinus  and  its  veins  from  dislocation 
of  the  cranial  bones  during  labour,  or  to  raised  pressure  from  asphyxia. 
These  infants  are  often  born  dead  or  die  soon  after  birth.  Atelectasis  is 
generally  present.  Subarachnoid  haemorrhage  causes  most  damage  to  the 
nerve  tissues.  Encephalitis  or  meningo-encephalitis  may  follow  on  the 
injury,  or  be  due  to  infection  or  toxaemia  before  or  after  birth.  Both  these 
affections  produce  secondary  sclerosis.  An  acute  onset,  with  fever,  and  a 
subsequent  tendency  to  improvement,  are  in  favour  of  germ  infection. 
Congenital  hemiplegia  is  due  to  unilateral  cerebral  defect,  or  to  endarteritis 


Cerebral  and   Cerebellar  Degenerations.  675 

.■and  thrombosis  of  the  middle  cerebral  artery,  or  syphilitic  disease  of  the 
veins  entering  the  superior  longitudinal  sinus. 

Post-natal  cases  are  generally  hemiplegic  and  the  result  of  focal 
■encephalitis,  embolism,  thrombosis  or  haemorrhage.  Quite  three-fourths 
begin  under  3  years  of  age.  They  occur  during  the  course  of  infective 
•diseases  (p.  697),  and  are  often  ushered  in  with  one  or  more  fits,  which  may 
prove  fatal.  Possibly  convulsions  may  cause  the  local  mischief,  if  a  haemor- 
rhage, but  they  are  more  likely  to  be  the  result  thereof.  As  the  child  recovers 
the  paralysis  becomes  obvious  and  the  subsequent  occurrence  of  sclerosis 
engenders  the  spasticity.  When  a  general  sclerosis  results,  as  after  a 
general  encephalitis,  the  sclerosis  and  its  effects  resemble  those  of  natal 
and  ante-natal  causation  and  can  only  be  distinguished  by  the  history,  that 
is,  they  date  in  onset  from  some  acute  illness  after  birth. 

Morbid  Anatomy. — Atrophy  of  the  cortical  regions  of  the  brain  is 
.always  present,  and  more  or  less  sclerosis,  with  or  without  porencephalus. 
In  pre-natal  cases  the  pyramidal  tracts  are  undeveloped  ;  in  post-natal 
■ones  they  show  degenerative  changes.  In  recent  natal  cases  extravasations 
■of  blood  over  the  cortex,  and  lacerations  of  the  cortex  of  the  cerebrum  and 
•cerebellum,  have  been  found.  Gross  lesions  are  characteristic  of  the  hemi- 
plegias and  general  sclerosis  of  the  diplegias.  Circumscribed  atrophic 
sclerosis,  superficial  shrunken  patches,  or  cysts  may  be  found.  Osier 
states  that  cerebral  sclerosis  is  found  in  50,  porencephalus  in  24,  meningeal 
hemorrhage  in  9,  and  embolism  in  7  per  cent.  The  cerebellar  cortex  may 
be  much  atrophied.  In  congenital  syphilis  the  pia-arachnoid  is  thickened 
and  the  cortex  atrophied. 

The  cell  degeneration  may  be  primary,  due  to  the  toxaemia  of  syphilis 
■or  some  infective  disease.  Or  it  may  be  secondary  to  pressure  from  haemor- 
rhage, thrombosis  of  the  veins  entering  the  superior  longitudinal  sinus, 
embolism  or  thrombosis  of  the  Sylvian  artery,  or  multiple  intra-cerebral 
haemorrhage  from  asphyxia  neonatorum.  Microscopical  examination  may 
reveal  degeneration  of  the  large  pyramidal  cells  ;  old  or  recent  degeneration, 
or  absence,  of  the  pyramidal  fibres  ;  and  degeneration  of  the  direct  and 
crossed  pyramidal  tracts. 

Symptoms. — Males  are  more  liable  than  females  because  they  are 
Jarger  at  birth.  In  ante-natal  and  natal  cases  the  affection  usually  shows 
itself  during  the  first  few  days  of  life  as  a  stiffness  of  the  limbs  which 
gradually  becomes  more  pronounced.  In  very  mild  forms,  and  among  the 
unintelligent,  it  may  not  attract  attention  for  several  months  or  not  until 
the  normal  child  is  expected  to  try  and  walk.  The  adduction  of  the  lower 
limbs  may  be  the  first  sign  to  attract  notice  and  may  not  be  observed  for 
several  months.  The  child  is  a  reflex  animal  at  first  and  myelinisation  of 
the  cord  is  not  complete  until  the  end  of  the  first  year.  Post-natal  cases  are 
generally  of  sudden  onset  in  the  first  3  years  of  life,  during  the  course  of  an 
.acute  illness,  ushered  in  by  fits,  and  hemiplegic.    Pre-frontal  sclerosis  may 


676  Chapter  LI. 

give  rise  fco  impaired  intelligence,  asymmetry  of  the  cranium,  slight  general 
rigidity,  and  backward  speech  if  it  is  on  the  left  side.  The  symptoms  vary 
with  the  site  of  the  lesion.  Palsy  and  spasm  are  generally  unequally 
combined. 

In  a  marked  case  of  diplegia  there  is  great  rigidity,  chiefly  of  the 
extensor  type,  and  paralysis.  The  rigidity  preponderates.  The  head  and 
upper  part  of  the  trunk  are  inclined  forward  and  move  as  if  inseparable. 
Backward  extension  and  lateral  deviation  of  the  head  are  due  to  involve- 
ment of  the  neck  muscles.  The  arms  are  applied  to  the  trunk  ;  the  fore- 
arms flexed  ;  the  hands  pronated,  flexed  at  the  wrists  and  inclined  toward 
the  ulnar  border,  and  the  fingers  and  thumbs  may  be  tightly  clenched. 
Sometimes  there  is  extension  or  hyper-extension  of  the  forearms  and 
hands.  Movements  are  awkward,  slow,  and  accompanied  by  rigidity. 
Grasping,  supinating  and  throwing  are  performed  with  difficulty.  In 
marked  contractures  movements  are  impossible  and  even  passive  ones  are 
violently  resisted.  In  contra-distinction  to  spinal  palsy  the  loss  of  power- 
is  greatest  in  the  hand.  The  lower  limbs  are  rigid,  rotated  inward,  and 
slightly  flexed  at  the  hip  and  knee.  The  thighs  are  strongly  adducted  as. 
far  as  the  knees  and  sometimes  crossed.  Below  the  knees  an  oval  space  is. 
formed,  owing  to  the  inward  rotation  of  the  limbs.  The  feet  tend  to  equinus,. 
because  of  contraction  of  the  gastrocnemii.     The  back  is  hollowed. 

The  rigidity  may  be  so  great  as  to  render  sitting  impossible.  In  milder 
cases,  on  sitting,  the  legs  are  held  rigidly  extended  on  account  of  the  flexor 
rigidity  at  the  hip  joints.  On  standing  it  is  usual  for  the  plantar  surface  of 
one  foot  to  rest  on  the  instep  of  the  other.  Movements  are  slow  and 
clumsy.  The  typical  gait  is  cross-legged  and  spasmodic.  Often  the  child  is. 
unable  to  walk  at  all  or,  even  when  supported,  can  only  make  very  imperfect, 
efforts  on  tip-toe,  with  short  rigid  steps  and  the  knees  closely  pressed 
together.  The  point  of  the  foot  is  drawn  along  the  ground  with  a  movement, 
of  circumduction  and  comes  to  rest  on  the  other  foot,  or  is  carried  forward 
and  across  in  a  "  cross-legged  "  manner.  All  these  movements  may  be- 
precipitate  because  of  a  kind  of  foot  clonus.  Other  muscles  are  more  or 
less  involved.  Those  least  under  the  influence  of  the  will  are  the  most 
likely  to  escape.  Spasmodic  rigidity  and  an  expression  of  stupidity  depend 
on  implication  of  the  facial  muscles.  Bisus  sardonicus  has  been  noted  in. 
one  instance.    The  legs  are  most  and  the  face  least  affected. 

The  eyes  are  usually  unaffected  unless  the  face  muscles  are  implicated. 
Squint,  generally  convergent,  is  due  to  spasm  or  hypermetropia.  Inequality 
of  the  pupils  is  not  uncommon.  Nystagmus  is  unusual.  Congenital  cataract,, 
primary  bilateral  optic  atrophy,  and  palsy  of  the  third  and  sixth  nerves  have 
been  noted.  Vision  is  usually  good.  Bulbar  symptoms  may  be  present.. 
The  tongue  may  be  protruded  slowly,  with  difficulty  or  not  at  all,  or  may 
deviate  to  the  sound  side.  Difficulty  in  swallowing  is  due  to  spasm  of  the 
pharyngeal  and  oesophageal  muscles.     The  child  may  only  be  able  to  take: 


Cerebral  and   Cerebellar  Degenerations.  677 

Hquid  01  semi-solid  food  for  some  years.  Slobbering  and  difficulty  in 
chewing  may  be  present.  Speech  is  often  affected.  It  is  slow  and  drawling, 
or  jerky  as  if  the  words  "  emerged  with  difficulty."  Sometimes  there  is 
aphonia,  stuttering  or  dumbness.  The  child  is  backward  in  learning  to 
speak  and  express  ideas  in  words.  The  defect  is  mental  or  due  to  rigidity 
and  articulatory  difficulty.  Crying  is  hoarse,  and  prolonged  if  there  is 
general  rigidity. 

The  rigidity  diminishes  during  sleep  and  is  increased  by  fear  and  other 
emotions.  There  is  no  true  muscular  atrophy.  The  affected  limbs  or  limb 
may  be  abnormally  small  from  non-development,  due  to  disuse  and 
deficient  innervation.  Sometimes  the  muscles  seem  actually  hypertrophied 
and  are  unduly  hard.  There  is  no  sensory  disturbance.  Intention  tremor 
is  present  in  mild  cases. 

All  the  deep  reflexes  are  greatly  exaggerated,  though  there  may  be 
difficulty  in  obtaining  them  because  of  the  rigidity.  The  periosteal  reflexes 
are  marked.  Ankleclonus,  patella  and  jaw  clonus  may  be  present.  The 
plantar  leflex  is  extensor  in  type.  Superficial  reflexes  are  lessened,  normal 
or  increased. 

Electrical  irritability  is  normal  or  increased.  In  rare  cases  tetanoid 
contraction  has  resulted  from  faradism.  There  is  no  alteration  in  muscular 
sense,  vasomotor  functions,  or  the  functions  of  the  bladder  and  rectum, 
except  a  tendency  to  spasm  in  some  instances.  At  times  the  affection  is  so 
slight  that  it  attracts  no  attention. 

Post-natal  hemiplegia  is  essentially  the  same  as  in  adults  except  in  its 
onset.  The  damage  may  be  slight,  transient,  or  last  for  a  few  months  and 
end  in  complete  recovery.  It  is  rarely  complete  ultimately.  The  grasp 
may  be  as  strong  as  on  the  sound  side  but  the  ordinary  performance  of 
voluntary  movements  is  interfered  with.  There  is  a  variable  degree  of 
rigidity  associated  with  a  variable  amount  of  mobility  in  the  form  of  mobile 
spasm,  athetosis,  chorea  or  tremor,  usually  the  intention  tremor  of 
disseminated  sclerosis  and  known  as  chorea  spastica.    The  leg  may  recover 

^  completely  or  exhibit  mere  clumsiness,  a  liability  to  trip  and  fall,  spasticity, 
or  a  varying  degiee  of  athetosis.  The  nutrition  and  development  of  the 
affected  limb  are  much  interfered  with.  Hemiplegia  is  rather  more  common 
on  the  right  side.  Initial  monoplegia  is  rare  and  apparent  monoplegia  is 
generally  due  to  partial  recovery.  Palsy  is  at  its  maximum  in  the  second 
week. 

There  is  not  much  palsy  of  the  face  and  trunk.  The  arm  is  more  affected 
than  the  leg,  and  the  distal  segments  more  than  the  proximal  ones.  There 
may  be  a  little  weakness  on  the  same  side  as  the  lesion  because  of  some 
"  uncrossed  fibres."  The  facial  palsy  is  most  apparent  on  laughing  and 
crying  and  may  be  associated  with  exaggerated  or  choreiform  movements. 
It  may  not  clear  up  though  the  arm  and  leg  recover.  The  limb  is  often 
reddish-blue  in  colour,  possibly  from  vasomotor  paresis.    Contractures  and 


678  Chapter  LI. 

distortions  result  in  bad  cases.  Chorea  and  athetosis  may  cause  muscular 
hypertrophy.  Aphasia  is  most  frequent  in  right  hemiplegia.  If  due  to  the 
depression  of  acute  illness  or  genera]  cerebral  disturbance  it  is  evanescent. 
It  is  indicated  by  backwardness  in  learning  to  speak.  Except  in  bilateral 
lesions  or  one  on  the  left  side  in  later  childhood  it  is  temporary,  for  the 
speech  centre  on  the  opposite  side  undertakes  the  functions  of  the  one 
destroyed  or  damaged. 

In  these  post-natal  cases  the  damage  may  be  too  slight  to  cause  per- 
manent palsy,  or  be  situated  outside  the  motor  area.  In  either  case  there 
is  a  tendency  to  fits.  Slight  degrees  of  paralysis  are  liable  to  be  overlooked  in 
infancy.  The  nerve  elements  in  the  damaged  cortex  are  softened  and 
destroyed.  Secondary  scar  tissue  forms  and  fits  are  set  up  by  irritation,, 
produced  by  the  slighter  damage  in  the  immediate  neighbourhood  of  this 
local  area  of  impaired  vitality.  They  are  Jacksonian  in  type  but  may  become 
generalised,  by  overflow  to  the  surrounding  cerebral  tissues. 

In  all  cases  of  cerebral  sclerosis  the  mental  state  must  be  carefully 
noted  for  on  this  depends  the  prognosis.  Except  possibly  in  agenesis  of  the 
motor  tracts  and  cases  in  which  the  damage  is  limited  to  the  motor  area  there 
is  always  some  mental  impairment.  The  child  may  be  intellectually  normal, 
merely  a  little  feeble-minded  or  deficient,  or  partially  or  completely  idiotic. 
There  are  many  gradations.  Placidity  is  common  but  the  child  is  often 
silly,  odd,  capricious,  shy,  timid,  impulsive,  disagreeable,  irritable, 
destructive,  vicious,  violent  and  dirty.  Even  in  the  mildest  cases  there  is  as 
a  rule  some  defect  but  it  may  not  be  noticed  until  he  enters  on  school  life 
and  into  competition  with  other  children. 

Complications  are  limited  to  fits  and  various  deformities,  such  as 
asymmetry  of  the  head,  facial  hemiatrophy,  microcephalus  and  hydro- 
cephalus ;  redaction  or  over-flexion  of  the  head  and  torticollis  ;  kyphosis, 
lordosis  and  scoliosis  ;  unequal  scapulae  and  pelvic  bones  ;  equino-varus  and 
pes  cavus  ;    and  various  forms  of  tremor,  chorea  and  athetosis. 

Diagnosis. — Cerebral  sclerosis  must  be  distinguished  from  tetanus 
neonatorum,  infantile  palsy,  amyotonia,  myotonia,  transverse  and  com- 
pression myelitis,  Friedreich's  disease,  disseminated  sclerosis,  endogenous 
myopathies,  cerebral  syphilis  and  hysteria.  A  double  lesion  in  the  brain 
might  cause  double  infantile  spastic  hemiplegia  but  must  be  extremely  rare. 
Most  of  the  above  diseases  can  be  differentiated  without  much  difficulty. 
Chief  stress  is  laid  on  the  spasticity,  exaggerated  reflexes,  mental  state,  and 
the  past  history.  Post-natal  cases  are  generally  hemiplegic  and  of  sudden 
onset.  A  mild  diplegia  may  become  hemiplegia  through  the  effects  clearing 
up  on  one  side.  Slight  degrees  of  rigidity  and  mere  clumsiness  are  not  always- 
recognised.  Athetosis  indicates  incomplete  destruction  of  the  motor  centre 
or  an  attempt  at  spontaneous  cure. 

Prognosis. — Few  severe  infantile  cases  survive  5  years.  If  they  do,, 
they  may  live  beyond  puberty.     In  cases  of  mild  or  medium  severity  the 


Cerebral  and  Cerebellar  Degenerations.  679 

outlook  as  regards  life  is  good,  but  as  regards  recovery  it  depends  primarily 
on  the  cause  and  secondarily  on  the  duration  and  extent  of  the  rigidity 
and  the  mental  state.  If  it  is  due  to  delayed  development  of  the  motor 
tract,  the  child  will  gradually  improve  and  though  for  years  he  may  be 
backward  in  learning  to  talk,  walk,  play  games  and  do  mental  work,  he 
may  eventually  differ  in  no  respect  from  the  normal  boy.  Complete 
acquirement  of  motor  power  and  skill  in  the  use  of  the  muscles  is  rare. 
The  child  commonly  betrays  some  clumsiness.  His  mental  backwardness 
depends  on  the  delay  in  teaching  or  in  learning  to  speak  properly.  Some 
of  these  children  stutter  badly.  A  few  are  mentally  precocious.  The 
rigidity  may  disappear  entirely  ;  first  from  the  face  and  neck,  then  from  the 
upper  extremities,  and  finally  from  the  lower  ones,  in  which  however  it  may 
be  permanent.  Mental  imbecility  may  be  present  though  the  other  signs 
clear  up.  If  so,  there  is  probably  cortical  agenesis  as  well  as  delayed 
development  of  the  motor  tracts.  Puberty  is  not  delayed.  The  disease  is 
not  transmitted  to  children. 

When  secondary  to  meningeal  haemorrhage,  the  prognosis  depends  on 
the  amount  of  the  haemorrhage  and  its  effect  on  the  mental  state.  In  fact, 
whenever  the  cause  is  not  one  of  mere  delay  in  development,  the  outlook 
depends  chiefly  on  the  degree  of  mental  incapacity,  and  is  progressively 
worse  as  this  approaches  idiocy.  Many  improve  a  little  and  then  remain 
stationary.  The  prenatal  cases  rarely  exceed  30  years  of  age,  and  the 
post-natal  ones  are  often  progressive  and  fatal  within  3  years. 

In  the  post-natal  type  recovery  is  rare,  if  rigidity  has  appeared.  Even  if 
the  palsy  clears  up,  there  is  some  impaired  development  of  the  affected  side. 
Mental  acuity  is  often  subnormal.  In  unfavourable  cases  athetosis,  Jack- 
sonian  epilepsy,  epilepsy  and,  less  often,  intentional  tremor  may  arise. 
The  paralysed  limb  does  not  grow  properly,  remains  small,  and  may  lead 
to  limping  and  scoliosis.  In  cerebral  monoplegia  only  one  limb  is  per- 
manently affected.  Epileptic  fits  sometimes  appear  at  the  onset  and 
remain  prominent  to  the  end,  but  they  may  cease,  or  may  develop  later. 
They  are  liable  to  increase  in  frequency,  and  may  end  in  status  epilepticus 
or  sudden  death.  Usually  death  is  due  to  malnutrition,  epilepsy  or 
intercurrent  disease.  Epilepsy  does  not  reduce  the  possibility  of  mental 
and  physical  improvement,  but  increasing  age  does  very  considerably. 

Treatment. — Rely  chiefly  on  warm  baths  followed  by  methodical 
education  of  the  limbs  by  passive  movements,  massage,  voluntary  move- 
ments and  gymnastics.  Massage,  galvanism,  passive  movements  and  warm 
garments  assist  in  maintaining  nutrition  until  voluntary  power  develops. 
It  may  be  advisable  to  tie  up  the  sound  limbs  to  encourage  the  use  of  the 
affected  ones.  Heavy  boots  are  injurious.  Dividing  the  tendons  of  spastic 
muscles  relaxes  the  spasm  of  adjacent  ones  as  well.  A  flexed  wrist  must  be 
hyperextended,  with  the  thumb  at  right  angles  to  the  palms,  for  1-2  years. 
Tenotomy  and  tendon  transplantation  are  of  value.     Eemedy  deformity 


680  Chapter  LI. 

which  limits  the  usefulness  of  the  limb.  Operative  treatment  is  useless  if 
paralysis  is  complete  and  spasm  constant,  and  in  cases  of  idiocy,  miero- 
cephalus,  athetosis  and  (?)  epilepsy.  Careful  education  of  the  speech, 
special  senses  and  mental  functions  is  essential.  These  children  must  be 
encouraged,  not  bullied.  The  mode  of  life  should  be  that  of  ordinary  children 
as  far  as  possible.  Success  depends  on  and  justifies  prolonged  systematic 
treatment. 

Infantile  Cerebral  Degeneration. — Syn. :  Diffused  Cerebral  Sclerosis. — 
This  is  probably  also  identical  with  the  "  family  chorea  and  hereditary 
family  athetosis  "  of  Massalongo  and  Oppenheim,  and  with  a  sub-vaiiety 
"  family  ophthalmoplegia."  It  is  an  endogenous  tendency  to  premature 
failure  of  nutrition  and  function  of  nervous  structures,  and  must  be  dis- 
tinguished on  etiological  grounds  from  sclerosis  due  to  encephalitis  or 
congenital  syphilis.  Possibly  some  cases  are  terminations  of  interstitial 
encephalitis.  Anatomically  there  is  found  extreme  cerebral  atrophy, 
sclerosis  of  many  convolutions  and  especially  of  the  white  matter  and 
basal  ganglia,  some  cerebellar  atrophy,  degeneration  of  the  pyramidal 
tracts  and  the  ascending  cerebellar  tracts,  and  isolated  patches  of  sclerosis. 
The  nerve  cells  are  abnormally  small. 

It  generally  begins  in  the  first  or  second  year  of  life.  An  apparently 
healthy  child,  if  able  to  walk,  begins  to  show  signs  of  difficulty  in  walking. 
This  increases  and  is  associated  with  spasticity,  exaggerated  reflexes,  and  a 
similar  defect  in  the  upper  limbs.  It  may  start  in  the  legs  or  in  all  four 
limbs.  The  muscles  of  the  face  and  mastication  become  involved.  The 
movements  are  sluggish  and  awkward.  There  is  inability  to  carry  out 
purposive  movements,  increased  muscular  tone,  rigidity  and  contractures. 
Tremors,  ataxia  and  athetosis  are  not  uncommon.  The  muscles  are  tense 
and  board-like.  There  is  no  true  palsy  or  atrophy,  and  no  change  in  electrical 
reactions.  Squint,  nystagmus,  conjugate  deviation,  choked  disc  and  optic 
atrophy,  and  pseudo-bulbar  symptoms  have  been  noted.  The  pupils  react. 
The  power  of  speech  is  rapidly  lost.  The  mental  state  is  rarely  unimpaired ; 
usually  there  is  increasing  idiocy.  The  disease  is  progressive,  spasticity 
becomes  extreme,  distressing  convulsions  occur,  and  death  results  from 
emaciation,  bedsores  or  intercurrent  disease.  The  above  symptoms  are 
combined  in  various  ways  in  different  cases  according  to  the  localisation 
and  extent  of  the  sclerosis. 

Higier  (1897)  reported  progressive  ophthalmoplegia  externa  in  4  sisters. 
The  symptoms  were  like  those  of  cerebral  sclerosis  but  the  onset  was  late, 
beginning  with  weakness  and  spasticity  in  the  legs  at  7-12  years  of  age. 
It  gradually  progressed  to  spastic  paraplegia  and  talipes  equino-varus, 
inability  to  stand,  walk  or  sit,  tremor  and  clumsiness  in  the  hands,  defective 
speech,  impaired  intelligence,  squint  and  optic  atrophy.  It  affects  both 
sexes  and  is  transmitted  by  either.  Sporadic  cases  are  rare.  In  other 
instances  the  levator  palpebrae  superioris  or  the  abducens,  perhaps  in 
conjunction  with  the  facial  nerve,  was  affected. 


Cerebral  and  Cerebellar  Degenerations.  681 

Infantile  progressive  bulbar  palsy  begins  at  6-10  years  of  age.  Speech, 
swallowing  and  expression  are  affected.  Dribbling  of  saliva  is  followed  by 
atrophy  and  tremor  of  the  tongue,  a  mask-like  aspect,  palatal  palsy,  weak- 
ness of  the  muscles  of  mastication,  irregularity  of  the  pulse  and  breathing. 
It  may  remain  stationary  for  some  time. 

Amaurotic  Family  Idiocy. — Syn.  :  Primary  Amaurotic  Mental  Defi- 
ciency (Warren  Tay) — Infantile  Degeneration  ivith  Changes  at  the  Macula — 
Arrested  Cerebral  Development — Family  Form  of  Idiocy — Agenesis 
Corticalis. — This  is  a  variety  of  cerebral  sclerosis  or  degeneration  described 
first  by  Warren  Tay  in  1881.  In  1901  Falkenheim  collected  64  cases,  of 
which  27  were  isolated  ones  and  37  occurred  in  13  families.  Four  of  the 
36  families  were  Gentiles.    A  good  many  cases  have  been  reported  since. 

The  disease  is  almost  peculiar  to  Jews,  especially  poor  Polish  and 
Russian  Jews.  It  occurs  in  families,  affecting  several  children  in  no  regular 
sequence.  No  etiological  factor  has  been  found.  The  children  are  usually 
normal  at  birth  and  breast-fed.  It  begins  between  the  second  and  tenth 
months,  generally  at  6  months  of  age,  with  weakness  of  the  muscles  of  the 
neck  and  back,  inability  to  support  the  head,  dull  expression  and  imperfect 
vision.  This  is  followed  by  apathy,  imbecile  aspect,  increasing  weakness, 
•acuteness  of  hearing,  and  perhaps  persistent  screaming.  Perception  of 
light  is  left  and  the  electrical  reactions  are  unchanged.  The  paralysis  is 
flaccid  or  spastic,  or  spasticity  may  follow  flaccidity  ;  the  reflexes  are 
normal  or  increased.  In  late  stages  there  is  atrophy  of  the  enfeebled 
muscles,  retraction  of  the  head,  rigidity  of  limbs,  progressive  emaciation  and 
idiocy.  Death  results  from  marasmus  or  intercurrent  disease.  At  birth 
the  eyes  are  normal.  Haziness  in  the  macular  region  is  the  first  sign  ; 
then  the  macula  becomes  occupied  by  an  oval  whitish-grey,  bluish-white, 
greenish-white  or  dead  white  patch,  about  twice  the  diameter  of  the  optic 
disc,  in  the  centre  of  which  is  a  round  cherry-red  spot,  the  fovea  centralis. 
These  changes  remain  stationary.  The  optic  disc  may  show  neuritis  or 
atrophy,  and  the  surrounding  pigment  disc  is  very  distinct.  Unequal 
pupils,  squint,  ptosis  and  nystagmus  are  sometimes  present.  The  pupils 
usually  respond  to  light. 

Hyperacusis  is  not  always  present.  Some  children  appear  deaf. 
Spasms  or  fits  may  be  induced  by  sudden  noises.  Explosive  laughter  and 
■dysphagia  or  disturbance  of  deglutition  have  been  reported.  The  terminal 
symptoms  suggest  meningitis,  and  death  may  be  unexpectedly  sudden. 
Out  of  38  cases  (Falkenheim)  35  died  \mder  2  years  and  the  other  3  under 
4  years  of  age.  The  characteristic  ocular  changes  axe  not  found  in  all 
cases. 

The  essentia]  change  is  a  degeneration  of  the  ganglion  cells  of  the 
retina,  and  of  the  optic  nerves  and  tracts.  In  McKee's  case  Spiller  found  the 
ganglion  cells  of  the  retina  increased  in  size,  more  globular,  and  much 
degenerated.  At  the  fovea  centralis  there  are  no  such  cells  and  the  red 
■choroid  is  visible  ;    but  at  the  margins  of  the  fovea  the  ganglion  layer  is 


682 


Chapter  LI. 


6-10  cells  deep  and,  being  swollen,  gives  rise  to  a  white  area  round  the- 
central  red  spot.  These  cells  are  genetically  part  of  the  central  nervous- 
system.  Degenerative  changes  were  found  in  the  optic  nerve  and  the  nerve 
cells  throughout  the  spinal  cord.  Hirsch  first  found  these  extraordinary 
cellular  changes  in  the  retina.  Spiller  could  not  find  a  single  normal  cell 
throughout  the  central  nervous  system.  The  disease  is  not  inflammatory, 
and  must  be  regarded  as  a  primary  degeneration  of  nerve  cells  and  secondary 
degeneration  of  nerve  fibres  ;  varying  in  distribution.  It  differs  from  in- 
fantile cerebral  sclerosis  in  the  cellular  changes. 

Possibly  these  cellular  changes  are  compatible  with  more  prolonged 
life.  More  probably  cases  in  older  children  are  different.  They  exhibit 
progressive  mental  degeneration  and  changes  in  the  fundus.  A  normal  child, 
at  3-14  years  of  age,  becomes  irritable,  bad  tempered  and  mentally  dull,, 
perhaps  timid  and  emotional.  The  ocular  symptoms  are  defective  sight, 
loss  of  centra]  vision,  moderately  dilated  pupils  which  react  badly  to  light,, 
perhaps  nystagmus,  pallor  of  the  discs,  and  mild  choroido-retinitis  in  the 
macular  region.  Spasticity,  inco-ordination,  and  absent  or  deficient  knee 
jerks,  may  be  present.  The  loss  of  central  vision  induces  a  crab-like  gait. 
It  progresses  to  blindness  and  imbecility.     Some  improve  on  pot.  iod. 

A  family  form,  analogous  to  family  spastic  paraplegia,  begins  about  the 
eighth  year  of  age.  It  is  very  slowly  progressive,  with  gradual  development 
of  spasticity,  and  is  possibly  due  to  overwork  of  the  neurons  at  the  time  of 
functional  activity. 

Juvenile  General  Paralysis. — This  is  due  to  congenital  syphilis,  though 
the  signs  thereof  may  be  absent  in  the  patient  yet  present  in  other  children. 
It  affects  both  sexes  equally.  It  begins  about  puberty,  sometimes  as  early 
as  the  eighth  year.  A  definite  family  history  of  syphilis  is  found  in  60-80' 
per  cent,  of  the  cases,  and  Mott  states  that  general  paralysis  occurs  in  the 
father  in  20  per  cent. 

Mott  describes  two  types.  In  one  there  is  an  arrest  of  development, 
and  the  child  is  infantile  in  body  and  mind.  In  the  other  there  is  fair- 
physical  and  mental  development  until  puberty  or  adolescence,  and  then 
progressive  decay  of  the  central  nervous  system.  The  degeneration  of  body 
and  mind  may  be  started  by  the  strain  of  school  life,  puberty,  accident,, 
acute  illness  or  spontaneously.  In  a  third  type  the  child  is  unduly  sharp 
and  intelligent. 

The  early  signs  are  an  aspect  of  worry  or  pre-occupation,  apathy,  loss 
of  memory  ;  outbreaks  of  crying,  passion  or  screaming,  symptoms  of 
cerebral  irritation  ;  attacks  of  partial  paralysis,  of  mental  stupor  or 
unconsciousness,  or  epileptiform  convulsions.  The  pupils  are  unequal, 
react  sluggishly  or  not  at  all  to  light,  and  optic  atrophy  may  be  present 
early.  Fine  tremors  of  the  tongue,  facial  muscles  and  hands  are  present. 
The  knee  jerks  are  exaggerated  early  and  lost  eventually.  Speech  is- 
indistinct,  slovenly,  slow  or  rapid  ;  and  sometimes  ceases.      Delusions  are^ 


Cerebral  and  Cerebellar  Degenerations.  683 

uncommon  and  megalomania  rare.  Childish  ideas  of  grandeur,  such  aa 
might  be  expected  at  the  particular  age,  occur  in  about  10  per  cent. 
Sometimes  there  are  attacks  of  excitement  and  depression. 

The  course  is  steadily  progressive  physical,  mental  and  moral  failure 
without  remission.  Weakness  of  the  limbs  is  followed  by  paralysis  and 
contractures.  The  face  is  expressionless.  Sucking,  chewing,  humming  and 
slobbering  occur.  The  sex  organs  undergo  fibrosis  and  there  are  no 
spermatozoa,  Graafian  follicles  or  catamenia.  The  testes  may  be 
undescended. 

Diagnosis  is  often  difficult.  Many  cases  are  mistaken  for  idiocy  or  a 
congenital  idiot  may  develop  the  disease.  The  exaggerated  reflexes, 
sluggish  light  reflex,  and  early  occurrence  of  paralytic  attacks  are  the  chief 
indications.  Evidence  of  congenital  syphilis  may  be  present,  e.g.  scarring  at 
the  angles  of  the  mouth,  interstitial  keratitis,  choroidal  atrophy  or  deafness. 
The  chief  difficulty  is  the  differential  diagnosis  from  endarteritis  of  the 
brain  of  specific  origin.  It  is  important  with  a  view  to  prognosis.  Fits  may 
simulate  epilepsy. 

The  average  duration  is  2-4  years,  varying  from  6  weeks  to  7  years. 
It  is  invariably  fatal,  and  a  chronic  diffuse  meningo-encephalitis  has 
frequently  been  found  after  death.  It  is  not  a  post-syphilitic  degeneration 
entirely. 

Cerebellar  Ataxia. — The  cerebellar  cortex  has  an  important  influence 
on  the  movements  of  skeletal  muscles.  Luciani  found  that  ablation  of  the 
cerebellum  caused  general  unsteadiness,  strabismus,  spasms  of  the  neck 
muscles,  flexions  of  the  fore-limbs,  hypotonia,  and  unsteadiness  of  the 
posterior  limbs  ;  the  symptoms  passing  off  in  a  few  months.  If  the  cortex 
was  damaged  in  the  region  of  the  sigmoid  gyrus,  the  symptoms  persisted. 
Therefore,  atrophy  and  even  complete  absence  of  the  cerebellum  can  exist 
without  symptoms.  Mild  cases  of  disease  may  recover.  Injury  to  the 
cortex  is  indicated  by  muscular  rigidity,  reflex  and  mental  symptoms. 

Marie  and  Sanger  Brown  have  described  Hereditary  Cerebellar  Ataxia. 
It  occurs  in  several  members  of  a  family  in  association  with  a  congenital 
cerebellar  defect.  It  begins  in  the  legs  and  then  affects  the  arms,  face  and 
speech.  The  gait  is  reeling,  rather  than  ataxic  ;  the  Argyll-Robertson  pupil 
is  sometimes,  nystagmus  rarely,  and  optic  atrophy  often  present ;  the 
knee  jerks  are  exaggerated  always  ;  and  there  are  articulatory  difficulties. 
It  is  closely  allied  to  Friedreich's  disease  (p.  715),  and  comes  on  at  15-35 
years  of  age.  Cerebellar  hypoplasia  and  secondary  degenerations  are  found 
after  death. 

Cerebellar  Ataxia  or  Diplegia  is  sometimes  an  ataxia  of  congenital 
origin  starting  in  early  life.  Batten  recognises  three  types  : — (1)  Noticed 
from  earliest  life  and  tending  to  improve.  (2)  Of  sudden  onset  during 
acute  illness,  and  perhaps  ending  in  recovery.  (3)  Of  gradual  development 
in  a  normal  child,  progressive,  and  of  bad  prognosis.     The  symptoms  are 


684  Chapter  LI. 

unsteadiness  of  the  head,  trunk  and  limbs  ;  unsteadiness  in  sitting,  standing 
and  walking  ;  slow  monotonous,  drawling,  sing-song,  indistinct  articulation  ; 
slowness  or  difficulty  in  swallowing.  Intelligence  is  unimpaired  ;  the  habits 
are  clean  ;  there  are  no  eye  symptoms,  and  no  rigidity.  Cases  must  be 
diagnosed  from  ataxia  due  to  tumours  of  the  cerebellum  or  mid-brain  and 
sometimes  seen  in  diphtheritic  palsy ;  from  cerebral  diplegia  with 
associated  choreiform  movements  or  ataxia  ;  from  Friedreich's  disease 
and  disseminated  sclerosis.  Some  of  them  are  mixed  cases  of  cerebral  and 
cerebellar  mischief.  In  these  there  is  usually  rigidity,  mental  impairment, 
exaggerated  knee  jerks  and  extensor  plantar  reflexes. 

The  disease  is  rarely  progressive  and  tends  markedly  to  recover. 
A  child  ataxic  and  unable  to  walk  at  2  years  of  age  may  walk  steadily  in 
another  2  years.  Treatment  is  directed  to  improving  co-ordination  by  the 
use  of  a  solitaire  board,  mozaic  puzzles,  etc.,  for  the  hands  ;  Fraenkel's 
exercise  board,  walking  and  various  combined  movements  for  the  legs. 

Functional  Familial  Disorders. — Though  not  degenerative  in  causation 
these  rare  affections  present  analogies  with  the  above  diseases  which  render 
it  convenient  to  consider  them  in  connection  therewith. 

Family  Periodic  Paralysis  was  first  reported  by  Hartwig  (1874)  as 
"  intermittent  spinal  paralysis."  Up  to  1907  about  85  cases  were  on 
record.  It  is  characterised  by  periodical  attacks  of  motor  paresis  or 
paralysis,  flaccid  in  type,  with  weakness  or  abolition  of  the  reflexes,  and 
partial  or  complete  loss  of  electrical  excitability.  Sensation  is  altered. 
It  may  affect  several  members  in  the  same  family.  It  begins  at  6-24  years 
of  age.    F.  Buzzard  has  reported  a  case  starting  in  infancy. 

The  attacks  come  on  gradually  during  a  period  of  rest  after  physical 
over-exertion,  usually  in  half  an  hour  or  so  and  often  during  the  night. 
They  may  be  preceded  by  a  sense  of  fatigue,  "  pins  and  needles  "  over  the 
trunk  and  limbs,  or  a  dull  aching  sensation  in  the  legs  and  a  sinking  sensa- 
tion in  the  epigastrium.  The  severity  varies  from  slight  temporary  paresis 
up  to  complete  immobility  ;  the  duration  from  an  hour  to  days  ;  and  the 
frequency  from  daily  ones  to  attacks  at  prolonged  intervals.  All  the 
voluntary  muscles  are  affected,  especially  the  proximal  limb  muscles.  It 
appears  in  the  legs,  arms,  trunk  and  neck  successively.  Except  in  severe 
attacks  the  muscles  of  respiration  and  those  supplied  by  the  cranial  nerves 
escape.  The  diaphragm  is  never  affected  and  breathing  is  entirely 
diaphragmatic.  There  is  no  sphincter  trouble,  but  weakness  of  the 
abdominal  muscles  interferes  with  micturition  and  defsecation.  Speech  and 
swallowing  are  affected. 

The  superficial  and  deep  reflexes  are  abolished  or  diminished.  There 
is  a  gradual  reduction  in  the  response  to  mechanical,  electrical  and  reflex 
stimulation,  in  proportion  to  the  loss  of  voluntary  power.  The  heart  often 
dilates,  is  irregular,  and  may  present  a  systolic  murmur.  Sensation  and 
consciousness  are  unimpaired.     Sweating  is  often  present. 


Cerebral  and  Cerebellar  Degenerations.  685 

Buzzard  ascribes  it  to  stagnation  of  lymph,  in  the  muscular  lymph 
spaces,  and  some  consequent  effect  on  the  muscle  plasma.  In  support  of 
this  view  is  the  fact  that  many  patients  can  walk  off  the  attack  ;  and  the 
escape  of  the  diaphragm  and  the  muscles  supplied  by  the  cranial  nerves,  for 
they  are  never  so  completely  at  rest  as  the  limb  muscles  and  therefore  do  not 
suffer  from  lymph  stasis.  Indiscretions  in  diet  and  constipation  are 
predisposing  causes,  and  increased  toxicity  of  the  urine  has  been  noted, 
suggesting  auto-intoxication.  Possibly  the  two  factors  are  combined  in 
action. 

Recovery  takes  place  in  inverse  order  to  the  onset.  The  disease  does  not 
shorten  life.  Attacks  become  less  severe,  less  frequent,  and  may  cease  as. 
age  increases.  Syncope  may  occur  from  the  cardiac  dilatation.  Treatment 
should  be  directed  to  the  prevention  of  toxsemia  and  auto-intoxication. 

Myotonia  Congenita  or  Thomson's  Disease,  is  a  spastic  contraction  of 
the  muscles  coming  on  after  sitting.  After  much  effort  the  patient  is  able 
to  walk  and  as  he  walks  the  movements  improve.  It  affected  12  out  of 
14  in  Thomson's  family.  Mikinoff  (1897)  collected  100  cases.  It  affects, 
more  males  than  females  and  is  transmitted  by  either  sex.  It  has  been 
observed  in  infants  at  the  breast  in  the  form  of  inability  to  open  the  mouth, 
immobility  of  the  face  on  beginning  to  cry,  inability  to  nurse,  frequent 
sighing  respiration,  interference  with  movements  of  the  limbs,  and  hyper- 
trophy of  the  leg  muscles. 

The  chief  signs  are  impediment  in  gait,  temporary  rigidity  at  the  onset 
of  effort,  and  the  disappearance  of  rigidity  with  return  of  suppleness  of  the 
muscles.  They  are  increased  by  fatigue,  damp,  heat,  cold  and  observation. 
All  the  muscles  may  be  involved,  even  the  eyes  and  tongue.  The  spasmodic 
state  is  universal  but  most  in  the  legs,  arms  and  face.  Muscular  develop- 
ment is  very  marked  ;  knee  jerks  active  ;  and  a  localised  muscular  swelling 
is  induced  by  a  sharp  tap.  A  very  small  faradic  current  induces  tetanic 
contraction,  or  clonic  contractions  which  persist  after  the  current  is  turned 
off.  The  muscles  are  easily  excited  by  galvanism,  and  the  reaction  of 
degeneration  has  been  noted.  This  disease  has  been  ascribed  to  auto- 
intoxication. If  so,  it  is  due  to  a  poison  which  has  exactly  opposite  effects, 
to  the  one  which  causes  family  periodic  paralysis.  It  runs  a  prolonged 
course,  with  periods  of  remission  and  improvement. 

Landry's  Paralysis.— Few  cases  occur  in  children.  It  is  an  acute 
intoxication  affecting  the  nerves,  cord  or  bulb,  and  causing  polyneuritis, 
neuritis  of  spinal  nerve  roots,  poliomyelitis  or  bulbitis.  It  may  begin  with 
bulbar  symptoms.  Generally  it  starts  in  the  feet  and  affects  the  bulbar 
region  finally,  causing  death  from  asphyxia  without  loss  of  consciousness. 
The  superficial  and  deep  reflexes  are  absent  and  electrical  irritability 
disappears.  The  sphincters  escape  and  there  are  no  trophic  effects.  It  is 
almost  always  fatal  in  5-10  days. 


686  Chapter  LI. 

Treatment. — In  all  the  organic  affections  described  in  this  chapter 
treatment  is  of  comparatively  little  value  for  curative  purposes.  It  must 
be  directed  to  maintaining  the  general  health,  conserving  strength,  and 
relieving  symptoms.  Anti-syphilitic  remedies  must  be  tried  if  there  is 
the  least  possibility  of  a  syphilitic  causation. 


CHAPTER    L1I. 

VASCULAR    AFFECTIONS— TUMOURS— ABSCESS. 

•Concussion — Intracranial  Hemorrhage — Thrombosis — Embolism — Cerebral 
and  Cerebellar  Tumours  and  Abscess. 

Concussion  of  the  brain,  if  severe,  causes  "bruising"  and  haemorrhagic 
■extravasation.  It  is  infrequent  in  children  and  rare  in  babies,  because  they 
do  not  often  fall  from  any  great  height  and  the  yielding  bones  allow  dis- 
placement of  the  brain.  Concussion  gives  rise  to  loss  of  consciousness, 
vomiting,  infrequent  pulse  and  retention  of  urine.  In  actual  bruising  of  the 
brain  there  may  be  aphasia,  transitory  palsy,  and  signs  of  cerebral  irritation, 
shown  by  irritability,  refusal  of  food,  vomiting,  and  the  curled  up  attitude 
in  bed  with  resentment  at  being  disturbed.  Mild  cases  of  concussion 
recover  in  a  few  hours  or  days.  Severe  ones  may  be  fatal.  It  is  advisable 
to  treat  even  the  mildest  case  with  rest,  quiet  and  careful  feeding,  for  it  is 
impossible  to  make  an  accurate  estimate  of  the  amount  of  damage  and 
time  must  be  allowed  for  its  repair. 

Intracranial  Haemorrhage. — The  bleeding  is  meningeal  or  intra-cerebral. 
Meningeal  haemorrhage  is  usually  vertical,  involving  one  or  both  con- 
vexities of  the  cerebrum,  and  may  extend  to  the  base  and  cerebellum.  It 
is  commonly  due  to  injury  at  birth  by  narrow  maternal  passages,  forceps 
or  prolonged  constriction  of  the  neck.  The  overlapping  bones  compress 
the  veins  of  the  longitudinal  sinus.  It  may  occur  in  normal  labour, 
especially  if  premature.  After  birth  it  results  from  injury,  pachymeningitis 
(p.  670),  pertussis,  the  haemorrhagic  types  of  specific  fevers,  sinus  throm- 
bosis, and  various  blood-states  such  as  scurvy,  purpura,  leukaemias  and 
haemophilia.  In  some  of  these  the  bleeding  takes  place  under  the  dura 
mater,  causing  a  subdural  haematoma  (p.  670)  ;  generally  it  is  from  vessels 
in  the  pia-arachnoid. 

Intra-cerebral  haemorrhage  may  be  intra-ventricular  from  the  choroid 
plexus  or  into  the  substance  of  the  brain.  Occasionally  it  occurs  in 
apparently  healthy  children  and  no  cause  can  be  found  after  death,  e.g.  into 
the  ventricles  at  2  months  (G.  Carpenter),  left  temporo-sphenoidal  lobe  at 
19  months  (Murray),  pons  at  6  years  (Collier),  cerebellum  at  9  years 
(H.  H.  Phillips),  frontal  lobe  at  lOyears  (Edwards).  The  usual  causes  are  the 
same  as  in  meningeal  haemorrhage,  or  malignant  endocarditis  and  embolism, 
occasionally  atheroma,  arterio-sclerosis,  aneurysm  and  syphilis. 


688  Chapter  LI  I. 

Symptoms. — At  birth  the  signs  are  often  those  of  asphyxia  only 
(p.  116),  subnormal  temperature  and  cyanosis.  Sometimes  there  are  con- 
vulsions, unequal  pupils,  shallow  irregular  breathing,  and  slow  pulse. 
Or  there  may  be  no  asphyxia,  but  fits  and  inequality  of  the  pupils  come  on 
in  a  few  days.  Fits  are  more  or  less  unilateral  when  late  in  onset.  Trismus, 
spasms,  exaggerated  reflexes,  ocular  palsies,  irregular  pulse  and  breathing, 
and  increasing  coma  or  palsy  are  sometimes  present,  and  probably  due  to 
increasing  effusion.  Usually  there  is  no  evidence  of  paralysis.  The  fon- 
tanelle  bulges  and  does  not  pulsate.  Generally  speaking  the  onset  is  with 
convulsions  or  coma,  and  the  sequel  is  spastic  paralysis.  In  older  children 
the  symptoms  are  the  same  as  in  adults,  viz.  headache,  coma,  delirium, 
convulsions,  palsy,  etc.     The  attack  may  begin  with  convulsions. 

Diagnosis  is  important  in  cases  due  to  injury  at  birth,  because  of  the 
possibility  of  relief  by  operation.  It  is  based  on  the  history  of  prolonged 
labour,  use  of  forceps  or  asphyxia,  and  the  fits  or  coma  with  bulging  fon- 
tanels. Trephining  is  necessary,  if  there  is  risk  of  death  from  pressure,  and 
might  be  adopted  more  readily  for  the  prevention  of  cerebral  spastic 
paralysis.  Cushing  (1905)  reported  operations  on  4  cases,  one  bilateral, 
with  2  recoveries.     Lumbar  puncture  may  reveal  blood. 

Haemorrhage  into  the  Spinal  Cord  or  Canal. — This  is  commonly  due 
to  birth  injury  and  on  the  ventral  surface,  perhaps  spreading  from  the 
vertex.  Small  haemorrhages  into  the  cord  are  frequent  and  apparently 
unimportant ;  large  ones  are  rare  and  possibly  produce  syringomyelia. 
The  causes  are  the  same  as  in  intracranial  haemorrhage. 

Thrombosis. — Primary  thrombosis  of  cerebral  sinuses  or  veins  is  due 
to  marasmus,  prolonged  diarrhoea,  broncho-pneumonia,  tuberculosis, 
congenital  syphilis,  acute  diseases,  etc.  Secondary  or  infective  thrombosis 
is  due  to  the  streptococcus,  pneumococcus,  staphylococcus  and  other 
organisms  ;  and  occurs  in  general  pyaemia,  local  abscess  by  extension 
through  the  wall,  otitis  media,  cellulitis,  mouth  affections,  etc.  It  gives 
rise  to  obstruction  of  the  circulation,  obliteration  of  the  vessel,  contraction 
of  the  clot,  breaking  down  in  the  infective  cases,  pyaemia  and  meningitis. 

Symptoms  may  be  absent  in  the  newborn,  cachexia,  and  incomplete 
cases.  Frequently  they  are  only  those  of  the  antecedent  disease.  The 
ordinary  cerebral  signs  are  headache,  restlessness,  vomiting,  delirium  and 
coma.  Infants  may  merely  be  somnolent  or  cry  out  at  night.  Vomiting, 
convulsions,  coma  and  death  occur  in  rapid  sequence  in  some  instances. 
Others  show  rigidity  of  the  neck,  trismus,  squint,  nystagmus,  unequal 
pupils,  irregular  pulse  and  breathing.  Optic  neuritis  may  be  present ;  and 
rigors  and  sweats  in  pyaemic  cases. 

In  pure  sinus  thrombosis  of  the  superior  longitudinal,  two  lateral  and 
cavernous  sinuses,  the  symptoms  are  severe  headache,  vertigo,  vomiting, 
dilated  pupils,  optic  neuritis,  and  perhaps  twitching  of  the  face  and  neck 
muscles.     It  is  indistinguishable  from  cerebral  tumour. 


Vascular    Affections —  Tumours — -  Abscess.  689 

Localising  signs,  often  absent,  are  cyanosis  and  cedema  of  the  forehead 
and  dilated  superficial  scalp  veins,  if  the  clot  is  in  the  superior  longitudinal 
sinus.  If  in  the  lateral  sinus,  the  superficial  veins  on  that  side  are  empty  ; 
pain  and  stiffness  extend  into  the  internal  jugular,  perhaps  causing 
dysphagia  and  lateral  inclination  of  the  head,  and  the  vein  may  be  palpable, 
as  a  tender  cord  under  the  anterior  edge  of  the  sterno-mastoid  ;  the  deep 
cervical  glands  are  enlarged  ;  tenderness  and  cedema  behind  the  mastoid 
result  from  thrombosis  of  the  mastoid  emissary  vein  ;  and  bulbar  symp- 
toms may  arise  from  pressure  on  nerves  passing  through  the  jugular  foramen. 
Cerebral  symptoms,  fever  and  rigors  indicate  septic  thrombosis  of  the 
lateral  sinus,  and  the  diagnosis  depends  on  a  thrombus  in  the  jugular  vein. 
When  the  cavernous  sinus  is  blocked  we  find  proptosis,  cedema,  amblyopia, 
swelling  of  the  optic  discs,  retinal  haemorrhages,  ocular  palsy  and  panoph- 
thalmitis. Thrombosis  of  the  ascending  frontal,  parietal  and  temporo- 
sphenoidal  veins,  may  lead  to  acute  red  softening  and  haemorrhage,  term- 
inating in  sclerosis  and  palsy.  Marasmic  cases  may  live  for  weeks.  A 
few  primary  ones  recover  by  contraction  of  the  clot.  Secondary  hydro- 
cephalus may  ensue  if  the  sinus  is  obliterated.  Pulmonary  embolism  may 
occur.  Pyaemia  is  indicated  by  high  fever,  rigors,  embolism  and  arthritis. 
Death  is  often  due  to  multiple  pyaemic  abscesses  in  the  lungs.  Ligature  of 
the  vein,  the  sinus  being  incised  and  the  clot  removed,  saves  a  few  patients 
with  thrombosis  of  the  lateral  sinus.    It  is  usually  due  to  ear  disease. 

Embolism  is  a  sequel  of  endocarditis,  or  thrombosis  of  an  artery  in  the 
brain  or  in  a  vein  elsewhere.  It  causes  red  softening,  an  acute  haemorrhagic 
inflammation,  followed  by  yellow  softening  from  necrosis  ;  occasionally 
white  softening,  from  deficient  blood  supply.  An  infective  embolus  pro- 
duces results  closely  allied  to  encephalitis.  Both  embolism  and  thrombosis 
are  most  frequent  in  the  Sylvian  artery  and  its  branches.  A  large  one  causes 
convulsions,  followed  by  coma,  local  paralytic  and  irritative  symptoms, 
occasionally  aphasia  and  sensory  defects.  The  prodromata  are  such  as  are 
due  to  endarteritis  or  arterial  thrombosis,  viz.  headache,  restlessness, 
vomiting  and  drowsiness.  It  terminates  in  scar  formation,  sclerosis,  cyst 
formation,  and  cerebral  infantile  palsy. 

Intracranial  Tumours  are  very  uncommon  under  2  years  of  age,  except 
the  pea-like  tuberculous  nodules  sometimes  present  in  tuberculous  menin- 
gitis. After  this  age  all  kinds  may  be  found,  but  in  quite  50  per  cent,  the 
tumour  is  tuberculous,  and  25  per  cent,  glioma  or  sarcoma.  Other  varieties 
are  rare  and  secondary  tumours  almost  unknown.  The  tuberculous  tumours 
are  often  multiple,  shaiply  limited,  rarely  break  down,  and  may  be  sur- 
rounded by  softening.  They  are  most  frequent  in  the  cerebellum  and  pons. 
They  are  often  latent,  dense,  have  a  greenish  tinge,  and  end  in  meningitis. 
A  local  source  of  infection  in  the  thoracic  or  mediastinal  glands,  occasionally 
in  the  skin,  is  almost  always  found.  Gliomata  are  epithelial  in  origin,  from 
the  neuroglia  cells,  infiltrating  in  character,,  and  liable  to  myxomatous 


690  Chapter  LI  I. 

degeneration,  softening  and  cystic  formation,  and  haemorrhage.  They  grow 
slowly  and  do  not  involve  the  bones  of  the  skull  or  cause  secondary  deposits, 
and  are  most  common  in  the  pons.  They  are  richly  cellular,  fibrillaiy, 
spider-celled,  spindle-celled  or  giant-celled  (Stroebe).  Sarcomata  are  most 
common  in  the  cerebellum.  They  are  single,  capable  of  removal,  grow 
slowly,  and  are  liable  to  haemorrhage  and  myxomatous  degeneration. 

Cystic  tumours,  due  to  the  cysticercus  01  echinococcus,  are  exceptional 
in  this  country  but  not  uncommon  in  Europe.  They  may  be  single,  form 
multiple  cysts  on  the  surface  of  the  brain  and  in  the  ventricles,  occur  in  the 
cranial  bones,  and  are  at  times  embolic,  the  result  of  dissemination  by  the 
blood  during  operation.  Small  ones  may  calcify.  The  progress  is  very  slow 
and  a  few  recover.  Gummata  are  exceptional  and  are  not  due  to  congenital 
syphilis.  Miliary  aneurysms  are  due  to  chronic  interstitial  nephritis,  infec- 
tive emboli,  or  micro-organisms.    Abscess  receives  separate  consideration. 

No  part  of  the  brain  is  exempt.  About  30  per  cent,  of  all  tumours  are 
cerebellar  and  10  per  cent,  pontine.  They  may  be  cortical,  cerebral,  or  basal. 
Supra-tentorial  tumours  are  very  rare  under  15  and  still  more  rare  under 
8  years  of  age,  if  tuberculous  nodules  are  excepted. 

Boys  are  twice  as  liable  as  girls,  possibly  because  they  are  more  likely 
to  injure  themselves.  It  is  quite  common  for  the  tumour  to  correspond  with 
the  site  of  an  injury,  though  it  is  difficult  to  believe  that  injury  is  an 
exciting  cause. 

General  Symptoms  depend  on  the  size,  rate  of  increase,  the  vascularity 
and  nature  of  the  growth.  They  are  headache,  vomiting,  optic  neuritis 
and  atrophy,  vertigo,  bradycardia,  and  changes  in  disposition  and  mental 
activity.  Yet  headache,  vomiting  and  optic  neuritis  may  be  absent  in  even 
large  tumours.  Headache  is  the  most  important  sign.  It  varies  in  site, 
extent  and  severity.  It  is  not  as  bad  as  in  adults,  severe  at  times,  and 
•constant  or  intermittent.  It  is  exaggerated  by  mental  effort  and  increased 
intracranial  pressure.  It  varies  from  a  dull,  aching  pain  to  paroxysmal 
agony  in  which  death  may  occur.  Marked  variation  may  depend  on  the 
vascularity  of  the  tumour.  It  is  most  valuable  as  a  sign  when  it  is  persistent 
and  localised.  Occasionally  it  is  over  the  site  of  the  tumour,  commonly 
frontal  or  occipital,  rarely  vertical  or  parietal.  It  is  most  constant  and 
severe  when  the  tumour  is  in  the  posterior  cranial  fossa,  the  pain  being 
occipital  and  radiating  into  the  neck.  The  pain  may  get  less  or  disappear 
when  hydrocephalus  is  apparent,  because  pressure  is  relieved.  It  is  least 
constant  and  severe  in  infants  for  the  skull  bones  can  separate  readily  ; 
and  is  difficult  to  diagnose  in  them,  perhaps  only  giving  rise  to  screaming 
attacks.  A  sense  of  fulness,  pressure  or  constriction  in  the  head  may  also 
be  present.  Tenderness  of  the  scalp  may  be  noted  in  cortical  tumours,  over 
a  limited  area  and  elicited  by  percussion.  Convulsions  are  the  next  most 
frequent  sign  in  children,  still  more  so  in  infants.  They  may  occur  singly 
at  long  intervals  or  as  often  as  20-30  times  a  day.  In  cortical  tumours  they 
may  be  of  the  type  of  Jacksonian  epilepsy.     Often  they  are  general  and 


Vascular    Affections — Tumours — Abscess.  691 

may  pass  through  the  stages  of  an  epileptic  fit,  ending  in  coma.  Occasion- 
ally they  leave  behind  a  general  fine  tremor  for  hours  or  days.  Optic 
Neuritis  and  Atrophy  are  sometimes  the  first  sign,  often  present,  almost 
always  double,  and  independent  of  the  size  of  the  tumour.  It  is  the  type 
known  as  "  choked  disc."  It  appears  in  one  eye  first  and  is  rarely  of  the 
same  degree  in  both  eyes.  Limitation  to  one  eye  indicates  disease  in  the 
•optic  nerve  anterior  to  the  chiasma  ;  if  in  the  chiasma,  there  is  hemianopia 
.also.  It  occurs  in  quite  75  per  cent,  and  may  be  advanced  though  sight 
seems  little  impaired.  Gradual  loss  of  sight  in  children  attracts  little  notice 
.and  the  blindness  may  be  thought  of  sudden  onset.  As  the  neuritis  increases 
there  is  limitation  of  the  field  of  vision  for  light  or  colour  and  finally  amauro- 
sis. It  comes  on  earlier  and  is  most  intense  in  tumours  of  the  cerebellum 
.and  basal  ganglia,  for  intracranial  pressure  is  most  likely  to  be  raised. 
True  neuritis  is  due  to  distension  of  the  nerve  sheath,  extension  of  irritation 
.and  inflammation  along  the  nerve,  or  meningitis.  Vomiting  is  more 
frequent  than  in  adults  and  is  cerebral  in  type.  It  may  or  may  not  be 
.accompanied  by  nausea,  may  occur  frequently  and  independently  of  food, 
is  generally  associated  with  optic  neuritis  and  often  with  severe  paroxysms 
•of  headache,  sometimes  with  vertigo  or  on  movement.  It  may  be  so  bad 
•as  to  cause  inanition.  It  is  rare  in  glioma  of  the  pons,  most  common  in 
sub-tentorial  tumours,  and  not  infrequently  absent.  Occasionally  it 
simulates  anorexia  nervosa. 

Vertigo  is  constant  or  paroxysmal  with  dizziness  and  sinking  feeling  in 
the  stomach  and  mental  confusion.  The  child  feels  as  if  falling  or  turning 
round  (subjective),  or  as  if  the  room  and  its  contents  are  in  motion 
(objective).  It  may  come  on  while  lying  down,  on  change  in  position,  or 
with  vomiting.  It  is  most  common  in  tumours  of  the  cerebellum  or  the 
posterior  fossa  of  the  skull.  It  must  not  be  confused  with  the  slight  vertigo 
due  to  ocular  palsies.  Nystagmus  may  be  present  in  late  stages,  and  in 
hydrocephalus  and  cerebellar  tumour.  Insomnia  is  rare.  The  pulse  is 
infrequent,  slow  and  irregular  ;  frequent  and  irregular  towards  the  end. 
Bradycardia  may  be  marked  at  the  height  of  the  headache.  The  pulse 
alters  noticeably  with  change  in  position.  Acceleration  may  depend  on 
vagus  palsy.  Attacks  of  syncope  are  rare.  Cheyne-Stokes  breathing  is 
often  present  in  late  stages.  Fever  results  from  secondary  meningitis. 
The  psychical  and  mental  changes  aie  first  irritability,  depression,  disinclina- 
tion for  amusement  and  games,  and  a  desire  for  quiet ;  sometimes  out- 
breaks of  irritability,  screaming  and  apparent  terror  ;  or  persistent  somno- 
lence and  gradual  cessation  of  speech.  In  older  children  there  is  dulness, 
stupidity,  lack  of  interest  and  intelligence,  and  forgetfulness.  Finally  the 
child  passes  into  coma,  imbecility  or  dementia.  In  a  few  instances  melan- 
cholia, hallucinations  and  maniacal  attacks  have  been  noted. 

Localising  signs  may  be  few  or  absent,  slight  at  first  and  increasing 
with  the  size  of  the  tumour.  A  sudden  increase  is  due  to  haemorrhage  into 
.the  growth  or  surrounding  tissues.    Some  of  the  symptoms  depend  on  local 


692  Chapter   LI  I. 

destruction  or  irritation,  others  on  interference  with  function  by  direct 
pressure,  or  on  circulatory  effects  from  pressure  by  disease  in  some  other 
part  of  the  brain.  They  are  the  same  as  in  adults  and  include  ataxia,, 
imperfect  gait,  disorders  of  equilibrium,  spasms,  tremor,  paralysis,  altered 
reflexes,  sensory  disturbances,  irregular  flushing,  polyuria,  glycosuria, 
interference  with  swallowing,  articulation  and  respiration,  hallucinations  of 
sight  and  hearing,  affections  of  the  special  senses,  hemianopia,  disturbance 
of  speech,  and  mental  action  and  psychical  changes. 

The  details  of  localisation  must  be  studied  in  works  on  the  nervous, 
system.  Cortical  tumours  may  give  rise  to  local  headache,  tenderness,  and 
localised  fits.  One  in  the  frontal  lobe  may  cause  dulness,  apathy  and 
inattention,  fainting  attacks,  petit  mal,  drowsiness,  enuresis  and  coma. 
If  it  extends  backward  it  produces  symptoms  referable  to  pressure  on  the 
motor  area,  and  convulsions  on  the  opposite  side  of  the  body.  Pressure  on 
the  olfactory  lobe  affects  smell.  Occasionally  the  growth  may  reach  a  large 
size  and  cause  little  mental  deterioration.  Motor  aphasia  and  agraphia  are 
due  to  backward  pressure  on  the  left  side.  A  tumour  in  the  ascending  frontal 
lobe,  or  pressing  on  this  lobe,  causes  motor  symptoms  and  spasms.  Atten- 
tion must  be  directed  to  the  point  of  origin  of  the  subjective  sensation  and 
spasm,  the  order  in  which  the  spasm  spreads,  and  the  point  of  greatest 
subsequent  paresis.  Monoplegia  is  apt  to  result  from  a  cortical,  and 
hemiplegia  fiom  a  sub-cortical  growth.  Sensory  aurse,  ushering  in  fits,  arc 
most  common  in  tumours  of  the  ascending  parietal  convolution.  A  growth 
in  the  angular  gyrus  may  cause  word-blindness  and  even  temporary  blind- 
ness of  the  opposite  eye.  Conjugate  deviation  of  the  eyes  to  the  left  is  said 
by  Wernicke  to  be  due  to  a  lesion  in  the  left  inferior  parietal  lobule.  Fits. 
of  all  kinds  occur  in  tumours  of  the  supra-marginal  and  angular  gyrus, 
sometimes  hemianopia  on  the  opposite  side,  and  impaired  smell  on  the  same, 
side.    Speech  is  unaffected  in  tumours  on  the  right  side. 

Tumour  in  the  occipital  lobe  causes  bilateral  homonymous  hemianopia 
on  the  opposite  side  and  sometimes  partial  loss  of  colour  vision.  If  on  the. 
left  side  there  may  be  word-blindness  and  psychical  blindness,  inability 
to  recognise  familiar  faces  and  objects.  Visual  hallucinations  may  depend 
on  cortical  irritation  of  these  lobes.  Word-deafness  is  due  to  a  tumour  in 
the  temporo- sphenoidal  lobe.  If  in  the  basal  ganglia,  the  signs  are  chiefly 
those  of  pressure  on  the  internal  capsule  and  on  the  cranial  nerves  outside- 
the  brain.  A  small  abscess  in  the  right  corpus  striatum  of  a  13-year  old 
girl,  due  to  infective  endocarditis,  caused  rigidity  of  the  limbs,  chiefly  on 
the  left  side,  and  left  facial  palsy.  Pontine  and  bulbar  tumours  affect  the. 
motor  and  sensory  tracts  on  the  opposite  side,  and  the  fifth  to  the  seventh 
cranial  nerves  on  the  same  side.  If  in  the  upper  part  of  the  pons,  the  third 
and  fifth  nerves  are  affected  ;  if  in  the  lower  part,  the  sixth,  seventh  and 
eighth ;  if  in  the  medulla,  the  ninth  to  the  twelfth  nerves  and  the  vasomotor 
centre  are  likelv  to  be  involved. 


Vascular   Affections — Tumours — Abscess.  693 

Cerebellar  Tumours  are  outside  and  press  on  the  cerebellum,  in  one 
lateral  lobe,  or  in  the  vermiform  process.  Headache  is  severe,  optic  neuritis 
common,  and  vomiting  nearly  always  present.  Tumour  is  most  frequent 
in  the  lateral  lobe  and  can  be  successfully  removed.  If  small,  and  not 
involving  the  median  lobe,  it  may  be  latent  or  only  cause  general  symptoms. 
If  the  middle  lobe  is  involved,  vertigo  and  ataxia  are  present.  The  vertigo 
is  severe,  fairly  constant,  and  always  in  the  same  direction.  It  is  exag- 
gerated when  the  headache  is  severe  and  less  marked  between  the  paroxysms. 
It  is  usually  subjective,  the  patient  turning  in  the  same  direction  if  the 
tumour  is  intra-cerebellar,  and  in  the  opposite  direction  if  it  is  extra- 
■cerebellar.  If  objective,  the  objects  move  in  a  direction  away  from  the 
tumour.  There  is  often  nausea,  faintness  and  general  bewilderment.  The 
gait  is  staggering,  as  if  intoxicated  or  on  ship-board,  the  steps  short  and 
irregular,  and  the  body  swaying  from  side  to  side.  In  severe  cases  the 
patient  cannot  stand  or  even  sit  up  in  bed.  If  the  tumour  invades  a  cerebral 
peduncle,  there  is  generally  a  tendency  to  fall  toward  the  tumour.  The 
ataxia  is  most  in  the  leg  on  the  side  of  the  tumour,  is  always  present  in 
tumour  of  the  middle  lobe,  and  less  with  the  eyes  shut.  In  tumour  of  the 
vermes  the  tendency  is  to  fall  backward  or  forward.  It  is  independent  of 
vertigo,  paralysis  and  loss  of  muscular  sense.  The  seventh  and  eighth 
nerves  are  most  often  affected  by  extra-cerebellar  tumours  and  tinnitus 
is  present ;  in  intra-cerebellar  ones  the  fifth  to  the  eighth  may  be  involved. 
The  knee  jerks  are  variable,  and  the  epigastric  and  plantar  reflexes  unaltered. 
In  tumour  of  the  vermes  there  may  be  fits  in  which  there  is  retraction  of  the 
head  and  arching  of  the  back.  Occasional  symptoms  in  late  stages  are 
tremor,  paresis  of  the  limbs  and  trunk  muscles,  ankleclonus,  head-rolling, 
retraction  of  head,  spastic  rigidity,  blindness,  deafness,  mental  disturbance, 
•convulsions  and  unconsciousness.  Hydrocephalus  is  common.  Cerebellar 
fits  may  be  due  to  pressure  on  the  pons  and  cerebellum,  or  irritation  of  the 
labyrinth.  There  is  increased  tinnitus,  vertigo,  blackness  before  the  eyes, 
occasionally  sudden  blindness  or  unconsciousness,  a  tendency  to  fall,  and 
extensor  tonic  spasm. 

Diagnosis.- — This  depends  on  the  general  symptoms  primarily  and 
localising  ones  secondarily.  Many  of  the  later  ones  are  due  to  circulatory 
disturbances  and  hydrocephalus.  James  Taylor  bases  a  table,  useful  for 
localisation,  on  the  presence  of  hemiplegia : — 

(1)  Pure  hemiplegia — the  tumour  above  the  tentorium. 

(2)  With  palsy  of  the  opposite  third  nerve — in  the  cms  cerebri. 

(3)  With  hemiataxy  and  nuclear  ocular  palsy — in  the  mesencephalon 

(4)  With  hemiataxy  on  either  side  and  palsy  of  the  fifth,  seventh  and 

eighth  nerves  on  the  same  side — in  the  pons  Varolii. 

(5)  Without  facial  palsy,  with  hemiataxy  on  the  opposite  side,  and 

with  alternate  palsy  of  ninth  to  twelfth  nerves — in  the  medulla. 


694  Chapter  LI  I. 

Hemiataxy  without  hemiplegia  indicates  a  sub-tentorial  tumour. 
The  diagnosis  from  abscess  is  considered  under  abscess.  Meningitis  may- 
simulate  and  is  more  common  than  either,  and  is  more  often  associated  with 
abscess.  Hydrocephalus  may  give  rise  to  symptoms  of  tumour  or  may  be 
secondary  to  it.  Occasionally  cerebral  sclerosis  may  be  suspected.  Intra- 
cranial haemorrhage  produces  well  marked  symptoms  but  they  are  not 
progressive. 

Prognosis. — Tuberculous  tumours  may  cease  growing  and  undergo' 
caseation.  A  similar  result  may  ensue  in  gummata  and  possibly  in  gliomata. 
Shrivelled  and  atrophied  tumours  have  been  found  after  death.  Recovery 
may  leave  behind  permanent  blindness.  For  this  reason  it  is  advisable  to 
trephine  if  there  is  optic  neuritis,  for  it  may  prevent  blindness.  Remark- 
able intermissions  occur  and  all  the  symptoms,  except  blindness,  disappear 
for  a  long  time.  Usually  the  course  is  progressive.  The  symptoms  increase 
in  intensity  and  others  develop  from  extension  of  the  growth,  pressure  and 
circulatory  disturbance.  Convulsions  may  be  present  throughout,  especially 
in  abscess,  or  only  appear  toward  the  end  and  as  a  terminal  event.  Death 
takes  place  from  meningitis,  suddenly  from  intense  headache  or  bulbar 
palsy,  haemorrhage,  or  progressive  coma  and  asthenia.  Acute  exacerbations- 
are  due  to  haemorrhage,  into  the  tumour  or  adjacent  tissues,  or  surrounding 
softening.     The  average  duration  is  less  than  two  years. 

Cerebral  Abscess. — An  acute  abscess  is  generally  traumatic  and 
situated  between  the  bone  and  dura  mater  (extra-dural),  or  between  the 
dura  mater  and  pia-arachnoid  (sub-dural)  and  shut  off.  Multiple  small 
pyaemic  abscesses  are  a  type  of  suppurative  encephalitis.  The  common 
intracranial  abscess  is  chronic,  encephalic,  and  due  to  ear  disease.  Some- 
times it  is  secondary  to  disease  of  the  nose,  orbit  or  cranial  bones,  and 
occasionally  no  cause  is  found.  It  may  be  secondary  to  infective  endo- 
carditis, empyema,  bronchiectasis,  pulmonary  gangrene,  thiush,  tuberculosis- 
and  infective  fevers,  being  generally  multiple  and  pyaemic  in  these  cases. 

Pathology. — The  inflammation  starts  in  the  white  matter  and  ends- 
in  local  suppuration.  Pyaemic  abscesses  are  multiple.  The  single  abscess- 
varies  in  size  from  a  pea  to  that  of  a  whole  hemisphere.  There  is  generally 
a  definite  limiting  membrane,  and  the  adjacent  tissue  is  cedematous,  softened 
or  inflamed.  Occasionally  it  becomes  encapsuled,  caseates,  and  remains- 
latent  until  fresh  inflammatory  action  leads  to  rapid  increase  in  size,  rupture 
into  the  ventricle  or  on  to  the  surface,  and  suppurative  meningitis.  The 
contents  vary  from  thick  and  greenish,  perhaps  inspissated  and  very  offen- 
sive pus  in  chronic  cases  to  thin,  watery,  brownish  sero-pus  in  acute 
abscess,  sometimes  gas  and  pus.  The  capsule  consists  of  thick  fibrous 
tissue  or  necrotic  brain  substance. 

Symptoms  and  Course. — It  may  be  so  acute  as  to  defy  diagnosis  or  so 
chronic  as  to  simulate  tumour.  In  its  initial  stage  there  may  be  no 
symptoms  or  a  more  or  less  acute  period  of  1-7  days  illness  with  headache, 


Vascular   Affections — Tumours — Abscess.  695 

vomiting,  prostration,  variable  fever  and  chilliness.  This  may  be  followed 
by  drowsiness,  vacancy,  constipation,  polyuria,  glycosuria,  coma,  and 
death  from  respiratory  failure  or  from  meningitis.  Or  it  may  pass  into  a 
stage  of  complete  latency  ;  or  incomplete  latency  in  which  the  symptoms 
are  variable  headache,  malaise,  slight  fever,  chills,  drowsiness,  and  perhaps 
convulsions,  optic  neuritis,  irritability  and  mental  changes.  Occasionally 
the  signs  are  acute  and  temporary,  due  to  a  local  meningitis.  The  period  of 
latency  is  rarely  more  than  a  few  months  but  may  last  for  years.  As  a 
sequence  of  this  or  of  the  initial  stage  an  acute  illness  ensues,  possibly  due 
to  suppurative  cerebritis  or  meningitis.  It  is  characterised  by  headache 
which  may  be  localised,  increased  by  cough  and  stooping  ;  vomiting, 
especially  in  cerebellar  abscess  and  on  standing  up  ;  convulsions,  loss  of 
memory,  stupor,  delirium,  and  a  normal  or  subnormal  temperature. 
Bradycardia,  arrhythmia,  intermittence,  tachycardia,  slow  breathing  and 
occasionally  Cheyne-Stokes  respiration  may  be  noted.  In  addition  there 
may  be  the  usual  symptoms  of  a  cerebral  tumour  and  localising  signs. 
Sometimes  the  symptoms  are  limited  to  persistent  severe  headache,  dulness 
of  intellect,  subnormal  temperature  and  infrequent  pulse.  Other  cases 
may  exhibit  high  fever,  delirium,  rigors,  convulsions,  etc.,  and  end  fatally 
in  7-10  days. 

The  abscess  of  ear  disease  is  twice  as  common  in  the  cerebrum  as  in 
the  cerebellum,  and  more  frequent  under  10  years  of  age  than  in  adults, 
in  males,  and  on  the  right  side.  It  is  single  in  90  per  cent.,  usually  in  the 
temporo-sphenoidal  lobe,  occasionally  in  the  lateral  lobe  of  the  cerebellum, 
and  most  liable  to  occur  when  the  dura  mater  is  implicated.  The  dura  and 
brain  between  the  diseased  bone  and  the  abscess  are   generally  affected. 

Extension  of  the  mischief  causes  thrombosis  of  the  lateral  sinus,  purulent 
meningitis  by  direct  spread  from  the  bone  disease  or  rupture  of  the 
abscess,  or  rupture  into  the  lateral  ventricle,  fourth  ventricle  or  ear. 
An  acute  abscess  is  generally  associated  with  sinus  phlebitis  and  a  chronic 
one  with  labyrinthine  disease.  A  boy,  3  years  old,  had  multiple  fits  for 
2  months,  somewhat  staggering  gait  and  tremor  of  the  hands.  After  a  few 
weeks'  interval  the  fits  recurred.  The  ataxia  was  chiefly  on  the  left  side. 
The  left  ear  discharged  pus  at  the  end  of  6  months.  He  became  drowsy, 
aphasic  and  comatose,  and  died  suddenly  in  a  fit  12  months  after  the  onset 
and  3  months  after  exploration  of  the  brain.  An  abscess  was  found  in  the 
temporo-sphenoidal  lobe  after  death.     Fever  was  almost  absent  throughout. 

Diagnosis.— In  disease  of  the  mastoid  and  middle  ear  the  abscess  is 
most  likely  to  be  temporo-sphenoidal  ;  and  there  may  be  word-deafness 
and  motor  aphasia,  if  it  is  on  the  left  side.  Unilateral  fits  and  hemiplegia 
are  in  favour  of  a  parietal  abscess.  In  disease  of  the  labyrinth  the  abscess 
is  more  likely  to  be  cerebellar  and  associated  with  rigidity  of  the  neck, 
ataxia,  vomiting  and  severe  headache.  Disorders  of  speech,  hemiplegia 
and  hemiparesis  point  to  the  cerebrum  as  the  site  of  the  mischief.      In 


696  Chapter  LI  I. 

differentiating  abscess  from  tumour  stress  must  be  laid  on  the  sudden  onset 
of  symptoms,  which  may  subside  and  become  latent;  headache  more  often 
absent,  optic  neuritis  less  common,  meningitis  probable,  course  short,  and 
mental  changes  rapid.  In  tumour  the  symptoms  come  on  slowly,  progress 
steadily,  headache  is  more  severe  and  paroxysmal,  optic  neuritis  common, 
mental  changes  more  gradual,  the  course  prolonged,  and  haemorrhage  into 
the  tumour  is  not  infrequent.  Yet  a  chronic  abscess  may  be  latent  and  the 
signs  those  of  a  tumour  ;  and  a  tumour  may  be  rapidly  progressive,  from 
haemorrhage  into  its  substance,  or  become  obsolescent.  In  doubtful  cases 
the  diagnosis  is  based  on  a  careful  estimation  which  is  the  more  probable. 
In  some  instances  the  signs  are  limited  to  those  of  atypical  meningitis,  or  of 
pyaemia  and  marasmus  with  no  definite  brain  symptoms.  The  diagnosis  of 
chronic  abscess  from  chronic  tympanic  disease,  sinus  thrombosis  or 
meningitis  is  often  impossible.  The  two  latter  affections  may  occur  as 
complications  and  obscure  the  primary  cause. 

Prognosis.— Abscess  may  terminate  in  purulent  meningitis  from 
external  rupture,  rare  except  in  cerebellar  abscess,  rupture  into  the 
ventricle,  sudden  and  unexpected  death,  or  death  from  respiratory  failure 
during  coma.  Rupture  into  the  ventricle  causes  severe  symptoms  and 
death  from  collapse  in  a  few  hours.  In  untreated  cases  the  ordinary  signs 
of  a  growing  tumour  develop.    Optic  neuritis  is  rarely  followed  by  atrophy. 

Treatment  of  Tumour  and  Abscess. — Many  tumours  being  tuberculous 
and  multiple  it  is  advisable  to  adopt  the  treatment  appropriate  for  tuber- 
culosis. If  there  is  the  least  possibility  of  cerebral  syphilis  mercury  and  pot. 
iod.  must  be  given.  Encapsulated  tumours  and  cysts,  especially  in  the 
frontal  and  parietal  regions,  are  the  most  amenable  to  successful  operation. 
Vascular  infiltrating  tumours  are  not  removable.  If  measures,  which 
increase  intracranial  pressure,  increase  the  severity  of  the  symptoms  it  is 
probable  that  the  tumour  is  a  vascular  one.  Trephining  is  advisable  for 
choked  disc  and  optic  neuritis.  As  much  as  7  dioptres  of  swelling  have 
subsided  and  left  perfect  vision,  but  white  exudation  about  the  disc 
generally  leads  to  some  impairment  of  sight  and  atrophy.  Lumbar  puncture 
may  relieve  pressure.  It  is  negative  in  abscess,  unless  there  is  meningitis. 
Both  tumours  and  abscess  are  difficult  to  locate,  to  find  at  operation,  and 
to  remove.  It  is  justifiable  to  explore  the  temporo-sphenoidal  lobe,  if  there 
is  evidence  of  intracranial  abscess  and  the  child  is  getting  worse.  Symp- 
tomatic treatment  is  directed  to  reducing  intracranial  pressure  and  cerebral 
congestion  by  rest,  quiet,  leeches  behind  the  ears,  mustard  foot  baths, 
calomel  and  saline  purgatives,  and  vaso-dilators.  Phenacetin  and  caffeine, 
bromide,  chloral,  morphia  and  other  hypnotics  may  be  needed  for  the 
relief  of  headache.  Nasal  feeding  is  often  necessary.  It  was  continued  for 
4  months  in  the  case  of  a  6-year  old  boy  with  tuberculous  tumour  of  the 
left  lobe  of  the  cerebellum  and  secondary  hydrocephalus. 


CHAPTER    LIIL 

POLIOENCEPHALITIS    AND    POLIOMYELITIS. 

Polioencephalitis. —  Syn.  :  Acute  Encephalitis — Cerebral  Infantile 
Paralysis. — This  disease  was  first  recognised  by  Striimpell  in  1884.  Since 
then  evidence  has  accumulated  in  favour  of  the  view  that  there  is  a  specific 
disease  of  the  nervous  tissues,  liable  to  occur  in  epidemic  01  family  out- 
breaks, and  apparently  the  result  of  the  action  of  some  toxin  rather  than  of  a 
specific  micro-organism.  No  such  organism  has  been  found  in  the  cerebro- 
spinal fluid  or  the  nervous  tissues.  This  suggests  that  the  poison  is  not 
produced  in  loco  but  is  carried  to  the  brain  and  cord  by  the  blood. 

Acute  encephalitis  is  due  to  many  causes.  It  is  apt  to  occur  in  specific 
fevers,  notably  measles,  cerebrospinal  and  purulent  meningitis,  and  as  a 
•complication  or  sequel  of  diphtheria,  influenza,  pneumonia,  pertussis, 
vaccination  and  affections  of  the  tonsils,  and  may  follow  bruising  of  the 
brain  by  traumatism.  Septic  infections  in  the  newborn  sometimes  produce 
it,  in  the  form  of  attacks  difficult  to  distinguish  from  toxaemia.  Predisposing 
causes  are  malformation  of  the  brain,  injury  at  birth,  prematurity,  cerebral 
syphilis  and  malnutrition.  A  localised  distribution  is  the  result  of  embolism 
in  infective  endocarditis,  and  thrombosis  or  haemorrhage,  as  in  pertussis 
and  diphtheria  ;  possibly  these  causes  only  acting  as  predisposing  ones  and 
the  actual  disease  being  due  to  secondary  toxaemia  or  infection.  One-third 
of  the  hemiplegic  cases  follow  acute  specific  fevers.  An  acute  purulent 
•encephalitis  may  be  associated  with  purulent  meningitis  and  due  to  infection. 

The  type  under  consideration  is  much  more  common.  It  is  a  primary 
specific  disease  of  the  grey  matter  of  the  central  nervous  system,  which  is 
divisible  according  to  its  distribution  into  the  following  groups.  Many  of 
the  cases  overlap  and  present  symptoms  of  more  than  one  group.  All 
parts  may  be  simultaneously  affected. 

I.  Polioencephalitis  superior,  localised  or  general  : — 

(1)  Pre-frontal,  causing  profound  mental  changes. 

(2)  Mid-cerebral,     affecting    the    motor    areas    and    producing 

hemiplegia  or  diplegia. 

(3)  Occipital,  perhaps  causing  blindness. 

(4)  Temporo-sphenoidal,  possibly  setting  up  deaf-mutism. 

(5)  Cerebellar,  causing  ataxia  and  disturbance  of  equilibrium. 


698  Chapter  LI  1 1. 

II.  Polioencephalitis  inferior  ;  located  in  the  pons  or  bulb  and  affecting; 

the  nuclei  below  the  level  of  the  corpora  quadrigemina,  pro- 
ducing palsy  of  one  or  more  of  the  cranial  nerves.  In  rare  instances 
there  is  a  polyneuritis  of  the  cranial  nerves  and  not  an  affection 
of  the  nuclei. 

(1)  Strabismus  and  varieties  of  ophthalmoplegia. 

(2)  Acute  bulbar  palsy,  affecting  one  or  more  of  the  nerve  nuclei. 

III.  Diffuse  disseminated  encephalo-myelitis,  in  which  multiple  inflam- 
matory foci  are  distributed  throughout  the  central  nervous 
system.  It  simulates  disseminated  sclerosis  but  may  end  in 
recovery. 

IV.  Poliomyelitis  or  acute  infantile  paralysis. 

V.  A  neuritic  type  in  which  the  main  stress  falls  on  the  peripheral 
nerves.  It  begins  with  pains  in  the  limbs  or  joints  and  is  followed 
by  paralysis,  with  ultimately  more  or  less  complete  recovery- 
It  may  be  limited  to  cranial  nerves. 

Pathology. — The  chief  anatomical  feature  is  the  occurrence  of  minute 
haemorrhages  in  the  parts  affected.  The  neuritic  cases  are  explained  as  the 
result  of  irritation  of  the  nerves  or  the  nerve  roots  by  extension  from  the 
pia-arachnoid  of  the  brain  or  cord,  which  is  believed  to  be  always  primarily 
affected.  The  post  mortem  signs  are  in  favour  of  a  toxic  degeneration  and 
opposed  to  inflammation,  except  in  the  cases  which  are  distinguishable  by 
the  definite  presence  of  purulent  or  cerebrospinal  meningitis.  Cantani 
produced  it  in  rabbits  by  injecting  the  toxins  of  dead  influenza  bacilli. 
In  many  cerebral  cases  it  might  be  spoken  of  as  a  general  non-septic  cere- 
britis,  especially  of  the  cortex  in  the  motor  area.  The  grey  matter  is 
reddish  in  colour  ;  the  pia  may  be  injected  and  adherent ;  and  on  section 
the  brain  shows  red  or  yellowish  points  surrounded  by  zones  of  oedema  and 
softening.  In  later  stages  there  is  found  degeneration  of  the  nerve  cells 
of  the  cortex  and  their  nerve  fibres,  and  descending  degeneration  of  the 
motor  tracts  ;  sometimes  sclerosis  and  hydrocephalus.  Similar  changes  are 
present  in  the  cerebellum,  if  affected.  The  anatomical  appearances  vary 
with  the  duration  of  the  illness.  Both  hyperemia  and  softening  are  present ; 
and  the  brain  may  be  soft,  fluid,  creamy,  and  contain  many  hsemorrhagic 
foci.  A  baby  developed  apparently  sudden  blindness.  The  pupils  were 
small,  equal  and  reacted  slowly  to  light ;  the  optic  discs  were  swollen 
temporarily.  After  death,  which  took  place  suddenly,  the  brain  showed 
nothing  except  extreme  softness.  Other  signs  of  infection  or  toxaemia.. 
occasionally  present,  are  myocardial  degeneration,  splenic  enlargement,., 
acute  nephritis,  and  haemorrhages  into  the  intestines,  mesentery  ancL 
serous  membranes. 


Polioencephalitis  and  Poliomyelitis.  699 

Although  the  disease  may  occur  at  any  age  in  the  brain,  quite  two- 
thirds  of  the  cases  are  under  3  years  and  it  is  rare  after  7  years. 

Symptoms. — The  onset  is  usually  sudden  with  headache,  vomiting, 
pain  in  the  back  and  limbs,  and  fever.  The  infant  passes  quickly  into 
stupor,  unconsciousness  or  coma  ;  or  may  develop  more  or  less  paralysis 
without  loss  of  consciousness.  Cases  differ  much  in  their  severity  and  may 
be  characterised  by  convulsions,  high  fever  and  vomiting  ;  fever  and 
drowsiness,  but  no  fits  ;  apyrexia  and  screaming  attacks  ;  aphasia  or 
almost  sudden  unconsciousness.  Coma  is  rarely  complete,  the  mental  state 
being  more  one  of  hebetude  or  stupor.  Convulsions  are  unilateral  or  general ; 
single,  multiple  or  continuous,  and  even  fatal.  In  infants  they  are  almost 
invariably  present  at  the  onset,  and  are  unrelieved  by  ordinary  measures. 
In  mild  cases  the  temperature  is  101-102°  F.  and  in  severe  ones  104-106°  F. 
The  pulse  is  feeble  and  frequent.  The  breathing  is  shallow  and  often  of 
Cheyne-Stokes  type  ;  and  attacks  of  asphyxia  may  occur.  Irritability, 
restlessness  and  general  hyperesthesia  are  not  rare.  Squint,  tense  fontanelle, 
slight  rigidity  of  the  neck  muscles,  retraction  of  the  head,  and  flexor 
rigidity  of  the  limbs  are  more  frequent.  At  the  onset  the  reflexes  are  often 
absent  if  the  cord  is  involved,  and  obtainable  in  cerebral  cases.  Sphincter 
control  is  usually  lost. 

The  other  symptoms  depend  on  the  extent  and  localisation  of  the 
mischief.  New  inflammatory  areas  may  give  rise  to  fresh  convulsions. 
Unilateral  ones  (Jacksonian  epilepsy)  occur  when  the  motor  area  on  one 
side  is  attacked  ;  and  paralysis  develops  immediately  and  severely,  or 
successively  in  the  face,  arm  and  leg.  The  loss  of  power  is  partial  or 
complete  ;  and  the  palsy  is  flaccid  at  first  and  spastic  subsequently.  It 
may  be  bilateral,  if  both  motor  regions  are  involved.  There  is  no  reaction  of 
degeneration  and  no  sensory  disturbance.  If  the  motor  region  escapes,  the 
signs  may  be  limited  to  affections  of  sight,  hearing  or  speech.  Occasionally 
there  is  optic  neuritis  and  atrophy,  aphasia  or  complete  deafness.  One  child 
showed  continuous  tremor  of  the  hands  and  forearms,  without  paralysis. 
Athetoid  movements  may  be  present. 

The  disease  may  chiefly  affect  the  cranial  nerve  nuclei.  A  4-year  old 
boy  was  taken  ill  with  fever,  shivering  and  nausea.  On  the  third  day  he 
vomited  and  had  a  fit  or  was  delirious.  Next  day  he  became  unconscious 
and  lost  sphincter  control.  He  presented  some  rigidity  of  the  neck  muscles, 
trismus,  conjugate  deviation  of  the  eyes  to  the  left,  and  a  temperature  of 
102-4°  F.  In  the  next  4  days  he  had  19  fits.  The  fever  subsided  in  24  hours. 
Consciousness  returned  on  the  eighth  day  of  the  illness.  The  conjugate 
deviation  of  the  eyes  persisted  for  2  weeks  ;  and  he  ultimately  recovered 
with  no  ill  effects  except  paresis  of  the  muscles  supplied  by  the  right  sixth 
and  left  seventh  nerves.  In  bulbar  cases  the  muscles  of  respiration  and 
deglutition  may  be  involved,  and  death  ensues  from  bulbar  palsy. 


700  Chapter  LI  1 1. 

Complications  and  Sequels. — Some  of  these  occur  during  the  course  of 
the  disease  and  may  be  strictly  regarded  as  symptoms.  Chief  among  them 
are  the  motor  defects,  viz.  hemiplegia,  monoplegia,  diplegia  and  crossed 
paralysis ;  clumsiness,  fine  or  coarse  tremor,  choreiform  movements, 
hemichorea,  athetosis  and  ataxia,  all  of  which  are  involuntary  in  some 
patients  and  in  others  only  occur  on  voluntary  movements  ;  slow,  stiff 
voluntary  movements  up  to  more  or  less  rigidity  ;  contractures  and  defor- 
mities ;  and  various  palsies  of  cranial  nerves,  chiefly  the  oculo-motor  ones. 
The  psychical  disturbances  are  delirium,  hallucinations,  delusions,  and 
screaming  or  apathy  during  the  attacks  ;  and  subsequently  weakness  of 
memory  and  intellect,  feeble-mindedness,  or  imbecility.  Deaf-mutism, 
blindness,  epilepsy  and  hysterical  convulsions  are  occasional  sequels. 
Epilepsy  is  general  or  Jacksonian.  The  child  is  not  free  from  the  liability 
to  it  until  some  years  after  puberty.  The  Jacksonian  type  usually  appears 
in  1-10  years  and  is  not  severe.  It  is  most  likely  to  develop  in  children,  over 
2  years  of  age  at  the  onset,  for  in  them  the  mischief  may  be  a  focal  hemor- 
rhagic encephalitis  in  the  motor  region,  with  red  softening,  yellow  softening 
and  sclerosis.  Probably  fits  develop  subsequently  in  about  half  these 
patients.  Focal  encephalitis  at  this  age  and  later  is  milder  in  type  than  the 
acute  encephalitis  of  infancy.  It  is  more  circumscribed,  and  more  likely  to 
end  in  recovery.  The  localising  signs  are  unilateral  tiemor  in  one  or  both 
limbs,  monoplegia  or  hemiplegia,  facial  palsy,  aphasia,  conjugate  deviation 
of  the  eyes  to  the  affected  side,  convergent  squint  and  perhaps  optic  neuritis. 
It  is  this  focal  type  of  encephalitis  which  gives  rise  to  cerebral  spastic 
paralysis,  and  occasionally  to  spastic  diplegia.  It  may  end  in  cystic  forma- 
tion, porencephaly,  abscess  or  sclerosis. 

Diagnosis.- — Encephalitis  is  liable  to  be  mistaken  for  meningitis, 
poliomyelitis,  sinus  thrombosis,  cerebral  abscess  or  tumour,  convulsions  from 
•other  causes,  and  the  onset  of  a  specific  fever.  Serous  apoplexy  at  first  gives 
rise  to  similar  symptoms  but  the  intracranial  pressure  is  generally  much 
higher.  In  encephalitis  it  is  by  no  means  always  raised,  so  lumbar  puncture 
is  of  assistance  in  forming  a  conclusion.  Frequently  it  is  impossible  to 
determine  the  exact  nature  of  the  illness  until  the  course  of  the  disease  and 
the  appearance  of  sequels  afford  further  infoimation.  Paralysis,  when 
present,  is  spastic  in  type. 

Prognosis. — The  course  is  variable.  Impairment  of  consciousness  may 
persist  for  a  day  or  two,  or  for  1-3  weeks.  The  fever  may  be  of  short 
duration,  or  last  for  2-3  weeks,  rarely  more  than  a  week.  The  early 
symptoms  indicate  much  more  extensive  mischief  than  there  is  evidence  of 
subsequently.  After  a  variable  period  the  effects  become  more  localised 
and  it  is  possible  to  estimate  the  extent  of  the  damage.  Rarely  the  disease 
is  subacute  or  chronic,  and  the  effects  appear  slowly.  Death  may  take 
place  from  cardiac  or  respiratory  failure  in  a  day  or  two,  before  accurate 
diagnosis  is  possible  ;    or  in  2-3  weeks  from  encephalitis,  bulbar  palsy,  or 


Polioencephalitis  and  Poliomyelitis.  701 

associated  infective  disease.  Other  patients  recover  gradually  ;  sometimes 
completely  in  6-8  weeks  ;  more  often  with  various  sequels  which  may  be 
permanent.  Mental  defect  is  quite  common.  Tremor,  ataxia  and  nystagmus 
may  persist  for  many  months  and  yet  disappear  eventually. 

Treatment. — Rest,  bed,  quiet,  a  dark  room,  and  cold  to  the  head  are 
required.  Calomel  by  mouth,  warm  foot  baths,  and  leeches  to  the  mastoids 
assist  in  cerebral  depletion.  Hydrotherapeutic  measures  are  needed  to 
reduce  high  fever.  Feed  carefully  on  light  diet  and  allow  no  alcohol. 
Rely  on  chloral  and  bromides  as  nerve  sedatives  and  for  convulsions.  Give 
pot.  iod.  if  there  is  evidence  of  syphilis.  Other  measures  are  such  as  are 
suitable  for  meningitis.  Lumbar  puncture  is  advisable,  if  the  fontanelle 
is  tense  and  as  an  aid  to  diagnosis. 

Poliomyelitis. — Syn.  :  Acute  Anterior  Poliomyelitis— Spinal  Infantile 
Paralysis  — ■  Infantile  Paralysis  —  Infantile  Atrophic  Paralysis  —  Acute 
Atrophic  Paralysis —  Essential  Paralysis  of  Children.  This  disease  may  be 
defined  as  an  acute  specific  infective  fever  of  which  poliomyelitis  is  a 
frequent,  but  not  essential  feature.  It  may  occur  without  paralysis.  If 
palsy  is  present  it  is  the  result  of  the  anterior  cornua  being  involved,  and 
possibly  this  sometimes  may  be  due  to  other  causes.  It  is  apparently 
analogous  to  encephalitis  and  similar  in  causation.  The  cord  may  be 
involved  alone,  or  with  the  peripheral  nerves,  or  the  peripheral  nerves  only 
may  be  affected.  In  its  purest  form  it  is  limited  to  the  grey  matter  in  the 
anterior  cornua.  It  is  sporadic  and  epidemic.  The  onset  is  more  or  less, 
acute,  usually  with  fever  or  gastro-enteric  disturbance  ;  and  palsy  develops 
in  a  few  hours  or  days.  Some  of  the  paralysed  muscles  undeigo  considerable 
atrophy,  many  recover,  but  it  is  rare  for  all  the  affected  muscles  to  regain 
power  completely.  The  usual  result  is  a  permanent  paralysis  and  atrophy 
of  one  or  more  muscles  or  gioups  of  muscles,  and  secondary  deformities 
from  unopposed  contraction  of  their  opponents. 

The  disease  was  described  by  Underwood  of  England  in  1774.  The 
first  really  good  clinical  account  was  published  by  Heine  in  1860,  he  having 
observed  it  20  years  previously  and  suggested  that  the  lesion  was  in  the  cord. 
The  spinal  lesion  was  demonstrated  by  Cornil  in  1863,  Prevost  in  1865,  and 
later  and  more  fully  by  Charcot,  Joffroy  and  Lockhart  Clarke. 

Etiology. — It  has  been  ascribed  to  cold,  wet,  injury,  teething,  over- 
exertion and  some  general  infection.  Epidemics  and  sporadic  cases  have 
followed  various  specific  fevers  and  other  infective  diseases.  Isolated  cases 
have  been  traced  to  sitting  on  wet  grass,  cold  stones,  or  in  a  draught  when 
heated.  Over-exertion  is  possibly  a  predisposing  cause  by  giving  rise  to 
fatigue  of  the  motor  cells.  Some  cases  have  followed  falls  and  injuries. 
Perhaps  injury  to  the  back  may  set  up  neuritis,  or  myelitis  from  extension 
up  the  nerve  roots.  Dentition  is  a  coincidence  rather  than  a  cause,  except 
that  it  may  predispose  by  giving  rise  to  fever  and  disordered  digestion. 
Most  children  are  in  perfect  health  at  the  onset.     Some  are  enfeebled  by 


702  Chapter  LI  1 1. 

diarrhoea  or  wasting  disease.  Often  the  attack  is  ushered  in  by  gastro- 
intestinal symptoms  ;  or  follows  a  specific  fever  or  sore-throat.  Accepting 
the  infectious  theory  of  origin,  even  the  mildest  sore-throat  may  prove  the 
point  of  entry  of  the  micro-organism.  The  disease  is  in  no  sense  of  the 
word  hereditary,  but  a  family  disposition  is  sometimes  noted.  The 
occurrence  of  several  cases  in  the  same  family  is  more  likely  to  mean 
•common  exposure  to  infection  than  predisposition. 

The  youngest  case  on  record  is  that  of  an  infant  in  whom  all  the 
■extremities  were  involved  a  few  days  after  birth  and  extreme  talipes 
-equinus  resulted  (Kahler,  1888).  Duchenne  saw  it  in  an  infant  aged  12  days. 
The  youngest  child  under  my  notice  was  6  weeks  of  age.  It  affects  children 
of  all  ages  from  infancy  to  adolescence.  Ninety  per  cent,  of  the  cases  occur 
•during  the  first  5  years  of  life  and  most  of  these  are  infants  under  1\  years. 
On  account  of  its  frequency  during  the  period  of  dentition  it  has  been 
■called  "  teething  paralysis."  It  is  most  common  at  12-18  months.  Boys  are 
-a  little  more  susceptible  than  girls,  and  after  the  age  of  10  years  girls  are 
very  rarely  affected. 

Numerous  epidemics  are  on  record  in  America,  Germany,  Italy, 
Austria,  Queensland,  Norway  and  Sweden.  From  1903-6  1,053  cases 
occurred  in  Norway  in  local  epidemics.  A  big  epidemic  visited  the  United 
States,  particularly  New  York,  in  1908;  about  3,000  cases.  About  three- 
quarters  of  the  cases  occur  during  the  months  of  June  to  September,  that 
is,  in  the  hot  time  of  the  year  when  infection  is  rife. 

Records  of  several  cases  in  the  same  family  are  of  considerable  interest 
and  illustrative  of  the  association  of  this  disease  with  encephalitis.  The  same 
.association  is  better  illustrated  sometimes  in  the  same  patient.  Pasteur 
(1897)  recorded  an  outbreak  affecting  7  children  of  one  family  within  3  weeks. 
All  had  moderate  fever  and  headache.  Three  developed  paralytic  symp- 
toms within  a  week  ;  in  2  fever  was  followed  by  tremors  for  a  few  days, 
with  temporary  squint  in  1,  but  no  paralysis  ;  in  the  remaining  2  no 
nervous  disturbance  was  noted.  Of  the  3  paralytic  cases  1  was  infantile, 
1  cerebral  hemiplegic,  and  the  other  spastic  spina]  in  type.  Of  2  sisters 
•one  developed  typical  spinal  palsy  and  the  other  cerebral  hemiplegia 
(Sanger  and  Mobius).  Cases  have  also  been  reported  with  spastic  paralysis 
of  one  leg  and  atrophic  paralysis  of  the  other  (Marie) ;  right  hemiplegia  and 
aphasia  with  spasticity  of  the  arm  and  subsequent  atrophy  of  the  leg 
(E.  C.  Williams)  ;  right  hemiplegia  and  infantile  palsy  of  the  left  leg 
(Neurath)  ;  spina]  palsy  and  facial  paralysis  (Oppenheimer) ;  acute  polio- 
myelitis and  ocular  palsy ;  and  spastic  hemiplegia,  ocular  palsy  and 
infantile  palsy  of  the  opposite  leg  (Calabresse). 

It  may  be  urged  in  favour  of  the  infectious  hypothesis  of  origin  that  the 
disease  frequently  occurs  in  epidemics  ;  may  affect  more  than  one  child 
in  the  same  family  ;  occurs  during  or  after  an  infective  disease,  and  is  most 
prevalent  in  hot  weather.    So  far  no  specific  organism  has  been  implicated. 


Polioencephalitis  and  Poliomyelitis.  703 

Possibly  it  may  follow  on  various  forms  of  infection.  Schultze  (1898) 
obtained  the  diplococcus  intracellularis  from  the  spinal  fluid  of  a  boy, 
aged  5  years,  with  acute  infantile  palsy  and  signs  of  meningitis.  Geirsvold 
(Norway)  also  isolated  a  diplococcus  from  the  cerebrospinal  fluid  before  and 
after  death.  It  was  Gram-positive,  produced  short  chains  in  broth,  was 
pathogenic  to  mice  and  rabbits  and  frequently  caused  paralysis  in  them. 
He  also  noted  that  mild  or  abortive  cases  without  palsy  occurred  during 
or  before  epidemics.  They  were  associated  with  rigors,  sore-throat, 
sweating,  and  sometimes  signs  of  irritation  of  the  central  nervous  system. 
In  addition  to  typical  paralytic  cases  he  noted  others  of  progressive,  and 
sometimes  fatal  palsy,  following  convalescence. 

Landsteiner  and  Popper  (1909)  transmitted  the  disease  to  monkeys 
by  inoculating  the  peritoneal  cavity  with  an  emulsion  of  spinal  cord  from 
a  fatal  recent  case.  Landsteiner  and  Levaditi  further  transmitted  it  from 
one  monkey  to  another,  and  ascertained  that  the  virus  could  pass  through 
a  Berkefeld  filter.  Flexner  and  Lewis  (1909-1910)  confirmed  these  results 
and  showed  that,  although  the  organism  was  invisible  under  the  microscope, 
it  would  grow  in  cultures,  best  in  human  ascitic  fluid  bouillon.  A  monkey 
inoculated  with  such  a  4-day  old  culture  developed  paralysis  on  the 
thirteenth  day. 

Morbid  Anatomy. — The  post  mortem  appearances  vary  with  the  date 
of  examination  after  the  onset  of  the  attack.  In  a  child,  aged  5  years,  who 
died  a  few  hours  after  the  onset,  Drummond  (1885)  found  the  grey  matter 
in  the  cornua  unduly  red,  the  capillaries  distended  and  the  vessels  running 
from  the  surface  to  the  cornua  also  distended,  minute  blood  extravasations 
in  the  grey  matter,  swelling  of  the  neuroglia  cells,  and  nerve  cells  which 
were  unduly  granular.  Examination  made  within  6  weeks  of  the  onset  has 
revealed  foci  of  inflammatory  softening  in  the  anterior  cornua,  generally  in 
the  cervical  and  lumbar  enlargements.  These  focal  lesions  do  not  usually 
■extend  beyond  the  neck  of  the  cornua  and  are  generally  situated  in  the 
•antero-internal  and  antero-external  parts,  even  encroaching  on  the  white 
matter  on  the  externa]  side.  Sometimes  small  haemorrhages  and  even  actual 
cavities  are  present.  The  nerve  cells  have  disappeared  or  are  undergoing 
degeneration,  with  more  or  less  disappearance  of  their  processes.     The 

I  inflammatory  process  is  rarely  limited  to  the  foci  but  is  usually  widely 
spread,  in  slight  degree,  and  may  extend  to  the  adjacent  white  columns. 
The  posterior  cornua  are  rarely  affected.  The  blood  vessels  in  the  anterior 
horns  are  dilated,  possibly  thrombosed,  and  their  walls  are  thickened  and 
show  nuclear  proliferation. 
After  many  years  the  affected  part  of  the  cord  is  often  smaller  than 
natural ;  perhaps  the  whole  of  one  lateral  half  shows  this  diminution  in 
size.  On  section  the  affected  grey  matter  is  more  translucent  than  normal. 
The  nerve  cells  may  have  totally  gone  or  the  few  that  remain  are  mere 
rounded,  shrunken,  deformed  masses  of  protoplasm  without  nerve  processes. 


704  Chapter  LI  1 1. 

The  nerve  fibres  have  disappeared  from  the  anterior  horns  and  the  neuroglia 
has  increased.  It  consequently  stains  very  deeply  with  carmine.  The  white 
matter  and  the  nerve  roots  are  smaller,  and  degeneration  may  be  traced 
down  the  nerve  to  the  muscles.  The  blood  vessels  in  the  cornua  are 
thickened  ;  the  posterior  horns  are  smaller,  sometimes  sclerosed  ;  and 
there  may  be  non-development  or  degeneration  of  Clarke's  column. 

The  focal  patches  are  usually  unilateral,  5-25  cm.  long,  and  may  exist 
in  the  cord,  bulb  and  pons.  They  may  be  multiple,  sometimes  bilateral, 
and  are  most  frequent  in  the  lumbar  region.  A  consideration  of  these 
anatomical  changes  shows  that  in  the  first  stage  there  is  acute  congestion  of 
blood  vessels  and  proliferation  of  the  cellular  elements  of  the  advcntitia. 
There  is  no  evidence  of  ante-mortem  thrombosis  or  changes  in  the  intima. 
The  perivascular  lymph  sheaths  are  crowded  with  round  cells  and  there 
is  an  intense  proliferation  and  cell  infiltration  round  the  blood  vessels  in 
those  parts  of  the  nervous  system  most  freely  supplied  with  blood.  It  is 
a  diffuse  inflammatory  infiltration,  and  may  be  spoken  of  as  an  interstitial 
anterior  poliomyelitis  with  subsequent  degenerative  changes  in  nerve  cells. 
The'atrophy  of  these  cells  follows  more  or  less  the  distribution  of  the  small 
arteries  in  the  anterior  horns,  very  suggestive  of  primary  blood  infection. 
More  probably  it  is  an  acute  perivascular  inflammation  of  the  pia-arachnoid 
which  extends  inwards,  especially  along  the  vessels  in  the  anterior  fissure. 
Cases  have,  however,  been  described  in  which  the  inflammation  is  appar- 
ently parenchymatous  in  type,  an  acute  degeneration  of  the  nerve  cells 
which  present  granular  degeneration  although  the  interstitial  tissue  is 
unaffected.  In  old-standing  cases  there  may  be  extremely  slight  inter- 
stitial change  in  contrast  with  the  marked  alteration  in  the  nerve  cells. 

The  muscles  are  greyish-red  or  yellowish-white  in  colour.  Their 
fibres  undergo  granular  degeneration  and  atrophy,  with  loss  of  transverse 
striation,  and  more  or  less  completely  disappear.  The  nuclei  of  their  sheaths 
and  of  the  interstitial  tissue  proliferate.  Only  a  few  fibres  may  be  affected. 
They  are  small,  and  may  be  replaced  by  interstitial  adipose  or  fibrous 
tissue.  Those,  in  which  granular  degeneration  is  slight,  may  recover  more  or 
less  completely.  Some  of  the  fibres  may  hypertrophy.  The  bones  are 
smaller  and  thinner  from  non-development,  and  the  whole  limb  smaller 
than  a  normal  one  ;   the  blood  vessels  are  truly  atrophied. 

Pathology. — The  inflammatory  lesion  is  due  to  some  organism  or  toxin 
conveyed  by  the  blood  stream.  The  nerve  cells  suffer  either  from  the  direct 
action  of  the  toxin  or  some  inflammation  of  the  supporting  tissue.  The 
changes  in  the  cord  are  the  effects,  not  the  cause,  of  the  constitutional 
state.  Both  are  due  to  the  same  morbid  process.  The  changes  are  located 
in  the  regions  supplied  by  the  anterior  arteries  of  the  cord  and  often  limited 
to  those  supplied  by  the  central  system  of  spinal  arteries.  The  anterior 
spinal  artery  gives  off  median  branches  which  pass  in  at  the  anterior  median 
fissure  to  each  horn.     These  are  terminal  arteries,  and  hence  infection  is 


Polioencephalitis  and  Poliomyelitis.  705 

purely  local.  There  is  no  evidence  that  it  is  due  to  infective  emboli  or 
thrombosis.    Probably  it  is  primarily  a  vascular  disease  of  the  pia-arachnoid. 

The  theory  of  toxin  eausation  is  supported  by  the  febrile  onset,  the 
distribution  of  the  anatomical  changes  in  the  region  supplied  by  the 
anterior  arteries  of  the  cord,  the  vascular  changes,  epidemicity,  and  the 
result  of  experiments  on  animals.  The  cerebrospinal  fluid  is  clear  and  may 
contain  an  excess  of  polymorphs,  but  no  organisms  are  found  in  it.  Inj  ections 
of  toxins  and  various  organisms  into  animals  produce  myelitis  by  direct 
action  on  the  nerve  parenchyma  or  on  the  vessel  wall.  Possibly  these 
two  processes  are  combined,  or  the  toxins  may  set  up  acute  degeneration  of 
nerve  cells. 

The  increased  vascularity  and  functional  activity  of  early  life  render 
these  regions  very  liable  to  disease.  The  paralytic  symptoms  depend  on  the 
degeneration  of  the  motor  cells,  which  also  leads  to  muscular  atrophy  and 
loss  of  reflexes.  If  the  cells  recover,  their  processes  undeigo  regeneration 
and  the  muscles  recover.  The  wide  distribution  of  the  initial  paralysis  is 
due  to  the  wide  distribution  of  the  inflammatory  mischief  in  the  cord  and 
perhaps  secondary  extension  to  the  white  columns.  Subsequently  the 
mischief  becomes  localised  and  its  effects  limited. 

In  cases  of  onset  so  sudden  as  to  suggest  focal  haemorrhage  it  is 
probable  that  there  are  mild  inflammatory  changes  in  the  cord,  not 
sufficiently  severe  to  give  rise  to  premonitory  symptoms.  Possibly  a  focal 
haemorrhage  results  therefrom.  It  is  unreasonable  to  suppose  that  local 
infective  processes  cannot  take  place  in  the  cord  without  the  antecedent 
condition  of  an  acute  constitutional  state. 

Symptoms. — The  common  type  is  associated  with  fever,  vomiting  and 
malaise  for  some  hours  or  days  before  the  onset  of  paralysis.  In  other 
cases  the  onset  is  sudden,  with  no  previous  sign  of  ill-health,  pain  or 
alteration  in  sensation.  These  latter  cases  are  most  frequent  during  the 
first  2  years  of  life  and  the  paralysis  is  usually  limited  to  1  limb.  In 
epidemics  there  are  numerous  aberrant  types. 

The  disease  may  be  divided  into  the  initial  stage  ;  the  paralytic  stage, 
primary  and  permanent ;  and  the  stage  of  atrophy  and  contractures. 
Or  one  may  speak  of  an  onset  lasting  1-7  days  ;  a  period  of  quiescence  or 
fixation  of  1-4  weeks  ;  partial  recovery,  1-6  months  ;  and  a  subsequent 
chronic  condition.     The  incubation  period  is  unknown. 

The  onset  is  very  variable  and  the  affection  frequently  overlooked  in 
the  early  stages.  In  many  cases  the  child  is  taken  to  the  doctor  because 
the  affected  limb  is  always  cold  and  does  not  grow  as  well  as  the  other. 
There  may  be  no  history  obtainable  as  to  when  the  loss  of  power  first  began. 
Sometimes  the  child  goes  to  bed  apparently  well,  may  be  a  little  restless 
during  the  night,  and  awakes  with  one  or  more  limbs  paralysed.  This  was 
called  by  West  "  paralysis  in  the  morning."  Or  the  palsy  may  come  on 
quite  suddenly  like  that  of  spinal  haemorrhage.    A  few  cases  occur  during 

2  z 


706  Chapter  LI  1 1. 

the  course  of  an  acute  fever  or  during  convalescence,  the  paralysis  being  the 
first  symptom  to  attract  attention.  Others  are  preceded  by  pain  in  the 
limbs,  commonly  ascribed  to  rheumatism  or  "  growing  pains." 

The  usual  mode  of  onset  is  a  febrile  attack  of  variable  severity  with  a 
temperature  of  101-105°  F.  It  is  generally  accompanied  by  gastro-enteric 
disturbance,  as  a  cause  or  consequence  of  the  fever.  Vomiting  is  a  frequent 
early  symptom,  and  diarrhoea  not  uncommon  ;  sometimes  there  is  con- 
stipation. Anorexia  and  general  malaise  are  present.  In  bad  cases  the 
fever  is  associated  with  severe  nervous  disturbance  ;  headache,  restlessness, 
insomnia,  twitchings,  convulsions,  delirium,  or  somnolence  passing  into 
coma  and  ending  fatally.  Head  retraction,  rigidity,  and  pains  in  the  head 
and  neck,  back  and  limbs,  may  lead  to  erroneous  diagnosis  of  cerebrospinal 
meningitis.  The  severe  limb  pains  are  due  to  involvement  of  the  nerve 
roots.  Sometimes  they  are  the  chief  symptom  (neuritic  type).  Screaming 
and  crying  may  be  present,  and  occasionally  general  immobility.  On  account 
of  the  vomiting  the  attack  is  often  ascribed  to  simple  stomach  disturbance 
and  its  true  nature  is  not  realised  until  paralysis  is  evident,  especially  if  the 
constitutional  disturbance  is  severe.  Loss  of  power  is  apt  to  be  ascribed 
to  the  weakness  and  inertia  of  illness.  Occasionally  the  constitutional 
disturbance  follows  the  onset  of  paralysis.  The  fever  varies  in  severity  and 
duration.  It  usually  lasts  for  a  few  days  to  a  week,  rarely  for  3  weeks,  and 
gradually  subsides. 

The  paralysis  comes  on  and  reaches  its  maximum  in  12-24  hours,  or 
may  be  the  first  symptom  ;  occasionally  it  takes  2  or  3  weeks  to  develop 
fully.  It  may  begin  in  1  limb  and  spread  to  the  others  in  a  few  hours  or 
days  ;  but  it  is  quite  exceptional  for  extension  to  occur  as  long  as  2  weeks 
after  the  onset.  Extremely  sudden  onset  may  be  due  to  haemorrhage  and, 
if  this  is  in  the  cervical  region,  paralysis  may  be  universal.  Cases  of  this 
type  may  possibly  be  due  to  other  causes,  but  their  effects  on  the  muscles 
are  the  same.  The  lumbar,  cervical,  dorsal  and  bulbar  regions  are  affected 
in  order  of  frequency. 

All  varieties  of  paralysis  are  produced.  The  left  side  of  the  body  seems 
rather  more  liable  than  the  right,  and  the  left  leg  most  of  all.  The  leg 
muscles  are  more  often  affected  than  those  of  the  thigh.  One  or  both 
legs  are  affected  in  quite  two-thirds  of  the  cases.  In  order  of  frequency  the 
paralysis  involves  1  lower  limb,  both  lower  limbs,  all  the  limbs  with  the 
neck  and  back  muscles,  1  upper  limb,  1  arm  and  1  leg  on  the  same  side, 
3  limbs,  an  arm  and  leg  on  opposite  sides,  both  upper  limbs.  The  para- 
lysis may  be  limited  to  1  muscle,  or  a  group  of  muscles,  usually  functionally 
associated.  Thus,  a  tibialis  anticus  may  be  affected  alone,  or  in  con- 
junction with  the  peronei  and  the  extensors  of  the  toes.  The  order  of 
frequency  in  the  various  muscles  of  the  legs  is  the  peronei,  tibiales,  extensors 
oi  the  toes,  quadriceps,  ham-strings  and  muscles  of  the  calf,  while  the  ilio- 
psoas generally  escapes.  Occasionally  the  psoas,  iliacus,  gluteus  and 
thigh  muscles  are  all  involved,  but  the  sartorius  is  spared.     In  the  upper 


Polioencephalitis  and  Poliomyelitis.  707 

-extremities  the  deltoid  ;  deltoid,  supraspinatus  and  infraspinatus  ;  the 
biceps  and  supinators  ;  and  the  flexors  of  the  hand,  is  the  usual  order  of 
frequency.  The  clavicular  part  of  the  deltoid  and  serratus  magnus  muscle; 
the  middle  and  posterior  parts  of  the  deltoid  with  the  infraspinatus  and 
rhomboids;  the  deltoid  and  the  intrinsic  muscles  of  the  hand;  the  serratus 
magnus  and  pectoralis  major  ;  the  middle  portion  of  the  trapezius  with  the 
•other  scapular  muscles  ;  are  combinations  of  muscles  which  may  be 
simultaneously  affected.  The  diaphragm  and  the  muscles  of  the  abdomen, 
•chest  and  neck  are  less  often  affected. 

Unilateral  paralysis  of  abdominal  muscles  leads  to  "  ballooning." 
Paralysis  of  the  erector  spinee  is  a  serious  cause  of  lateral  curvature.  The 
muscles  supplied  by  the  cranial  nerves  and  the  muscles  of  swallowing  are 
.affected,  if  the  bulbar  and  pontine  region  is  involved. 

The  sphincters  generally  escape,  unless  the  centres  in  the  lumbar  cord 
sire  involved  or  the  attack  is  very  severe.  Incontinence  occurs  in  about 
1  per  cent,  and  retention  in  5  per  cent.,  but  is  generally  dependent  on  the 
severity  of  the  fever  or  on  stupor.    Sphincter  trouble  is  not  permanent. 

Initial  loss  of  power  is  greater  than  permanent  paralysis,  and  rarely 
passes  completely  away.  Improvement  begins  in  a  few  days  though  little 
change  is  noticeable  for  2  or  3  weeks.  This  is  the  stage  of  regression,  fixation 
■or  quiescence.  The  parts  first  affected  are  the  last  to  show  improvement. 
There  may  be  no  definite  signs  of  improvement  for  some  weeks.  Usually 
In  3  months  those  muscles,  which  will  not  be  permanently  affected,  recover 
almost  completely.  In  the  others  distinct  wasting  commences  in  2-3  weeks 
and  steadily  progresses.  In  very  fat  children  it  may  not  be  evident  to  the 
•eye,  but  the  muscles  feel  flabby  and  measurement  shows  decrease  in  size. 
Atrophy  persists  when  it  is  once  developed,  though  there  may  be  con- 
siderable recovery  due  to  hypertrophy  of  unaffected  muscle  fibres. 

The  affection  may  end  in  complete  or  partial  recovery  or  complete 
paralysis.  In  partial  recovery  some  of  the  muscle  fibres  remain  paralysed, 
•eventually  atrophy,  and  are  replaced  by  fibrous  tissue.  The  tone  of  the 
muscle  is  diminished  and  it  becomes  stretched  by  the  action  of  its  opponents. 
This  is  still  more  marked  in  complete  paralysis  for  the  muscle  fibres  are 
replaced  by  fibrous  and  fatty  tissue.  The  opponent  muscles  are  physio- 
logically shrunken  by  over-contraction,  producing  a  deformity  which  can  be 
•easily  overcome.  If  neglected  it  ends  in  pathological  shrinking  and  a  certain 
amount  of  fibrosis,  with  contractures  and  permanent  deformity.  Eventually 
fascia,  ligaments  and  even  bones  become  involved. 

Electrical  Examination. — Loss  of  faradic  irritability  may  be  evident 
as  early  as  the  fifth  day.  The  muscles  in  which  the  reaction  is  diminished, 
and  not  abolished,  recover.  When  atrophy  is  complete,  loss  of  faradic 
irritability  is  permanent.  Muscles  which  react  at  the  end  of  2  weeks  may 
recover  in  a  fairly  short  time.  Faradic  irritability  usually  returns  in  6-12 
.months,  on  recovery  of  some  of  the  muscle  fibres.    Galvanic  irritability  is 


708  Chapter  LIII. 

increased  at  first  in  the  muscles  in  which  paralysis  will  persist,  but  it  slowly 
diminishes  as  atrophy  continues  and  is  lost  in  a  year  or  two.  If  the  muscles, 
are  persistently  treated  by  electrical  methods,  the  reaction  to  galvanism 
may  persist  for  years  although  there  is  no  return  of  power.  The  reaction  of 
degeneration  is  present  in  the  atrophied  muscles.  Idio-muscular  con- 
tractility may  be  increased  in  the  muscles  which  will  be  permanently 
affected,  and  subsequently  disappears.  The  motor  nerves  degenerate  and 
lose  faradic  irritability. 

Reflexes. — The  skin  reflex  is  lost  with  the  loss  of  muscular  power  and 
returns  if  recovery  takes  place.  The  knee  jerk  is  lost  in  paraplegic  cases  and 
if  the  vastus  internus  of  the  knee  is  even  slightly  affected.  The  Tendo 
Achilles  reflex  is  lost  if  the  calf  muscles  are  paralysed.  Exaggeration  of 
reflexes  may  be  due  to  slight  degeneration  of  the  motor  tract,  from  an 
extension  of  inflammatory  processes.  It  is  most  likely  to  be  found  in  severe. 
affections  of  the  cervical  portion  of  the  cord  or  sudden  haemorrhage.  The 
lower  limbs  are  then  completely  paralysed  but  soon  recover. 

Sensory  Effects  are  due  to  the  inflammatory  processes  involving  the 
sensory  tracts  in  the  cord,  the  nerves  or  nerve  sheaths,  or  to  spinal  menin- 
gitis. In  the  last  event  marked  rigidity  of  one  or  more  limbs  is  associated 
with  pain  in  early  stages,  and  induced  by  movement.  Pain  is  not  infre- 
quently felt  in  the  nerves,  muscles,  or  limb  as  a  whole.  It  is  most  common 
in  the  back.  Sometimes  there  is  pain  in  the  joints,  the  back  and  the  neck 
and  occasionally  the  pain  in  the  neck  is  associated  with  slight  rigidity.. 
There  may  be  marked  tenderness  in  addition.  Tingling,  pins-and-needles. 
and  formication  have  been  noted  in  patients  old  enough  to  describe 
their  sensations.  Anaesthesia  has  occurred  in  severe  involvement  of  the 
lumbar  cord,  persisting  for  some  weeks  and  associated  with  incontinence 
of  urine. 

Trophic  Effects  develop  later.  The  growth  of  the  limb  is  retarded  or 
completely  arrested.  The  younger  the  child  at  the  onset  of  the  attack 
and  the  greater  the  severity,  the  more  marked  is  the  subsequent  difference 
between  the  2  limbs.  The  skin  is  thin  and  liable  to  excoriations,  ulcers 
and  chilblains.  It  is  colder  than  natural,  mottled  like  marble,  and  becomes 
red  and  blue  in  cold  weather.  Hypertrophy  of  the  hair  and  excessive  secre- 
tion of  sweat  have  been  noted.  Considerable  adipose  tissue  may  be 
deposited  in  the  wasted  muscles,  (the  local  obesity  of  Landouzy),  and  cause 
a  pseudo-hypertrophy.  The  bones  are  thinned  and  readily  fracture.  The 
joints  are  liable  to  partial  or  complete  dislocation,  from  relaxation  of  the 
ligaments  and  lack  of  support  by  the  tendons  of  paralysed  muscles.  The 
movements  of  such  a  joint  are  flaccid  and  flail-like. 

Deformities  are  many  and  varied  and  depend  on  the  unopposed  action 
of  the  unaffected  or  less  affected  muscles,  which  contract  and  become 
permanently  shortened.  Partly  they  depend  on  extraneous  causes.  The 
weight  of  the  bed  clothes  assists  in  the  production  of  talipes  equinus  ;  and 


Polioencephalitis  and  Poliomyelitis.  709 

shortening  of  a  limb  causes  lateral  curvature.  The  common  deformities 
are  those  dependent  on  the  common  distribution  of  paralysis.  The  extensors 
of  the  thigh  are  much  more  often  affected  than  the  flexors.  Talipes  equinus 
is  the  most  frequent.  T.  valgus  due  to  the  paralysis  of  the  tibialis  anticus, 
and  T.  varus  due  to  paralysis  of  the  peronei,  are  both  associated  with  a 
certain  amount  of  equinus.  T.  calcaneus,  due  to  paralysis  of  the  calf 
muscles,  is  rare.  Pes  planus  is  due  to  paralysis  of  the  peronei  and  plantar 
flexors.  In  the  upper  arm  the  type  of  paralysis  may  be  that  known  as 
Erb's  paralysis  or  the  "  upper  arm  type,"  but  usually  the  triceps  is  also 
involved.  Club-hand  is  not  uncommon.  Paralysis  of  the  serratus  magnus 
produces  the  "  winged  scapula."  Lateral  curvature  of  the  spine,  unilateral 
distension  of  the  abdomen,  and  other  deformities  also  occur. 

Diagnosis  depends  on  the  paralysis,  atrophy,  loss  of  reflex  action, 
electrical  reactions,  and  absence  of  sensory  disturbance.  The  early  febrile 
stage  may  be  ascribed  to  other  febrile  causes  or  to  disorder  of  the  stomach. 
Paralysis  may  be  mistaken  for  weakness  or  prostration,  although  pros- 
tration does  not  cause  complete  immobility.  Cases  in  which  there  are 
sensory  disturbances,  pains  in  the  course  of  the  nerves  in  the  paralysed  limbs 
or  in  the  back,  and  subjective  sensations  such  as  formication  and  tingling, 
may  be  put  down  to  rheumatism,  spinal  meningitis  or  peripheral  neuritis. 
In  generalised  peripheral  neuritis  the  pain  along  the  course  of  the  nerves 
is  very  definite,  the  attack  is  more  gradual  in  onset,  and  it  can  be  traced  to  an 
antecedent  diphtheria,  influenza,  arsenic,  etc.  ;  and  the  paralysis  clears  up. 
If  however  the  acute  symptoms  have  subsided,  the  presence  of  paralysis, 
atrophy,  and  electrical  reactions  similar  to  those  of  acute  poliomyelitis, 
Tenders  a  differential  diagnosis  impossible.  The  wide  distribution,  even  at 
the  end  of  some  weeks,  and  subsequent  recovery  are  in  favour  of  multiple 
neuritis.  Some  of  these  cases  are  instances  of  the  neuritic  type  of  the  disease. 
The  paraplegia  is  readily  distinguished  from  that  of  transverse  myelitis  in 
which  are  found  exaggerated  knee  jerks,  anaesthesia,  sphincter  troubles, 
tendency  to  bed  sores,  no  reaction  of  degeneration,  and  only  slight  wasting. 
Transverse  myelitis  is  usually  dorsal  and  due  to  spinal  caries.  Cerebral 
palsy  is  distinguished  by  rigidity,  exaggerated  reflexes  and  no  reaction  of 
•degeneration.  Paralytic  chorea  of  a  severe  type  creates  considerable  diffi- 
culty, unless  the  muscles  are  examined  electrically.  There  is  usually  a 
history  of  chorea  and  evidence  of  some  choreic  movement  on  examination, 
■and  possibly  some  cardiac  affection.  Limitation  of  palsy  to  1  shoulder  in 
«arly  life  may  be  mistaken  for  a  birth  paralysis  of  the  upper  arm  type,  but 
the  infraspinatus  escapes  and  there  is  no  inward  rotation  of  the  arm. 

The  disease  has  to  be  differentiated  from  the  pseudo-paralysis  of  scurvy 
and  congenital  syphilis,  the  extreme  paraplegic  debility  of  rickets,  and  the 
delayed  development  of  the  lower  limbs  and  of  walking  in  backward  and 
imbecile  children.  Other  affections  to  be  borne  in  mind  are  progressive 
muscular  atrophy,  spinal  muscular  atrophy  (Werdnig-Hoffmann),  Tooth's 


710  Chapter  LI  1 1. 

peroneal  type,  muscular  dystrophies,  myatonia,  spina  bifida  occulta., 
haemorrhage  into  the  spinal  cord  and  hysteria. 

Prognosis. — The  disease  is  rarely  fatal,  even  in  its  most  acute  stages,, 
though  it  may  end  in  death  if  the  bulb  is  involved.  Possibly  some  deaths- 
from  acute  fever,  before  the  paralysis  has  developed  and  made  the  diagnosis- 
evident,  are  due  to  this  disease.  If  the  respiratory  muscles  are  involved 
death  may  ensue  from  bronchitis  or  pulmonary  catarrh.  Complete  recovery 
is  possible  but  rare.  In  the  "  transient  form  of  paralysis  "  the  effects  clear- 
up  in  a  few  days.  Almost  always  some  permanent  palsy  and  atrophy 
remain.     In  epidemics  death  and  complete  recovery  are  more  common. 

Even  in  the  worst  cases  the  relatives  may  be  assured  that  considerable 
recovery  will  take  place.  The  outlook  depends  largely  upon  the  results  of 
electrical  examination,  made  when  there  is  no  progressive  palsy,  that  is 
7-14  days  after  the  onset.  Loss  of  faradic  irritability  soon  after  the  onset  or 
during  the  first  fortnight  indicates  that  the  muscles  will  waste  rapidly  and 
probably  remain  permanently  paralysed  ;  the  earlier  it  is  lost,  the  worse  is 
the  prognosis.  If  the  response  to  faradism  is  normal,  the  muscles  will- 
recover  in  4-6  weeks.  If  there  is  a  fairly  good  response  at  the  end  of  10  days- 
and  somewhat  more  diminished  response  at  the  end  of  2  or  3  weeks,  there- 
is  a  fair  chance  of  recovery.  The  return  of  faradic  irritability  is  a  sign  of 
improvement  and  that  considerable  recovery  will  take  place.  If  it  is  absent 
for  6  months  the  muscles  are  unlikely  to  recover  and  after  12  months  prac- 
tically certain  not  to,  for  it  indicates  persistent  nerve  degeneration.  If  there- 
is  response  to  faradism  at  the  end  of  2  years,  there  is  still  possibility  of 
further  improvement  by  electrical  treatment.  If  there  is  no  response  to> 
either  faradism  or  galvanism  after  2  years,  the  chance  of  improvement  is  very 
small.  The  presence  of  galvanic  irritability  shows  that  the  muscle  fibres 
have  not  undergone  destructive  degeneration,  but  if,  after  3  months,  there 
is  no  return  of  voluntary  power  in  these  muscles  and  faradic  irritability  is 
still  absent,  there  will  be  no  recovery.  As  long  as  the  reaction  of  degeneration 
is  present  there  is  hope  of  improvement  for  the  cells  in  the  anterior  cornua. 
are  not  completely  destroyed. 

Generally  speaking,  more  or  less  recovery  takes  place  for  2  years  and 
then  the  residual  paralysis  must  be  regarded  as  permanent.  Late  improve- 
ment is  merely  one  which  has  been  delayed  by  the  too  early  use  of  mechani- 
cal appliances,  or  is  due  to  volitional  adaptations  in  the  process  of  growth 
and  development.  The  apparent  exaggeration  of  the  paralytic  effects  is  due- 
to  the  arrested  growth  of  the  affected  limb.  Progressive  atrophy,  starting 
in  the  affected  limb  or  the  parts  adjoining,  is  a  rare  sequel.  It  is  quite 
exceptional  for  any  sequelae  to  occur  beyond  the  mechanical  effects,  due  to> 
the  paralysis,  and  the  trophic  effects  due  to  the  deficient  nerve  and  blood 
supply.    The  disease  does  not  diminish  the  expectation  of  life. 

Treatment. — During  the  acute  stage  the  child  is  kept  in  bed  in  the  prone 
or  lateral  position  on  light  diet,  and  the  fever  treated  on  general  principles- 


Polioencephalitis  and  Poliomyelitis.  711 

by  diaphoretics,  diuretics  and  mild  purgatives.  It  is  doubtful  whether 
hydrotherapeutic  measures  for  the  reduction  of  fever  have  any  effect  on  the 
process  in  the  cord.  Local  applications  of  poultices,  fomentations,  ice 
bags,  dry  cupping,  mustard  paste  and  Pacquelin's  cautery  may  be  tried. 
Salicylates,  aspirin,  ergot  and  belladonna  have  all  been  recommended,  and 
opium  for  severe  pain.  It  is  impossible  to  be  certain  that  the  treatment  in 
any  particular  case  has  any  definite  effect  on  the  course  of  the  disease.  The 
limbs  must  be  kept  dry  and  warm;  and  belladonna  and  glycerine  may  be 
applied  for  the  relief  of  pain. 

After  the  acute  stage  give  drugs  which  improve  the  general  nutrition. 
In  3-4  weeks  strychnia  or  nux  vomica  can  be  used.  Drugs  to  maintain  or 
improve  the  general  nutrition  are  just  as  beneficial.  As  soon  as  the  acute 
symptoms  have  subsided  or  after  the  lapse  of  2-4  weeks,  massage  and 
electrical  treatment  may  be  commenced.  It  maintains  and  improves  the 
nutrition  of  the  muscles  during  the  time  the  nerve  elements  are  recovering. 
A  weak  faradic  current  may  be  employed  for  those  muscles  which  react  to 
it.  Some  say  that  the  faradic  current  increases  the  tendency  to  atrophy. 
Lewis  Jones  advocates  the  use  of  the  sinusoidal  current  from  the  mains 
in  electric  baths.  Galvanism  is  more  readily  applicable.  Use  2  flat 
electrodes,  applying  the  kathode  to  the  affected  limb  and  the  anode  to  the 
spine.  Begin  with  a  current  just  sufficient  to  cause  contraction,  or  none  at 
all  for  a  day  or  two  if  the  child  is  frightened.  At  first  apply  it  on  alternate 
days  and  then  daily  for  10  minutes  at  a  time  for  a  few  months,  using  weak 
currents.  Continue  it  2  or  3  times  a  week,  as  long  as  there  is  any  improve- 
ment or  for  at  least  a  year.  The  galvanic  bath  is  most  suitable  for  para- 
plegic cases.  Friction  and  massage  must  be  carried  on  systematically  for 
months,  to  maintain  nutrition  and  prevent  deformity.  Begin  passive  and 
active  movements  of  the  affected  muscles  as  soon  as  the  palsy  is  quiescent. 
The  child  at  this  stage  is  kept  on  ordinary  diet.  The  affected  limbs  must 
be  warmly  clad  and  a  warm  bottle  used  if  necessary.  Hot  salt  baths  do 
no  harm.      From  the  onset  a  cradle  must  be  used  to  prevent  T.  equinus. 

The  treatment  may  be  summed  up  in  a  few  lines.  Maintain  the 
nutrition  of  the  muscles.  Keep  the  limb  in  a  normal  position,  for  stretched 
paralysed  muscles  recover  badly.  Prevent  contractures  and  stretching  of 
muscles,  tendons  and  ligaments.  Use  simple  malleable  splints  as  supports 
by  night  and  day.  Continue  electrical  treatment  for  6-12  months,  massage 
for  1-2  years,  and  then  rely  upon  growth  and  systematic  education  of  the 
muscles.  For  this  it  is  not  necessary  to  send  the  child  to  a  specialist  or  a 
foreign  professor  of  gymnastics.  The  ordinary  medical  attendant  can 
devise  suitable  exercises  and  teach  the  nurse  to  carry  them  out. 

Mechanical  treatment  helps  to  prevent  deformity  and  overcome 
deformity  already  present.  If  the  lower  limb  is  affected,  keep  it  in  the 
position  of  slight  inward  rotation  of  the  hip,  with  the  knee  extended  by 
sand  bags  ;    and  apply  a  tin  splint  to  the  foot,  keeping  the  ankle  at  right 


712  Chapter  LI  1 1. 

angles.  If  the  deltoid  is  affected,  support  the  weight  of  the  arm  and  keep 
it  at  a  right  angle  with  the  trunk,  to  prevent  subluxation  of  the  humerus. 
A  support  will  enable  the  child  to  sit  up  when,  from  weakness  of  the  spinal 
muscles,  he  can  not.  It  will  enable  the  child  to  walk  at  an  earlier  period 
and  thus  keep  in  action  the  muscles  which  would  otherwise  remain  idle.  No 
support  must  be  constantly  worn,  for  under  such  circumstances  the  muscles 
become  still  feebler  from  disuse,  instead  of  increasing  in  strength.  All 
mechanical  treatment  must  be  supplemented  by  exercises  to  develop  the 
affected  muscles  which  are  weakened  by  palsy,  disuse  and  stretching. 

Surgical  measures  after  the  lapse  of  6  months  may  be  required  to  correct 
deformity  and  enable  the  child  to  walk  better.  Many  muscles  are  supposed 
to  be  paralysed  though  merely  powerless  from  disuse.  One  group  of 
muscles  may  be  placed  at  a  mechanical  disadvantage  and  become  useless 
because  an  opposing  group  has  recovered  first  and  contracted.  Tenotomy 
often  enables  the  child  to  plant  the  foot  flat  and  firmly  on  the  ground.  Both 
simple  section  and  shortening  of  the  tendon  are  often  of  only  temporary 
benefit,  because  the  unaffected  muscles  still  act  too  strongly.  Transplanta- 
tion of  tendon  or  muscle,  or  the  splitting  of  the  tendon  of  a  healthy  muscle 
and  attaching  a  portion  of  it  to  the  tendon  of  a  paralysed  opponent  (muscle 
grafting)  are  often  of  more  benefit.  The  artificial  production  of  anchylosis 
{arthrodesis)  in  flail  joints  is  beneficial,  but  should  not  be  done  under 
10  years  of  age  or  possibly  not  until  the  patient  is  old  enough  to  decide 
whether  he  would  prefer  an  apparatus  to  a  stiff  joint.  In  the  case  of  a  flexed 
wrist  considerable  improvement  may  result  from  cutting  the  flexors  and 
placing  the  wrist  in  a  position  of  hyper-extension  for  many  months,  to  allow 
contraction  of  the  stretched  extensors,  provided  that  on  further  flexion  the 
patient  can  slightly  extend  the  fingers.  Nerve  anastomosis  may  do  good, 
if  done  4-6  months  after  the  onset. 

Unfortunately  in  many  cases  all  treatment  proves  unavailing  to 
completely  restore  the  damaged  functions  and  the  best  that  can  be  hoped 
for  is  a  more  or  less  imperfect  cure.  Severe  deformities  in  simple  cases  are 
generally  the  result  of  insufficient  care  in  directing  the  treatment  to  the 
prevention  of  their  occurrence. 


CHAPTER    LIV. 

THE    SPINAL    CORD    AND    THE    NERVES. 

Myelitis — Friedreich's  Disease — Tabes  Dorsalis — Insular  Sclerosis — 
Paralysis  Agitans — Tumours — Birth  Palsy — Pressure  Paralysis — 
Peripheral  and  Cranial  Nerves— The  Sympathetic  Nervous  System. 

Myelitis  is  an  occasional  sequel  of  measles,  typhoid  fever  and  other 
infections.  It  commonly  attacks  both  the  cervical  and  lumbar  regions  ;  and 
gives  rise  to  paraplegia,  exaggerated  reflexes,  sphincter  and  sensory  troubles, 
and  bed-sores. 

Pressure  Myelitis. — Syn.  :  Pressure  or  Spastic  Paraplegia — Spinal 
Caries — Pott's  Disease —  Angular  Curvature. — Apart  from  a  cerebral 
•origin,  the  common  cause  of  spastic  paraplegia  in  children  is  the  pressure 
secondary  to  tuberculous  caries  of  the  vertebral  column,  which  produces 
angular  curvature  of  the  spine.  The  process  starts  in  the  body  of  the 
vertebra,  attacks  several,  causes  destruction  of  those  affected,  and  ends  in 
approximation  of  the  unaffected  discs.  The  cartilages  are  little  or  not  at  all 
involved.  Inflammation  spreads  to  the  membranes,  and  produces  so  much 
granulation  tissue  and  thickening  that  the  cord  is  compressed,  and  a  mild 
form  of  myelitis  is  set  up.  (Edema  and  softening  are  followed  by  sclerosis 
and  descending  degeneration  of  the  motor  tracts  and  some  degeneration  of 
the  ascending  tracts.  The  nerve  roots  are  often  involved  and  give  rise  to 
sensory  and  motor  symptoms,  little  noticeable  if  the  caries  is  dorsal.  Marked 
angular  curvature  may  exist  without  signs  of  pressure,  but  the  cord  and 
nerves  can  be  compressed  by  the  falling  together  of  the  vertebral  bodies. 
Abscess  and  bony  sequestra  pressing  on  the  cord  are  rare.  A  posterior  abscess 
is  more  common  than  an  anterior  one,  and  both  may  co-exist.  The  etiology  is 
that  of  tuberculosis.  Sometimes  there  is  a  history  of  a  fall  or  injury.  It 
may  be  present  at  birth  or  any  subsequent  age. 

The  symptoms  vary  with  the  site  of  the  disease.  It  is  most  common  in 
the  dorsal  or  dorso-lumbar  region,  less  frequent  in  the  cervical,  and  least 
common  in  the  lumbar.  Either  pain  or  paralysis  may  be  the  first  sign.  In 
the  early  stages  of  dorsal  caries  there  are  vague  pains  in  the  back  and 
disinclination  or  inability  to  play  games.  The  child  is  easily  tired  in  the 
legs  and  disinclined  to  use  them,  sometimes  lame,  and  may  suffer  from 
-starting  pains  and  nocturnal  enuresis.    Or  there  may  be  stumbling,  due  to 


714  Chapter  LIV. 

catching  the  toes,  dragging  the  feet,  and  a  girdle  pain  which  may  be 
described  as  stomach-ache.  Gradually  the  weakness  increases  and  the  gait 
becomes  stooping,  with  the  back  held  rigid. 

On  examination  we  find  rigidity  of  the  spinal  column,  and  inability  to 
flex,  extend  and  bend  it  fully  in  various  directions  without  discomfort  or 
actual  pain  ;  and  perhaps  pain  on  applying  sharp,  sudden  pressure  to  the 
head  or  shoulders,  or  on  lateral  pressure  on  the  spine  in  the  rigid  area. 
Sometimes  there  is  local  tenderness.  The  legs  show  rigidity,  exaggerated 
reflexes,  weakness  and  paraplegia.  Ankleclonus  and  an  extensor  plantar 
reflex  are  often  present.  Spastic  paraplegia  is  progressive,  with  impairment 
or  lack  of  sphincter  control,  girdle  pains,  and  slight  or  no  sensory  distur- 
bance. Bed-sores  appear.  The  angular  curve  is  not  present  in  early  stages,, 
and  is  found  more  often  in  dorsal  than  in  cervical  or  lumbar  caries.  It 
develops  gradually,  and  varies  in  extent  and  its  effects  with  the  site  and 
extent  of  the  disease. 

Cervical  caries  is  characterised  by  a  striking  manner  of  holding  and 
moving  the  head.  It  is  moved  as  a  whole  with  the  shoulders,  and  held  as  if 
the  child  was  carrying  a  burden  on  the  top  and  was  afraid  of  dropping  it. 
There  is  much  thickening  and  infiltration  of  the  tissues  adjacent  to  the 
spine,  little  or  no  curvature,  occasionally  marked  kyphosis,  great  rigidity,, 
muscular  spasm  and  sometimes  torticollis.  There  may  be  loss  of  power  in 
the  thoracic  and  abdominal  muscles,  involvement  of  the  phrenics  and,  if 
the  disease  is  in  the  first  and  second  vertebrae,  bulbar  symptoms  and  sudden 
death.  The  upper  limbs  are  affected  as  well  as  the  lower  ones.  Occasionally 
it  is  unilateral  in  its  effects,  and  there  is  often  some  wasting  of  the  small: 
muscles  of  the  hands.  Numbness  and  weakness  are  early  signs.  The 
sphincters  frequently  escape. 

In  lumbar  caries  the  rigidity  of  the  spinal  column  is  marked,  lordosis 
pronounced,  the  muscles  waste,  the  knee  jerks  may  be  lost,  and  there  is 
greater  liability  to  bed-sores. 

Complications. — Psoas  abscess  is  due  to  direct  infection  of  the  muscle- 
by  extension  from  the  vertebra,  generally  in  the  lumbar  but  occasionally 
tracking  down  from  the  dorsal  region.  The  abscess  eventually  points  below 
Poupart's  ligament  and  external  to  the  main  vessels,  above  this  ligament,  or 
behind  in  Petit's  triangle. 

Diagnosis. — Kyphosis  is  conclusive  proof  that  spastic  paraplegia  is  due 
to  angular  curvature,  provided  that  the  kyphosis  from  general  convex 
curvature  of  the  spine  in  severe  rickets  is  excluded.  Eigidity  occurs  in 
other  diseases.  X-rays  may  be  of  assistance.  Psoas  abscess  may  be  the- 
only  symptom. 

The  prognosis  is  fairly  good  if  suitable  and  prolonged  treatment  can  be- 
carried  out.  It  depends  on  the  general  health.  About  half  the  patients- 
die.    Paralysis   is    rarely   complete    and   usually  subsides   more   or  less- 


The  Spinal  Cord  and  the  Nerves.  715 

completely  after  3-9  months  treatment.  Death  may  be  due  to  general 
tuberculosis  or  lung  disease.     Meningitis  is  comparatively  rare. 

Treatment. — If  Pott's  disease  is  properly  treated  from  the  onset, 
paraplegia  will  not  develop.  The  chief  measures  are  seaside  and  sanatorium 
treatment ;  good  hygiene,  food  and  nursing  ;  cod-liver  oil  and  syr.  fer.  iod.  ; 
and  complete,  rest  in  the  recumbent  posture  with  extension  and  counter- 
extension,  if  necessary,  and  fixation  of  the  spine  by  sand  bags, 
poroplastic  splints  and  such-like  measures.  Rigid  supports  must  be  con- 
tinued for  months  after  the  pressure  symptoms  have  subsided. 

Operation  is  indicated  in  acute  cases  which  involve  sensory  nerves,  the 
bladder  and  rectum  ;  if  prolonged  expectant  treatment  fails  ;  and  in  cervical 
caries,  if  there  is  pressure  on  the  phrenics  and  interference  with  breathing. 
It  is  contra-indicated  in  the  presence  of  tuberculous  disease  elsewhere,  if 
mechanical  treatment  has  not  been  well  tried,  and  if  there  are  insufficient 
means  for  proper  operation,  nursing  and  subsequent  treatment.  Except  in 
those  cases  in  which  granulation  tissue  or  a  caseous  mass  presses  on  the 
cord,  operation  is  unnecessary  and  recovery  will  ensue  equally  well  or 
better  under  simpler  measures.  Chipault  collected  15  recoveries  out  of  103 
cases  treated  by  laminectomy.  It  must  be  followed  by  prolonged  rest  and 
sanatorium  treatment.  If  the  bodies  of  2  or  more  vertebra  are  destroyed 
and  the  laminse  are  then  removed,  there  is  no  support  left  for  the  spinal  cord. 
The  less  sensation  is  affected  the  better  is  the  prognosis,  whether  the  case  is 
treated  by  rest  or  by  operation. 

A  psoas  abscess  is  treated  by  aspiration  if  the  wound  cannot  be  kept 
aseptic.  Otherwise  it  should  be  evacuated.  Make  a  small  incision  where 
the  abscess  points,  irrigate  with  normal  saline  until  the  fluid  returns  clear, 
and  then  sew  up  the  wound.  The  injection  of  iodoform  emulsion  is  liable 
to  set  up  toxic  symptoms. 

Friedreich's  Disease. — Syn.  :  Hereditary  Ataxia — Hereditary  Tabes. — 
There  are  three  varieties  of  hereditary  ataxia.  In  the  cerebellar  ataxia  of 
Marie  and  Sanger  Brown  the  cerebellar  symptoms  predominate  and  the 
disease  begins  in  later  life  (p.  683).  In  Friedreich's  disease  the  spinal 
symptoms  are  in  excess.  In  a  third  type  there  are  additional  muscular 
changes.  Intermediate  varieties  exist.  Freidreich's  ataxia  was  described 
by  him  in  1863  as  a  form  of  locomotor  ataxia.  It  is  a  familial  endogenous- 
affection  of  the  spinal  cord,  of  very  gradual  development,  a  slow  and 
progressive  ataxia.  In  about  one-fourth  of  over  200  recorded  cases  there 
was  some  form  of  ataxia  in  one  of  the  parents.  No  definite  etiological  factor 
has  been  found.  The  influence  of  acute  febrile  disease  in  precipitating  an 
attack  has  been  frequently  noted.  Several  children  in  a  family  may  be 
affected,  usually  at  about  the  same  age  and  of  the  same  sex.  Isolated  cases 
are  more  likely  to  occur  in  small  families.  About  one-fourth  of  the  cases 
begin  before  the  commencement  of  the  second  dentition,  a  few  in  infancy, 
and  three-fourths  before  puberty.    It  rarely  begins  after  16  years  of  age. 


716  Chapter  LIV. 

Symptoms. — The  first  signs  are  weakness  and  unsteadiness  in  the 
muscles  of  the  lower  extremities,  perhaps  a  difficulty  in  getting  upstairs 
because  of  weakness  of  the  leg  muscles.  Rarely  it  begins  in  the  arms  or  with 
bulbar  symptoms.  The  symptoms  are  motor,  sensory,  reflex,  ocular,  cerebral, 
genito-urinary,  trophic  and  vasomotor.  First  in  importance  comes  the 
disorder  of  gait.  It  is  usually  described  as  oscillatory,  reeling  (cerebellar 
reel), or  like  that  of  a  drunken  man,  with  lateral  projection  of  the  feet  instead 
of  the  forward  tendency  seen  in  tabes.  The  legs  are  wide  apart  and  the 
steps  irregular  and  awkward,  but  not  so  violent,  so  sudden  or  so  unreason- 
able as  in  tabes.  The  toes  may  be  in-turned.  The  ataxia  is  often  more 
marked  on  closing  the  eyes.  Static  ataxia  is  present  in  about  half.  Rom- 
berg's symptom  is  often  present  at  the  same  time  but  is  less  frequent  in  the 
spinal  than  the  cerebellar  type.  Inco-ordination  may  be  so  marked  as  to 
render  the  child  unable  to  walk  without  the  aid  of  crutches.  In  a  few  yeais 
ataxia  is  present  in  the  upper  limbs  on  movement  and  is  at  times  increased 
by  closing  the  eyes.  In  prehension  the  hand  is  spread  out  like  a  claw, 
from  weakness  of  the  interossei.  Similar  claw-like  movements  may  occur 
in  the  foot,  from  hyper-extension  of  the  toes.  Retraction  of  the  big  toe  is 
an  early  sign. 

Tremor,  like  that  of  insular  sclerosis  and  probably  due  to  static  ataxia, 
is  not  often  present.  Abrupt,  choreiform  movements,  rather  like  those  of 
chorea,  may  occur  in  the  limbs,  face  and  neck.  Spasmodic  contraction  of 
the  lower  limbs,  while  sitting  or  lying,  begins  early.  Later  signs  are  per- 
manent contractures  such  as  talipes  cavus,  equinus  and  equino-varus,  and 
scoliosis.  Talipes  cavus  with  full  extension  of  the  toes  is  most  typical.  The 
deformity  may  be  the  cause  of  the  child  coming  under  observation. 
Apparent  palsy  in  early  stages  is  due  to  inco-ordination.  True  loss  of 
power,  especially  in  the  flexors  of  the  leg  and  the  spinal  muscles,  is  of  later 
development.    The  reaction  of  degeneration  is  rarely  present. 

Muscular  sense  is  unaffected.  Anaesthesia  and  analgesia  seldom 
occur.  Cutaneous  sensibility  is  sometimes  diminished,  rarely  increased. 
Slight  pain  is  not  infrequent  in  the  early  stages.  Pareesthesiae  and  girdle 
sensation  are  rare. 

The  reflexes  vary  with  the  predominance  of  cerebellar  or  spinal 
symptoms,  and  may  be  different  in  the  two  legs.  In  the  spinal  type  the 
knee  jerk  is  lost  early.  In  the  cerebellar  type  it  is  diminished,  normal  or 
even  exaggerated.  Other  deep  reflexes  show  similar  changes.  Babinski's 
sign  is  present.  The  cutaneous  reflexes  diminish  as  the  disease  progresses. 
Muscular  atrophy  is  due  to  disuse  and  most  marked  in  the  lower  limbs. 
There  may  be  peroneal  or  other  types  of  atrophy. 

Disorder  of  speech  depends  on  motor  disturbance  of  the  muscles  of 
articulation  and  is  most  common  in  the  spinal  type.  Speech  is  slow, 
awkward,  jerky,  stuttering,  scanning,  or  moderately  rapid  and  inter- 
rupted by  sudden  irregular  pauses.     Pronunciation  is  indistinct.     Some- 


The  Spinal  Cord  and  the  Nerves.  717 

times  speech  is  unaffected.  Fibrillary  tremor  of  the  tongue  is  not  uncommon . 
Mastication  and  deglutition  are  rarely  affected. 

The  expression  is  vacant  and  apathetic.  The  pupils  react  normally. 
Nystagmus  is  common  in  the  spinal  and  absent  in  the  cerebellar  type. 
In  the  latter  there  may  be  squint,  ptosis,  diplopia  and  optic  atrophy. 
Vertigo  may  be  constant  or  occur  in  paroxysms.  Later  and  rarer  symptoms 
are  headache,  migraine,  enuresis,  disorders  of  the  bladder  and  rectum, 
delayed  sexual  instinct  and  menstruation,  impotence,  palpitations, 
tachycardia,  salivation,  profuse  sweating,  dyspnoea  and  gastric  symptoms. 
Some  of  these  are  of  bulbar  origin.  At  first  the  intellect  is  unimpaired  ; 
later  it  is  weak  relatively  and  there  may  be  dementia.  There  is  much 
emotional  instability  and  proneness  to  laughter.  (Edema  and  trophic  ulcers 
of  the  legs  have  been  noted  in  some  prolonged  cases  (A.  R.  Moody,  1910). 

Morbid  Anatomy. — -The  cord  is  reduced  to  two-thirds  the  normal  size 
in  the  dorsal  region.  The  posterior  root  zones  are  degenerated  and  the 
columns  of  Goll,  from  the  lower  end  to  the  tip  of  the  calamus  scriptorius, 
are  sclerosed.  Burdach's. columns  are  less  affected.  The  direct  cerebellar 
tract  is  sclerosed  throughout,  especially  in  the  upper  dorsal  region,  and 
the  column  of  Clarke  generally  involved,  its  cells  being  reduced  in  size  and 
number  and  the  nerve  fibres  more  or  less  wanting.  The  lateral  columns 
are  sclerosed  but  the  damage  does  not  correspond  accurately  with  the 
crossed  pyramidal  tract.  The  lesion  diminishes  from  below  upward  and  is 
chiefly  in  the  external  portions.  Lissauer's  zone  is  often  affected.  The  bulb 
and  pons  are  sometimes  small  and  the  bulb  may  contain  degenerated  nerve 
fibres.  The  brain  is  unaffected.  Apparently  the  disease  is  a  combination  of 
degeneration  and  sclerosis,  and  the  sclerosis  is  intermediate  in  character 
between  posterior  sclerosis  and  ataxic  paraplegia  or  insular  sclerosis. 
Sclerosis  of  the  posterior  columns,  alone  or  with  sclerosis  of  the  pyramidal 
tracts,  and  cerebellar  hypoplasia  may  be  present  as  isolated  lesions  or  more  or 
less  combined.  Possibly  the  cases  following  infective  disorders  are  toxic 
in  origin,  not  dependent  on  abiotrophy,  and  not  familial.  The  hereditary 
cases  are  perhaps  due  to  arrested  development  of  some  nerve  tracts  in 
foetal  life  and  slowly  progressive  degeneration. 

Diagnosis. — This  disease  has  to  be  differentiated  from  tabes  dorsalis  and 
ataxic  paraplegia,  both  rare  in  childhood.  The  various  types  of  cerebellar 
and  spinal  hereditary  ataxia  must  be  distinguished  from  each  other  and 
from  cases  of  post-natal  origin. 

Course. — The  earliest  symptoms  are  disorders  of  gait,  hyper-extension 
of  the  great  toe,  loss  of  knee  jerk,  and  sometimes  disturbance  of  speech. 
Ataxia  develops  in  3-5  years  and  is  progressive.  Finally  the  patient  is 
unable  to  walk,  has  difficulty  in  using  the  fingers,  is  confined  to  bed  and  may 
be  completely  crippled,  speech  becoming  unintelligible.  Remissions  and 
aggravations  occur  but  it  is  steadily  progressive.  Recovery  is  unknown. 
The  duration  is  indefinite.  Death  results  from  marasmus,  intercurrent- 
disease,  or  suddenly  from  bulbar  palsy. 


718  Chapter  LIV. 

Treatment. — Maintain  the  general  health  and  nutrition,  making  use  of 
massage,  passive  movements,  galvanism  and  exercise.  Provide  a  support 
for  the  spine. 

Hereditary  Spastic  Spinal  Paralysis. — Spiller  (1902)  reported  14  cases 
in  5  generations  of  1  family.  It  does  not  always  begin  in  childhood. 
It  is  more  common  in  males  than  females.  The  child  becomes  easily  tired, 
awkward  in  movement  and  drags  the  feet.  Later  signs  are  spasticity, 
rigidity,  pes  equinus,  and  bending  forward  of  the  trunk ;  increased 
difficulty  in  walking  without  actual  paresis  ;  persistent  spasm,  even  while  at 
rest ;  exaggerated  reflexes,  ankleclonus,  Babinski's  signs  and  hyper-extension 
of  the  big  toe  ;  and  generally  some  diminution  of  intelligence.  The  course 
is  tedious  and  after  death  there  is  found  sclerosis  of  the  lateral  tracts,  and 
-to  a  slight  extent  of  the  lateral  cerebellar  tracts  and  columns  of  Goll. 

Family  Myopathic  Sclerosis  is  a  sub-variety  with  progressive  muscular 
atrophy  and  degeneration  of  the  motor  nerve  cells  in  the  cord  and  bulb. 

Tabes  Dorsalis. —  Like  general  paralysis  this  is  the  result  of  congenital 
syphilis  and  not  a  family  disease.  In  rare  instances  it  is  due  to  syphilis 
acquired  in  the  early  months  of  life.  It  differs  from  Friedreich's  disease  in 
the  presence  of  a  pre-ataxic  stage,  and  the  absence  or  late  development 
of  inco-ordination.  It  affects  both  sexes  equally  ;  and  begins  at  8-20, 
commonly  at  10-12  years  of  age,  in  1  instance  (Marburg,  1908)  at  2  years. 
The  early  signs  are  enuresis,  lightning  pains,  amblyopia  and  gastric  crises  ; 
and  weakness,  sluggish  knee  jerks,  Argyll-Robertson  pupils,  sometimes 
loss  of  knee  jerk  and  optic  atrophy,  paraesthesiee  of  the  legs  and  feet.  Later 
symptoms  are  absent  knee  jerks,  unequal  pupils,  Romberg's  sign  and  slight 
ataxia.  In  the  infantile  type  bladder  and  micturition  troubles  are  the 
first  indications  and  are  followed  by  ocular  and  sensory  symptoms,  ataxia 
being  absent.  About  100  cases  are  on  record.  Some  end  in  general  paralysis. 
The  progress  is  occasionally  rapid.  Usually  it  is  slow  and  the  disease 
remains  stationary  for  years. 

Disseminated  Sclerosis. — Syn.  :  Insular  or  Multiple  Cerebral  and 
Spinal  Sclerosis. — The  existence  of  the  adult  type  of  this  disease  in  children 
is  doubtful.  Recorded  cases  have  generally  followed  an  infective  disease, 
notably  measles,  scarlatina  and  diphtheria.  Probably  these  are  cases  of 
diffuse  encephalitis  or  encephalomyelitis  with  secondary  connective  tissue 
proliferation.  Others  are  perhaps  of  the  nature  of  a  diffuse  sclerosis 
or  focal  myelitis  from  congenital  syphilis.  The  chief  symptoms  are 
scanning  speech,  nystagmus,  intentional  tremor,  disordered  gait,  exag- 
gerated knee  jerks  and  epigastric  reflex,  and  mental  deficiency  ;  sometimes 
defective  ocular  movements,  bladder  weakness  and  sensory  disturbances. 
True  multiple  sclerosis,  with  proliferation  of  the  neuroglia,  is  possibly  a 
diffuse  gliosis  and  analogous  to  a  neoplasm. 

Paralysis  Agitans- — Lannois  (1894)  reported  a  case  in  a  boy,  11  years 
old.     Tremor  developed  a  few  months  after  measles.     From  12-18  years 


The  Spinal  Cord  and  the  Nerves.  719 

•of  age  lie  did  not  grow.  The  tremor  increased,  was  exaggerated  by  emotion, 
heat,  cold  and  voluntary  movement,  and  absent  during  sleep.  It  affected 
the  whole  body,  chiefly  the  upper  limbs,  but  not  the  face.  He  had  a 
"  Parkinsonian  "  attitude  on  standing  and  walking.  Possibly  this  was  a 
sequel  of  mild  encephalitis. 

Tumours  of  the  cord  are  rare,  usually  diffuse  and  inoperable.  Some 
are  tuberculous  and  end  fatally  from  meningitis.  Batten  has  reported 
diffuse  sarcomatosis  of  the  brain  and  cord  in  a  boy,  aged  10  years.  During 
an  illness  of  9  months  the  symptoms  were  headache,  vomiting,  optic 
neuritis,  loss  of  sight  and  hearing,  exaggerated  reflexes,  leucocytosis, 
endothelial  cells  in  the  cerebrospinal  fluid,  convulsions,  emaciation  and 
flexor  rigidity.    The  symptoms  of  tumour  vary  with  the  site. 

Peripheral  Birth  Palsy. — Syn.:  Paralysis  of  the  Newborn — ErVs 
Paralysis — Obstetrical  Paralysis  of  Duchenne — Upper  Arm  Palsy. — 
Erb's  paralysis  or  birth  palsy,  to  use  the  most  common  names,  is  a  paralysis 
■of  one  or  both  upper  arms  from  injury  to  the  brachial  plexus  during  labour. 
It  was  ascribed  by  Danyau  to  forceps  in  1851.  Duchenne  noted  cases  after 
•difficult  labour  and  Erb  fully  described  it.  Other  varieties  or  modifications 
may  occur  from  a  like  cause,  e.g.  paralysis  of  one  or  both  lower  arms,  a 
lower  arm  type. 

Etiology. — In  my  experience  most  cases  have  resulted  from  vertex 
presentations  in  primiparse.  Usually  it  is  ascribed  to  extraction  in  breech 
presentation,  the  injury  being  inflicted  by  pulling  on  the  shoulder  to 
facilitate  delivery  of  the  head  ;  pulling  down  the  arm  when  it  is  above 
the  head  ;  elevation  of  the  arm  upward  and  backward,  causing  compression 
■of  the  nerves  between  the  head  of  the  clavicle  and  the  first  rib  or  the 
transverse  processes  of  the  vertebrse,  possibly  aided  by  traction  on  the 
•clavicle.  In  cranial  presentations  it  may  be  due  to  the  pressure  of  forceps 
on  the  lower  nerves  of  the  plexus  ;  depression  of  the  shoulder  with  the  head 
bent  to  the  opposite  side  and  rotated  ;  lack  of  flexion  in  face  presentations  ; 
traction  on  the  head  producing  strong  pressure  on  the  shoulder ;  or  to 
traction  on  the  neck  by  the  finger  or  hook  in  the  axilla.  It  has  been  noted 
after  apparently  normal  labour,  with  no  undue  difficulty  or  instrumental 
interference.  In  a  few  instances  it  has  been  ascribed  to  constriction  of  the 
neck  by  the  umbilical  cord  or  in  the  pelvic  passage  during  prolonged 
labour. 

Site  of  the  Lesion. — The  damage  is  located  in  the  fifth  cervical  nerve 
<(  Wilfred  Harris)  ;  in  the  sixth  cervical,  and  the  fifth  to  a  less  extent ; 
in  the  fifth  and  sixth  always,  seventh  frequently,  eighth  and  first  dorsal 
•occasionally  (Clark,  Prout  and  Taylor,  1905).  In  5  operation  cases 
Kennedy  found  the  damage  involved  the  junction  of  the  fifth  and  sixth 
■cervical  nerves,  anterior  divisions  ;  complete  rupture  in  4  and  cicatricial 
pressure  in  the  fifth.    This  may  be  accepted  as  the  common  site,  namely, 


720  Chapter  LIV. 

at  or  just  below  the  junction  of  these  2  nerves,  below  the  origin  of  the 
nerves  supplying  the  rhomboids  and  the  spinati. 

The  nature  of  the  damage  is  a  complete  rupture,  rupture  of  a  few  nerve 
fibres,  rupture  or  stretching  of  the  nerve  sheath  and  fibres  with  laceration 
and  haemorrhage,  interstitial  haemorrhage,  direct  or  indirect  compression 
or  bruising  of  the  nerves.  Cicatricial  changes  and  neuritis  are  secondary. 
The  axis  cylinders  are  destroyed  and  new  connective  tissue  forms  between 
their  ends,  showing  under  the  microscope  strands  of  scar  tissue  among 
intact  bundles  of  nerve  fibres. 

The  muscular  affection  depends  on  the  extent  of  the  damage  and  on 
anatomical  variations  in  plexus  formation.  In  an  uncomplicated  case 
of  fifth  root  palsy  the  deltoid,  spinati,  biceps,  brachialis  anticus,  supi- 
nators and  radial  extensors  of  the  wrist  are  affected.  The  pectorals, 
latissimus  dorsi  and  triceps  suffer  if  the  sixth  nerve  is  involved  ;  and 
the  extensors  of  the  fingers  if  the  seventh  nerve  suffers.  In  avulsion  of 
the  whole  plexus  the  limb  is  entirely  paralysed.  The  pectorals  and  latis- 
simus are  partly  supplied  by  the  eighth  nerve.  The  "  lower  arm  "  type 
of  palsy  is  usually  the  remains  of  total  arm  palsy  but  may  occur  inde- 
pendently. In  3  reported  cases  the  cause  was  over-extension  of  the 
head  in  face  or  chin  presentations.  The  seventh  cervical,  and  to  a  less 
extent  the  eighth  cervical  and  first  dorsal  nerves,  were  damaged  far  enough 
from  the  cord  for  the  ocular  fibres  of  the  sympathetic  in  the  first  thoracic 
root  to  escape.  A  bilateral  upper  arm  palsy  under  my  care  was  associated 
with  paralysis  of  the  sterno-mastoids  and  diaphragm.  The  trapezius 
was  also  involved.  As  a  rule  the  deltoid  is  the  muscle  chiefly  affected, 
then  the  biceps,  brachialis  anticus,  supinator  longus,  and  less  frequently 
the  spinati  and  the  coraco-brachialis.  Occasionally  the  deltoid  suffers 
alone. 

Symptoms. — Severe  cases  attract  immediate  attention.  Milder  ones 
may  not  be  noticed  for  some  weeks.  The  arm  hangs  down  loosely  by  the 
side  of  the  trunk  and  is  not  moved.  It  is  close  to  the  trunk  and  rotated 
inward  ;  the  forearm  extended,  pronated  and  incapable  of  flexion  or 
supination  ;  and  the  hand  in  the  "  tipping  "  or  "  policeman  "  position, 
turned  back  and  somewhat  flexed.  Sensation  does  not  suffer,  except  in 
severe  cases  in  which  there  may  be  anaesthesia  over  the  outer  part  of  the 
arm,  over  the  area  supplied  by  the  circumflex  and  external  cutaneous 
nerves.  A  slight  degree  of  anaesthesia  is  unrecognisable  in  infants. 
Wasting  of  the  muscles  comes  on  in  a  few  weeks.  The  muscles  are  so 
small  and  well  covered  with  fat  in  babies  that  wasting  is  not  noticeable 
for  a  considerable  time.  In  bad  cases  the  reaction  of  degeneration  may  be 
present.  Rigidity  may  occur  early  from  unopposed  action  of  the  opponent 
muscles,  and  later  from  contraction  of  the  affected  ones.  Involvement  of 
the  sympathetic  causes  narrowing  of  the  palpebral  fissure,  retraction  of  the 
eyeball  and  myosis.     The  injury  may  be  complicated  by  fracture  of  the 


The  S final   Cord  and  the  Nerves.  721 

humerus  or  clavicle,  separation  of  the  head  of  the  humerus,  facial  palsy 
or  wry-neck. 

Diagnosis  is  easy  in  the  upper  arm  type  dating  from  birth.  Cerebral 
palsy  is  rarely  monoplegic  and  still  more  rarely  limited  to  one  group  of 
muscles.  Epiphysitis,  separation  of  an  epiphysis,  fracture  and  dis- 
location of  the  clavicle  must  be  excluded.  In  these  affections  there  is 
pain,  no  true  paralysis,  and  no  electrical  changes.  At  a  later  age  it  may  be 
impossible  to  be  certain  whether  the  palsy  is  a  "  birth  palsy  "  or  due  to 
poliomyelitis  of  the  fifth  segment  of  the  cord.  The  history  and  grouping 
of  the  paralysis  are  the  most  reliable  features.  Similar  palsy  may  result 
from  wounds,  pressure  of  enlarged  glands  or  tumours,  neuritis  and  spinal 
caries. 

Prognosis. — Mild  cases  show  little  or  no  discomfort  and  tend  to 
recovery.  In  more  severe  ones  the  child  is  peevish  and  irritable  ;  and 
the  signs  of  pain  and  anaesthesia  indicate  considerable  damage  and 
laceration  of  the  nerve  elements.  The  outlook  is  nevertheless  fairly  good 
in  these  severe  cases,  but  they  may  last  for  years  or  be  permanent.  Partial 
recovery  is  common.  Complete  rupture,  with  separation  of  the  divided 
ends  and  cicatrisation,  is  almost  certain  to  be  incurable  without  operation. 
There  is  little  piospect  of  recovery  unless  signs  thereof  are  present  by  the 
ninth  month.  Mild  cases  begin  to  improve  in  1-3  months  and  are  well  in 
a  year.  Flexion  of  the  elbow  is  the  first  sign  of  improvement  and  may  be 
the  only  one.  The  deltoid  recovers  last.  In  the  presence  of  R.D.  recovery 
will  be  slow  or  absent,  yet  it  may  be  complete.  If  the  muscles  respond  to 
faradism  recovery  is  rapid.  Some  writers  regard  the  prognosis  as  much 
more  grave.  Rotch  states  that  most  cases  never  recover  and  that  partial 
recovery  cannot  be  expected  for  years.  Warrington  and  Jones  (1906) 
say  that  30-40  per  cent,  end  in  useful  recovery.  Atrophy,  contractures 
and  maldevelopment  of  the  arm,  shortening  of  the  tendon  of  the  sub- 
scapular muscle,  and  sometimes  subluxation  of  the  head  of  the  humerus, 
are  the  chief  sequels. 

Treatment. — Keep  the  arm  at  rest,  to  allow  time  for  repair  of  the 
damaged  tissues.  Wrap  it  in  cotton  wool  and  fix  it  to  the  side,  as  in 
fractured  clavicle.  Keep  overstretched  muscles  mechanically  relaxed 
for  months,  e.g.  wrist  drawn  by  a  sling  toward  the  neck  to  keep  the  flexors 
of  the  forearm  relaxed,  and  hyperextension  of  the  wrist  if  the  extensors 
are  paralysed.  Maintain  the  nutrition  of  the  affected  muscles  by 
cutaneous  friction,  massage,  salt  baths,  exercises  and  electricity.  Use 
the  weakest  available  faradic  current,  if  the  muscles  react,  and  make  each 
muscle  contract  20  times.  Use  galvanism,  making  and  breaking  the 
current,  if  there  is  no  response  to  faradism,  but  replace  it  by  faradism  as 
soon  as  faradic  irritability  returns.  At  first  apply  galvanism  daily,  5 
milliamperes  for  5-10  minutes,  with  the  arm  and  the  negative  pole 
in  a  water  bath  and  the  positive  pole  between  the  shoulders.    After  a 

3   A 


722  Chapter  L  IV. 

few  days  make  the  muscles  contract  daily  and  later  on  only  on  alternate 
days. 

Operation  has  been  successfully  done.  The  damaged  portions  of  the 
nerve  are  excised  and  the  divided  ends  sutured.  It  must  be  advised  as 
soon  as  it  is  evident  that  recovery  will  not  take  place.  The  younger  the 
child,  the  better  is  the  result.  It  must  not  be  done  before  the  third  month 
of  life  and  not  then,  if  improvement  is  progressive.  It  is  preferable  to  wait 
until  1  year  of  age  for  the  risk  of  shock  is  less,  the  field  for  operation 
larger,  the  amount  of  paralysis  denned,  and  the  cicatrix  localised.  Marked 
benefit  has  accrued  as  late  as  14  years  of  age  (Kennedy).  At  the  operation 
test  the  exposed  nerves  by  electrical  stimulation  to  ascertain  their 
distribution.  Nerve  anastomosis,  crossing  and  transplantation  have  all 
been  adopted.  Massage  and  electrical  treatment  must  be  continued 
afterward. 

Radial  Palsy  or  paralysis  of  the  musculo-spiral  nerve  causes  palsy  of 
the  extensors  of  the  wrist,  wrist-drop  and  flexion  of  the  fingers.  •  It 
may  be  congenital,  due  to  an  amniotic  band  or  intra-partum  pressure 
on  the  nerve  ;  or  acquired,  due  to  lead  poisoning,  pressure  during  sleep, 
or  fracture  of  the  humerus.  The  crural  nerve  may  be  damaged  at  birth 
and  cause  a  "  lower  limb  "  birth  palsy.  Peroneal  palsy  may  be  due  to 
traumatism,  or  damage  at  birth.  Paraplegia  may  arise  from  injury  to  the 
spine  and  cord  in  difficult  labour  ;  and  possibly  some  of  the  bilateral  birth 
palsies  ascribed  to  injury  of  the  sixth  cervical  nerves,  notably  those  in 
which  the  sterno-mastoids  are  involved,  really  depend  on  injury  to  the 
spinal  cord. 

Pressure  Paralysis. — Syn.  :  Ischcemic  Paralysis  or  Myositis  —  Volk- 
mann's  Contracture. — If  bandages  or  splints  are  applied  too  tightly,  the 
Mood  supply  to  the  subjacent  muscles  is  interfered  with  and  they  become 
swollen  by  oedematous  infiltration.  The  extremity  of  the  limb  swells  and 
the  whole  limb  is  painful  or  uncomfortable.  In  the  forearm,  in  which  it 
is  most  frequent,  the  hands  and  fingers  may  be  discoloured,  blue  and 
swollen.  Often  pressure  sores  are  present  on  the  skin,  usually  near  the  bend 
of  the  elbow.  The  muscles  appear  paralysed  and  the  fingers  and  wrist 
become  flexed,  perhaps  within  a  few  days.  The  nature  of  the  contracture 
depends  on  the  flexors  being  stronger  than  the  extensors.  There  is  no  true 
paralysis  and  no  sensory  changes.  It  is  generally  a  sequel  of  fracture 
about  the  elbow  joint  and  rapid  in  onset.  The  forearm  is  pronated 
and  slightly  flexed  at  the  elbow.  The  wrist  is  markedly  flexed 
a,nd  the  metacarpo-phalangeal  joints  are  extended.  The  phalangeal 
joints  of  the  thumb  and  fingers  are  so  flexed  that  the  fingers  are 
often  buried  in  the  palm.  If  the  wrist  is  extended,  it  is  impossible 
to  extend  the  fingers.  The  muscles  can  be  moved  to  an  extent 
limited  by  the  degree  of  contracture.  Subsequently  the  muscles  undergo 
interstitial  fibrosis,  becoming  smaller,  harder,  and  contracted.     W.  Harris 


The  S final  Cord  and  the  Nerves.  723 

^1908)  found,  in  7  out  of  9  cases,  severe  neuritis  of  the  median  and  ulnar 
nerves  with  anaesthesia,  wasting,  and  R.D.  in  the  intrinsic  muscles  of  the 
hands.  The  R.D.  may  be  present  in  the  flexors  of  the  wrist  and  fingers. 
It  is  therefore  a  combination  of  myositis  and  neuritis  in  many  instances. 
Treatment  is  of  little  value  if  fibrosis  has  taken  place.  Warm  baths  and 
massage  twice  a  day  may  prove  beneficial,  and  possibly  the  injection  or 
inunction  of  thiosinamine  or  fibrolysin.  Surgical  measures  are  required 
for  the  relief  of  deformity. 

Facial  Palsy. — As  a  birth  palsy  facial  paralysis  results  from  the 
pressure  of  forceps,  fracture  of  the  base  of  the  skull,  or  from  pressure  by  a 
faulty  pelvis  or  intra-pelvic  tumour  in  prolonged  labour.  Subsequently 
it  is  due  to  meningitis,  tumours,  mischief  in  the  ear,  or  causes  affecting  the 
nerve  after  its  exit  from  the  stylo-mastoid  foramen.  In  rare  instances  it  is 
.associated  with  paralysis  of  the  sixth  or  eighth  nerve,  possibly  from  nuclear 
degeneration. 

Bell's  palsy  is  the  acquired  variety,  affecting  the  frontal  and  inferior 
branches  of  the  nerve.  It  is  due  to  cold,  pressure,  injury  and  other  causes 
•of  neuritis,  or  middle  ear  disease.  Cases  due  to  cold  often  show  a  family 
"tendency,  several  children  becoming  affected.  They  are  rare  in  the  first 
2  years  of  life.  So-called  "rheumatic"  cases  are  sometimes  due  to  transient 
acute  otitis  media.  Infants  are  less  susceptible  than  older  children  to 
facial  palsy  from  ear  disease,  for  the  inflammatory  products  cannot  exert 
the  same  amount  of  pressure  in  an  incomplete  bony  canal.  Henoch  and 
Goodhart  regard  this  combination  as  pathognomonic  of  tuberculosis,  but 
it  may  occur  independently.  Caries  or  necrosis  of  the  aqueductus  Fallopii 
is  followed  by  extension  of  the  destructive  process  to  the  nerve,  or  a  simple 
inflammatory  effusion  in  the  aqueduct  may  compress  the  nerve.  Facial 
palsy  in  chronic  otorrhoea  is  a  grave  sign  for  it  shows  necrosis  of  the  temporal 
bone  is  present. 

If  the  cause  is  at  the  base  of  the  brain,  the  auditory  and  other  nerves 
may  be  involved  and  there  are  cerebral  symptoms  ;  if  in  the  geniculate 
ganglion,  there  may  be  disturbance  of  lachrymation  and  palsy  of  the  soft 
palate  ;  if  external  to  the  ear,  the  signs  are  those  of  a  pure  motor  palsy. 
Bilateral  facial  palsy  is  rarely  due  to  ear  disease,  and  is  more  likely  to 
■depend  on  congenital  syphilis  and  be  associated  with  or  followed  by  deafness. 

The  prognosis  depends  on  the  cause.  Pure  motor  palsy  from  injury  at 
birth  or  cold  is  rarely  permanent,  though  I  have  known  it  persist  in  a  mild 
form  in  a  case  which  came  on  during  infancy.  The  outlook  depends  on  the 
•electrical  reactions  during  the  first  2  weeks,  e.g.  diminished  irritability, 
R.D.,  or  absence  of  response.  Many  aural  cases  recover  completely,  others 
incompletely.  Recovery  is  rare,  if  the  canal  is  necrosed;  usual,  if  the  nerve 
is  only  compressed  by  effusion.  Conjunctival  irritation,  from  imperfect 
closure  of  the  lids,  and  herpetic  eruptions  are  occasional  sequels.  The 
treatment    consists    of    persistent    galvanism     with    a    current     of     3-5 


724  Chapter  LIV. 

milliamperes  and  facial  massage.  Nerve  anastomosis  may  be  tried  in 
permanent  cases. 

Other  cranial  nerves  are  rarely  affected  except  as  the  result  of  polio- 
encephalitis inferior  or  bulbar  disease.  A  periodic  oculo-motor  palsy  of 
one  or  more  nerves,  partial  or  total,  may  be  associated  with  migraine  and 
last  for  days  or  months  (p.  764). 

Polyneuritis  is  described  under  the  head  of  diphtheritic  palsy,  and  may 
follow  other  infections.  Occasionally  it  is  epidemic,  a  variety  of  acute- 
anterior  poliomyelitis,  or  due  to  lead,  arsenic  and  alcohol. 

Sympathetic  Nervous  System. — Paralysis  or  irritation  of  the  sympathetic 
nerves  in  the  neck  results  from  the  pressure  of  glands,  thyroid,  etc.,  injury 
at  operation,  disease  of  the  spinal  cord,  first  dorsal  and  eighth  cervical 
roots,  injury  of  the  brachial  plexus  at  birth,  syringomyelia  and  tuberculous 
meningitis.  Paralysis  causes  contraction  of  the  pupil  and  palpebral 
aperture,  sometimes  retraction  of  the  eyeball  (enophthalmos),  redness  and 
anidrosis  of  the  affected  side  of  the  face.  Irritation  causes  dilatation  of  the 
pupil  and  palpebral  aperture,  sometimes  exophthalmos,  and  hyperidrosis. 

General  hyperidrosis  occurs  in  neurasthenia,  hysteria,  Graves'  disease 
and  epilepsy.  It  is  localised  in  hemiplegia,  affections  of  the  spinal  cord  and 
tuberculous  meningitis.  It  may  be  paradoxical,  occurring  under  con- 
ditions which  normally  inhibit  it ;  or  abnormal  in  distribution  and  unilateral.. 
It  may  be  limited  to  the  hands,  feet,  tip  of  the  nose  or  forehead.  For  this 
variety  ergot  is  sometimes  useful.  Chilblains,  Raynaud's  disease,  angio- 
neurotic oedema,  migraine,  syncope  and  swooning,  epilepsy  and  eclampsia 
may  depend  on  the  disorders  of  the  sympathetic  nervous  system  which 
induce  vaso-constriction  or  vaso-dilatation. 


CHAPTER    LV. 

THE  MUSCULAK  ATROPHIES. 

Werdnig-  Hoffmann  Type — Peroneal   Atrophy — Pseudo-hypertrophic    Para- 
lysis—  Facial  Type — Era's  Juvenile  Type — Amyotonia  Congenita. 

The  Myopathies  as  distinguished  from  myelopathies  are  characterised 
by  the  absence  of  definite  changes  in  the  spina]  cord.  In  recent  years  there 
has  been  a  tendency  to  favour  the  view  of  a  spinal  origin.  There  is  no 
sharp  line  of  demarcation  for  intermediate  types  occur.  Degenerative 
changes  in  the  cells  of  the  cord  in  cases  of  long  standing  are  probably 
secondary.  These  diseases  are  essentially  congenital  or  endogenous  in  that 
they  depend  upon  some  defective  tendency  in  development  of  the  muscular 
tissues.  The  tendency  is  a  potential  one  and  the  atrophy  may  not  develop 
for  many  years.  Excluding  the  spinal  and  neural  types  it  is  an  inherited 
weakness  in  the  muscle  fibres.  It  affects  more  males  than  females  and  is 
transmitted  by  the  mother.  The  same  type  occurs  in  members  of  the  same 
family.  Groups  of  muscles  of  the  same  period  of  development  are  affected 
simultaneously.  The  onset  is  during  childhood,  sometimes  in  adolescence. 
Perhaps  there  is  a  past  history  of  awkwardness  and  difficulty  in  learning 
"to  walk. 

The  general  features  are  slow  progressive  paralysis  in  muscles  or  groups 
•of  muscles,  and  atrophy  or  hypertrophy  of  those  affected.  The  palsy  is 
flaccid  in  type  and  fibrillary  contraction  is  absent.  There  is  no  qualitative 
■electrical  change  nor  a  decreased  reaction.  Muscular  tone  is  often  present 
and  the  tendon  reflexes  are  preserved  for  some  time.  Foot  contractures  are 
common.  There  is  no  affection  of  muscles  in  groups  corresponding  to 
groups  of  cells  in  the  cord.  The  extrinsic  muscles  of  the  eyes  and  the 
muscles  of  the  larynx,  pharynx  and  diaphragm  are  never  attacked.  The 
course  is  slow  and  the  patients  eventually  become  bedridden.  Death  is  due 
to  tuberculosis  or  intercurrent  disease. 

The  essential  change  is  a  wasting  of  muscle  fibres,  which  may  or  may 

I  not  be  associated  with  an  overgrowth  of  interstitial  tissue  or  a  marked 
tendency  to  deposition  of  fat.  The  muscle  fibres  undergo  granular  degenera- 
tion, and  the  muscles  are  pale  red  or  yellowish  in  colour.  At  first  the  muscle 
is  not  uniformly  affected.  The  wasting  depends  upon  the  congenital 
defect  rather  than  on  pressure  from  overgrowth  of  the  interstitial  tissue, 


726 


Chapter  L  V. 


proportion  to  the  atrophy.  Possibly  in  some  instances  there  is  a 
quantitative  as  well  as  a  qualitative  defect,  and  the  muscle  may  be  smaller 
than  normal. 

Classification. — The  division  into  2  groups  of  (1)  Simple  Atrophy, 
and  (2)  Atrophy  with  Hypertrophy,  or  Pseudo-hypertrophic  Paralysis, 
is  unsatisfactory.  In  some  cases  of  pseudo-hypertrophic  paralysis  there  is 
no  increase  in  the  bulk  of  the  muscle  and  there  are  intermediate  types 
showing  connection  between  these  varieties.  The  following  classification 
shows  the  connection  between  the  spinal,  neural  and  purely  muscular 
affections  : — 

A.  Spinal  Type  or  Progressive  Muscular  Atrophy. 

(1)  As  seen  in  adults  (rare). 

(2)  Early  Infantile,  or  AVerdnig-Hoffrnann  Type. 

B.  Peroneal  Atrophy  ;    a  neural  type. 

C.  Muscular  Dystrophies. 

(1)  Pseudo-hypertrophic   Paralysis, 

(a)  with  hypertrophy ; 

(b)  Avithout  hypertrophy  ;   idiopathic  muscular  atrophy. 

(2)  Idiopathic  Atrophy  ;    with  wasting  of  nearly  all  the  muscles, 

occasionally   a   little   pseudo-hypertrophy,    and  probably   a 
variety  of  the  previous  group. 

(3)  Amyotonia  Congenita  ;    an  infantile  or  congenital  type. 

(4)  Facio-scapulo-humeral    Type    of    Landouzy-Dejerine    (Facial 

Type). 

(5)  Erb's  Juvenile  Type,  possibly  a  variety  of  the  last  group. 

(6)  Intermediate  or  combined  forms. 

Many  of  these  types  may  occur  in  different  members  of  the  same 
family.  The  facial  type  and  Erb's  juvenile  form  are  more  frequently  asso- 
ciated than  the  others.  All  types  are  connected  by  intermediate  forms  with 
pseudo-hypertrophic  paralysis.  The  latter  disease  and  the  peroneal  type 
breed  most  true.  In  the  muscular  dystrophies  the  extrinsic  muscles  of  the- 
hand  are  rarely  affected.  It  is  rare  for  any  one  variety  to  occur  sporadically 
or  to  be  limited  to  one  generation.  The  sexual  distribution  is  variable. 
Sometimes  the  females,  more  often  the  males,  are  most  affected,  perhaps 
because  males  do  not  live  long  enough  to  transmit  the  disease.  It  may  be 
transmitted  by  unaffected  females.  In  other  instances  both  sexes  suffer 
equally.  Consanguinity  may  be  a  cause.  Usually  no  direct  exciting  factor 
can  be  found  :   a  few  cases  have  followed  infective  fevers. 


The  Muscular    Atrophies.  727 

Werdnig-Hoffmann  Type. — This  is  an  infantile  progressive  muscular 
atrophy  of  spinal  origin.  About  30  cases  are  on  record.  It  begins  at  6-12 
months  of  age  with  weakness  of  the  legs,  back,  neck  and  shoulder  muscles, 
and  then  those  of  the  hands  and  feet.  Gradually  complete  paralysis  ensues 
with  atrophy,  rarely  pseudo-hypertrophy,  disappearance  of  knee  jerks 
and  sometimes  fibrillary  twitching.  Intelligence,  sensation,  speech,  cranial 
nerves  and  the  sphincters  are  unaffected.  Death  takes  place  in  1-4  years 
from  involvement  of  the  respiratory  muscles,  pneumonia,  or  enteritis.  The 
anatomical  changes  are  atrophy  of  the  cells  in  the  anterior  cornua,  degenera- 
tion of  the  root  fibres  and  motor  nerves,  and  muscular  atrophy. 

The  hereditary  type  of  Leyden  is  probably  of  the  same  nature.  It  attacks 
many  members  of  the  same  family,  is  more  common  in  males,  and  usually 
begins  at  8-10  years  of  age.  The  early  signs  are  weakness  and  wasting  in  the 
muscles  of  the  back  and  lower  extremities,  lordosis  and  difficulty  in 
walking. 

Peroneal  Atrophy. — Syn.  ;  Spinal  Neuritic  Atrophy  (Bernhard) — 
Progressive  Neural  Muscular  Atrophy  (Hoffmann). — This  type  was  fully 
described  by  Tooth  (1886)  in  a  thesis  entitled  "  The  Peroneal  Type  of 
Muscular  Atrophy  "  ;  and  by  Charcot  and  Marie  in  the  same  year.  Many 
cases  had  been  reported  previously  though  the  special  characters  had  not 
been  recognised. 

The  disease  is  hereditary,  familial  and  transmitted  indiscriminately  by 
both  sexes.  Herringham  traced  it  through  5  generations,  20  males  being 
probably  affected  but  no  females.  The  disease  was  transmitted  by  healthy 
females  to  the  male  children.-  Affected  males  did  not  transmit  to  their 
children,  and  only  to  their  grandchildren  through  healthy  daughters. 
In  this  family  the  mode  of  inheritance  was  similar  to  that  of  pseudo- 
hypertrophic paralysis.  In  A.  J.  Whiting's  group  (1909)  transmission 
took  place  from  the  affected  to  children  of  the  opposite  sex.  The  usual  sex 
incidence  is  1  female  to  2  males  (1-5,  Sainton).  Several  members  of  a  family 
are  generally  affected  and  isolated  cases  are  rare.  A  sporadic  case  in  a  girl, 
7  years  old,  was  possibly  a  sequence  of  measles  at  6  months  of  age.  It 
commonly  begins  in  the  second  half  of  childhood,  usually  before  10  years 
of  age,  and  rarely  after  20  years.  Sainton  gives  the  limits  of  age  as  2-40 
years. 

Symptoms. — The  earliest  symptom  is  weakness  and  a  tendency  to 
"  drag  the  leg  "  or  "  turn  in  "  the  feet.  The  atrophy  is  first  conspicuous 
in  the  peroneal  regions  and  then  spreads  to  the  other  muscles  of  the  upper 
and  lower  extremities.  Sometimes  it  begins  in  the  extensor  longus  pollicis, 
the  extensor  communis  digitorum,  the  peronei,  the  intrinsic  muscles  of  the 
foot,  or  even  the  gastrocnemius.  Several  of  these  muscles  may  be  affected 
simultaneously.  Later  on  the  anterior  tibial  group  of  muscles  and  those 
of  the  calf  and  thigh,  especially  the  vastus  internus,  are  involved.  After 
many  years,  and  in  rare  instances  at  the  same  time,  the  hands  are  affected. 


728  Chapter  L  V. 

Here  it  begins  in  the  muscles  of  the  thenar  and  hypothenar  eminences  and 
.the  interossei.  It  then  spreads  to  the  muscles  of  the  forearm,  either  extensors 
.or  flexors  suffering  first  or  most.  The  facial  muscles,  and  usually  the 
supinator  longus  and  the  muscles  of  the  shoulder,  neck  and  back  escape. 
■Ultimately  the  muscles  of  the  pelvic  and  shoulder  girdles  may  be  involved. 
.The  disease  is  generally  symmetrical.  Club-foot  or  pes  cavus  results 
.early  from  unequal  involvement  of  the  leg  muscles.  The  main  en  griffe, 
:a  "  claw-like  "  deformity  of  the  hands,  is  due  to  the  intrinsic  muscles  being 
-affected.  It  is  an  extremely  rare  condition  in  early  life  from  any  other  cause. 
Scoliosis  is.  sometimes"  present  early,  perhaps  due  to  unilateral  club-foot. 

Muscle  reflexes  are  diminished  or  absent  in  the  affected  parts.  Both  the 
knee  jerks  and  Achilles  tendon  reflexes  are  generally  lost.  The  knee  jerk 
may  be  present,  if  the  thigh  muscles  are  not  affected,  although  the  atrophy 
below  the  knees  is  extensive.  The  cutaneous  reflexes  show  variable  altera- 
tions. Electric  irritability  to  faradism  and  galvanism  is  diminished  earlier 
and  to  a  greater  extent  than  in  muscular  dystrophy.  Faradic  irritability 
soon  becomes  extinct  and  the  reaction  of  degeneration  is  usually  present 
at  an  early  stage.  Even  muscles,  which  are  not  atrophied,  can  only  be 
stimulated  with  great  difficulty.  Patients  are  remarkably  insensitive  to 
faradism,  possibly  on  account  of  some  peculiarity  in  the  skin  (analgesia). 

Fibrillary  tremor  is  usually  present.  Cutaneous  sensibility  is  sometimes 
impaired  or  lost,  especially  where  atrophy  is  greatest  and  on  the  soles  of  the 
feet.  Pain,  hypersesthesia,  coldness  and  blueness  of  the  limb,  increased 
sweating  and  spasmodic  muscular  contractions  have  occasionally  been  noted. 
There  is  no  sphincter  trouble. 

The  disease  may  remain  stationary  for  years  or  even  permanently  ; 
usually  it  progresses  slowly  with  periods  of  intermission.  Cases  vary 
somewhat  in  type.  In  those  described  by  Charcot  and  Marie  both  upper 
and  lower  limbs  were  profoundly  affected.  In  5  members  of  the  same 
family,  aged  7-28  years,  there  was  marked  atrophy  of  the  intrinsic  muscles 
of  the  hands  and  feet,  pes  cavus,  and  weakness  of  the  leg  muscles  in  some 
•eases  (Lewis  Jones,  1898).  Electrical  examination  showed  extreme  insensi- 
bility to  faradism,  very  great  loss  of  muscular  excitability  to  faradism  and 
slight  diminution  to  galvanism.  In  1,  a  boy  aged  7  years,  the  analgesia 
to  faradism  and  loss  of  excitability  were  greatest  in  the  hands,  although  the 
muscles  were  supposed  to  be  unaffected. 

Pathology. — It  is  not  an  affection  of  the  anterior  cornua  for  there  is  no 
diminution  in  the  number  of  cells.  Some  of  them  show  an  advanced  state 
pf  ehromatolysis.  Other  degenerative  changes  have  been  found  in  the  cord, 
similar  to  those  due  to  section  of  peripheral  nerves  or  anterior  nerve  roots, 
and  are  probably  secondary.  The  chief  lesion  is  sclerosis  of  the  posterior 
columns.  There  is  evidence  that  some  cases  are  due  to  idiopathic  muscular 
dystrophy,  some  secondary  to  neuritis,  while  others  may  depend  on  a  com- 
bination of  the  two  factors.    Thus  it  may  be  due  to  a  congenital  tendency  to 


The  Muscular  Atrophies.  729 

nerve  or  muscle  degeneration,  which  may  be  excited  by  toxins  setting  up  a 
neuritis  or  acting  directly  on  nerve  or  muscle.  In  favour  of  neuritis  is  its 
tendency  to  follow  acute  specific  fevers,  notably  measles  ;  a  chronic  peri- 
pheral neuritis  has  been  found  in  two  cases.  The  presence  of  fibrillary 
contractions  and  of  the  reaction  of  degeneration  also  supports  this  theory. 
On  the  other  hand  the  hereditary  and  familial  cases  appear  to  depend  upon 
premature  failure  of  nutrition  in  the  peripheral  neive  fibres. 

Pseudo-hypertrophic  Paralysis.  —  Syn.  :  Pseudo-muscular  Hyper- 
trophy—  Lipomatous  Muscular  Atrophy. — This  disease  is  transmitted  by 
females  though  the  females  often  escape,  whereas  the  males  affected  rarely 
live  to  propagate  the  disease.  Children  of  the  same  woman  by  different 
husbands  may  suffer.  Many  children  in  the  same  family  may  be  affected, 
sometimes  only  the  males.  Males  are  much  more  often  affected  than 
females  and  more  severely.  Isolated  cases  occur.  The  type  may  vary  in 
different  members  of  the  family.  It  begins  during  the  period  of  develop- 
ment and  in  75  per  cent,  before  the  tenth  year.  In  rare  instances  it  begins 
as  late  as  18  years  of  age.  In  a  case  under  my  notice  no  symptoms  were 
present  until  21  years  of  age.  Usually  the  child  has  been  walking  and 
running  about  for  some  years  before  it  is  noticed.  In  25  per  cent,  it  shows 
itself  when  the  child  first  attempts  to  walk  and  in  such  instances  there 
is  often  backwardness  in  acquiring  this  function  ;  in  a  few  cases  the  child 
has  never  walked.  Sometimes  attention  is  not  drawn  to  the  disease  until 
after  puberty,  although  the  increase  in  size  and  the  weakness  of  the  muscles 
have  been  present  previously. 

Morbid  Anatomy. — The  spinal  cord  and  motor  nerves  are  usually 
normal.  The  muscles  are  abnormally  small  and  atrophic  ;  they  may  be 
just  like  masses  of  adipose  tissue  and  exhibit  under  the  microscope  only  a 
few  atrophied  muscle  fibres  with  little  or  no  transverse  striation.  Occasion- 
ally no  trace  of  muscle  can  be  found.  Other  muscles  may  show  a  large 
■amount  of  interstitial  connective  tissue  and  a  variable  quantity  of  adipose 
tissue  between  the  atrophied  muscle  fibres.  The  greater  the  amount  of 
connective  tissue  the  greater  is  the  wasting  in  the  muscles.  When  much 
adipose  tissue  is  deposited  the  wasting  is  not  as  a  rule  so  profound.  In 
portions  of  muscles  removed  during  life  some  muscle  fibres  have  been  found 
larger  than  normal. 

Pathology. — The  first  obvious  change  is  an  overgrowth  of  connective 
tissue  in  which  fat  may  or  may  not  be  deposited.  Muscular  atrophy  is 
mainly  primary,  partly  secondary  to  the  interstitial  growth,  while  the 
increase  in  bulk  is  due  to  the  deposition  of  fat.  In  late  stages  the  fat  is 
reabsorbed. 

Symptoms. — It  commences  with  weakness  of  the  lower  limbs.  Atten- 
tion may  be  drawn  to  the  disease  because  of  clumsiness  in  walking,  inability 
to  walk,  difficulty  in  maintaining  the  erect  position,  difficulty  in  rising  from 
the  ground  after  falling  or  from  a  low  chair,  or  in  going  up  stairs.     The 


730  Chapter  LV. 

muscular  enlargement  may  have  been  present  for  some  time,  and  may  have- 
been  regarded  with  pride  as  a  sign  of  muscular  strength.  It  develops 
gradually  and  is  conspicuous  in  a  few  years.  It  may  go  on  increasing  for 
a  time  and  then  diminish  as  the  muscular  atrophy  and  absorption  of  fat 
continue.  The  muscles  have  no  longer  the  elastic  feel  of  healthy  muscles 
but  are  hard,  wooden  and  inelastic,  even  though  small.  Some  muscles 
show  marked  wasting  without  antecedent  hypertrophy  and  in  certain  cases 
which  no  doubt  belong  to  this  same  group  none  of  the  muscles  show  any 
increase  in  bulk  (Idiopathic  Muscular  Atrophy).  The  muscles  most  com- 
monly hypertrophied  are  the  gastrocnemius,  gluteus,  deltoid,  triceps  and 
infraspinatus.  Those  which  are  atrophied  are  usually  the  biceps,  latissimus 
dorsi,  serratus,  lower  part  of  the  pectoralis  major,  flexors  of  the  thigh,  and 
extensors  of  the  leg.  The  calf  muscles  are  often  affected  and  may  reach  a 
very  large  size.  Although  so  bulky  they  are  very  weak  and  the  child  is  not- 
able to  raise  himself  on  the  toes.  The  intrinsic  muscles  of  the  hand  usually 
escape  and  those  of  the  forearm  are  rarely  affected.  The  masseters  are 
sometimes  enlarged,  but  usually  all  the  face  and  neck  muscles  escape. 
The  erectors  of  the  spine  are  generally  involved.  Hypertrophy  of  the 
infraspinatus  and  atrophy  of  the  lower  part  of  the  pectoralis  major  are  the 
two  most  common  features. 

The  effects  of  the  disease  show  themselves  in  the  position  of  the  body 
on  standing,  in  the  gait,  and  in  the  mode  of  getting  up  from  the  supine 
position.  In  order  to  enlarge  the  base  of  support  the  legs  and  feet  are  kept 
wide  apart.  The  head  is  erect,  shoulders  thrown  back,  and  belly  pro- 
tuberant. To  counteract  the  weakness  of  the  flexors  of  the  hips  there  is- 
marked  lordosis  in  the  lumbar  region.  This  disappears  in  a  sitting  posture, 
the  back  becoming  convex  backward  from  weakness  of  the  erector  spina) 
muscles.  The  gait  is  peculiar  and  waddling.  The  feet  are  kept  wide  apart 
and  the  body  sways  from  side  to  side  so  as  to  bring  the  centre  of  gravity 
over  each  foot  in  turn,  while  the  pelvis  is  tilted  to  enable  the  child  to  swing 
the  foot  clear  of  the  ground.  The  child  is  liable  to  fall  if  any  obstacle  is  met- 
with..  In  order  to  rise  from  the  supine  position  the  child  first  turns  on  the 
side  or  face.  He  then  raises  himself  on  his  hands  and  feet,  lowers  the  head, 
and  gradually  pushes  the  body  and  hands  backward  until  he  is  able  to  get 
first  one  and  then  the  other  hand  on  the  thighs.  Having  done  this  he  is- 
able  to  push  himself  up  to  the  erect  posture  by  climbing  with  his  hands  up 
the  thighs.  Or  instead  of  getting  on  to  the  hands  and  feet  he  gets  first 
on  to  the  hands  and  knees,  next  places  his  hands  on  the  thighs,  then  plants 
his  feet  on  the  ground  and  proceeds  to  climb. 

Knee  jerks  may  remain  normal  if  there  is  no  disease  of  the  extensors  of 
the  knee,  especially  the  vastus  internus.  If  these  muscles  are  affected  the 
knee  jerk  is  gradually  abolished.  The  electrical  reaction  is  normal  at  first 
but  as  the  wasting  progresses  the  response  to  galvanism  and  faradism 
diminishes.      There   is   never   a   reaction   of  degeneration.      There  is  no- 


The  Muscular  Atrophies.  731 

fibrillary  muscular  contraction,  no  disorder  of  sensation,  and  no  affection 
of  the  sphincters.  Mentally  the  child  may  be  ahead  of  his  equals  in  age,  but 
in  some  cases  there  is  an  associated  mental  weakness  or  imbecility,  from 
defective  development  of  the  brain. 

Deformities  arise  from  contraction  of  the  affected  muscles,  or  from 
unopposed  action  of  the  muscles  which  are  little  or  not  at  all  involved.  The 
knees  and  elbows  may  become  contracted  in  the  flexed  position.  Talipes 
equinus  results  from  contraction  of  the  calf  muscles  and  much  deformity 
of  the  ankle  joint  may  ensue.  Lateral  curvature  is  not  uncommon. 
Epilepsy  and  vesical  complications  have  been  recorded. 

The  state  of  the  muscles  varies  in  different  cases.  They  may  be  large 
or  small ;  or  one,  or  a  few,  may  be  large  and  the  remainder  small.  In  other 
cases  the  muscles  may  be  small  and  atrophied  from  the  onset.  Gradually 
the  affected  muscles  waste  and  the  weakness  increases  until  the  patient  is 
unable  to  walk  or  stand,  becomes  bedridden,  and  dies  from  some  inter- 
current disease,  usually  bronchitis,  broncho-pneumonia,  pneumonia  or 
tuberculosis.  Lung  affections  are  liable  to  develop  from  the  enfeeblement 
of  the  respiratory  muscles.  The  progress  is  slow  and  irregular.  Periods  of 
intermission  are  not  uncommon  and  at  times  there  may  be  definite  improve- 
ment. After  puberty  it  progresses  more  slowly,  but  when  once  the  patient 
is  confined  to  bed  it  rapidly  increases  and  deformities  become  more  marked, 
until  he  is  quite  helpless  except  for  some  power  in  the  hands.  It  is  less 
severe  and  more  slowly  progressive  in  females.  Sometimes  it  advances 
rapidly  and  rarely  remains  quite  stationary.  If  it  begins  before  puberty 
the  patient  is  unlikely  to  attain  adult  age. 

The  diagnosis  is  based  on  the  muscular  weakness  and  enlargement,  the 
age,  the  peculiar  gait  and  method  of  getting  up  from  the  ground,  and  the 
absence  of  fibrillary  contraction  and  the  reaction  of  degeneration.  The 
hands  and  forearms  rarely  suffer.  Muscular  weakness  is  of  more  impor- 
tance than  change  in  volume,  especially  if  it  has  come  on  gradually  or  has 
started  in  infancy.  Enlargement  of  the  calf  muscles,  with  contracture 
which  cannot  be  overcome,  is  very  significant,  and  importance  must  be 
attached  to  the  enlargement  of  the  infraspinatus  with  weakness  of  the 
pectorales  and  latissimus  dorsi.  It  must  not  be  forgotten  that  muscles 
may  be  badly  affected  without  there  being  any  actual  alteration  in  size,  but 
they  feel  very  different  from  healthy  ones.  The  peculiar  method  of  rising 
from  the  ground  is  not  pathognomonic  and  may  occur  in  other  affections  in 
which  there  is  weakness  of  the  extensors  of  the  hips  and  knee.  Care  must  be 
taken  not  to  confuse  the  disease  with  spastic  paraplegia  or  infantile  paralysis. 

Treatment. — In  order  to  maintain  and  develop  the  nutrition  of  the 
unaffected  muscles  fibres  the  patient  should  continue  muscular  exercise, 
short  of  fatigue,  as  long  as  possible.  Carefully  regulated  gymnastic  exercises 
are  useful.  Massage  may  help  nutrition.  Electrical  treatment  is  of  little 
or  no  value,  and  no  advantage  is  obtained  from  drugs  beyond  that  derived 


732  Chapter  LV. 

from  tonics  such  a  cod-liver  oil,  iron  and  arsenic.  Tenotomy  may  be 
necessary  to  remedy  deformities  which  interfere  with  walking.  The  general 
health  must  be  maintained,  and  the  patient  guarded  against  exposure  to 
cold  and  other  causes  of  lung  affections  and  intercurrent  disease. 

Facial  Type,  or  Facio-scapulo-humeral  type  of  Landouzy-Dejerine, 
called  by  Duchenne  "Progressive  Muscular  Atrophy  of  Infants." — This  has 
been  traced  through  5  generations.  It  seldom  begins  in  childhood  but  may 
start  as  early  as  2  years  of  age.  Usually  it  commences  in  the  second  decade, 
or  not  until  the  fourth  decade  of  life.  It  begins  in  the  orbicularis  muscles 
of  the  eyes  and  mouth  and  the  masseters,  and  extends  to  those  of  the  arms 
and  shoulders.  It  is  usually  symmetrical  and  the  face  acquires  a  charac- 
teristic dull,  expressionless  look,  the  "  myopathic  face."  The  atrophy  of  the 
orbicularis  oris  causes  separation  of  the  lips,  inability  to  pout  and  im- 
perfect labial  articulation.  Sometimes  the  lip  muscles  are  hypertrophied. 
The  smile  is  altered  from  paresis  of  the  levator  labii  superioris  and  the 
zygomatics.  The  buccinators,  frontales  and  orbiculares  palpebrarum  are 
less  often  affected.  The  gluteal  and  thigh  muscles  may  be  wasted  ;  those 
of  the  forearm  and  leg  are  well  developed.  The  sphincters  are  unaffected 
and  the  reflexes  are  lost  if  the  atrophy  is  extreme.  It  may  be  limited  to  the 
muscles  first  attacked  or  spread  slowly,  with  intervals  of  years  between  each 
extension.    Death  is  due  to  intercurrent  disease. 

Juvenile  Type  of  Erb. — This  differs  from  the  facial  type,  for  the  face  is 
unaffected  and  occasionally  hypertrophy  occurs.  It  begins  in  late  childhood 
or  early  youth  with  progressive  wasting  and  weakness  of  certain  groups  of 
muscles.  Usually  it  begins  symmetrically  or  unilaterally  in  the  muscles  of 
the  nipper  arm  and  shoulder,  namely  those  affected  in  pseudo-hypertrophy. 
Thus  it  may  begin  in  the  lower  part  of  the  pectoralis  major  and  the 
latissimus  dorsi.  It  involves  the  biceps,  triceps,  supinator  longus,  upper 
part  of  the  pectoralis  major,  pectoralis  minor,  trapezius,  and  rhomboids  ; 
less  frequently  the  serratus  magnus  and  spinati,  rarely  the  deltoid.  The 
other  muscles  of  the  forearms  and  hand  and  those  of  the  leg  may  remain 
intact  for  a  long  time.  The  muscles  of  the  pelvic  girdle,  thigh  and  back  are 
usually  affected,  especially  the  extensors  of  the  hip,  flexors  of  the  knee,  and 
less  often  the  glutei.  In  some  cases  the  lower  limbs  suffer  but  little,  and  in 
others  the  peroneal  type  of  atrophy  is  present.  In  late  stages  the  inter- 
cOs'tals"  and  diaphragm  may  suffer,  and  rarely  the  abdominal  muscles. 
It  may  be  associated  with  pseudo-hypertrophy  of  some  muscles,  especially 
the  deltoid  and  infraspinatus. 

General  Diagnosis.— These  muscular  dystrophies  are  all  apparently 
of  the  same  endogenous  causation  and  differ  merely  in  their  distribution, 
age  of  onset,  sex  liability  and  mode  of  transmission,  and  the  relative 
distribution  of  atrophy  and  pseudo-hypertrophy.  In  all  cases  the  electrical 
reactions  are  unaltered  or  merely  quantitatively  diminished.  There  is  no 
reaction  of  degeneration.     There  is  no  fibrillary  twitching.     There  is  no 


The  Muscular    Atrophies.  733 

sensory  disturbance  or  sphincter  trouble  ;  the  intrinsic  muscles  of  the  hand 
and  muscles  of  the  forearm  escape  or  remain  intact  for  a  very  long  time  ; 
and  the  knee  jerks  are  unaffected,  or  lost  if  the  thigh  muscles  are  atrophied. 
They  show  distinct  differences  from  progressive  muscular  atrophy  of  spinal 
origin  and  from  the  neural  form  as  seen  in  the  peroneal  type.  In  every  case 
the  course  and  prognosis  are  the  same.  The  treatment  is  that  advised  for 
pseudo-hypertrophic  paralysis.  Intermediate  varieties  occur  in  which 
pseudo-hypertrophy  or  muscular  atrophy  is  combined  with  trophic  changes, 
in  the  anterior  cornua. 

Amyotonia  Congenita. — Syn.  ;  Myotonia,  Hypotonia  or  Atonia 
Congenita — Congenital  Muscular  Atrophy — Congenital  Amyoplasia. — 
This  affection  was  described  by  Oppenheim  in  1900.  It  differs  from  my- 
opathy in  several  features.  There  is  no  hereditary  tendency,  no  familial 
distribution,  and  no  true  paralysis.  Silvestri  (1909)  reported  a  case  at 
45  days  of  age.  A  maternal  aunt  died  of  progressive  muscular  atrophy. 
The  mother  developed  osteomalacia  in  the  eighth  month  of  pregnancy. 
Her  first  child  showed  a  similar  condition  at  birth,  recovered  partially  and 
at  16  years  presented  Erb's  juvenile  paralysis.  The  fourth  child  was. 
myxcedematous.  The  affection  is  present  at  birth.  It  has  developed  in 
the  first  year  of  life  after  an  acute  illness  and  after  bronchitis  at  1  year  of 
age.  It  may  be  general,  chiefly  or  entirely  in  the  legs,  or  limited  to  the 
head  and  trunk.     There  is  no  tendency  to  spreading. 

The  muscles,  especially  those  of  the  legs,  are  thin,  flabby  and  weak, 
soft  and  atonic,  but  not  truly  atrophic.  The  weakness  varies  with  the  size. 
The  neck,  trunk  and  intercostal  muscles  may  be  affected.  Occasionally  the 
arm  and  trunk  muscles  escape.  The  periphery  of  the  limbs  is  most  affected, 
including  the  intrinsic  muscles  of  the  hand  if  the  arm  is  involved.  The 
diaphragm,  sphincters,  and  muscles  supplied  by  the  cranial  nerves  are  not 
involved.  Inability  to  close  the  eyes  has  been  noted  in  3  out  of  28  cases  on 
record  (1907-8).  There  are  no  sensory  changes,  no  trophic  changes,  no 
fibrillary  tremor,  no  reaction  of  degeneration,  and  no  disorder  of  the 
sensory  organs  or  brain.  The  electrical  reactions  and  the  reflexes  are  weak 
or  absent. 

The  child  is  unable  to  stand  or  walk,  and  assumes  a  squat,  frog-like  or 
huddled  up  attitude.  The  limbs  are  flaccid  and  motionless.  The  loss  of 
power  varies  from  impaired  voluntary  action  up  to  almost  total  functional 
paralysis.  Weak  voluntary  contractions  can  be  detected.  The  joints  are- 
flail-like  from  hypotonia  and  flaccidity,  so  much  so  that  it  may  be  possible 
to  hyperextend  the  legs  on  the  abdomen  until  the  heels  lie  behind  the  head, 
or  to  hyperextend  the  foot  until  the  dorsum  touches  the  shin.  Other  joints, 
are  similarly  mobile.  Contractures  have  been  reported  in  the  lower  limbs. 
The  mental  state  is  normal. 

Morbid  Anatomy. — In  a  child  aged  22  months  no  changes  were  found 
by  Spiller  (1905)  in  the  nervous  system.    The  muscles  were  small  and  pale. 


734  Chapter  LV. 

Under  the  microscope  they  had  a  hyaloid  appearance  with  much  fatty 
connective  tissue,  small  muscle  fibres  and  indistinct  longitudinal  striation. 
Baudouin  (1907)  found,  in  a  child  of  4  months  old,  deficient  myelination 
of  the  anterior  lumbar  roots  and  various  nerves.  The  muscles  were  very 
pale,  embedded  in  fat,  and  contained  an  excess  of  connective  tissue,  the 
muscle  fibres  varying  in  size.  Collier  and  Holmes  (1909)  found  similar 
muscular  changes,  small  anterior  spinal  roots  and  a  marked  deficiency 
and  atrophy  of  the  anterior  horns.  All  these  changes  have  been  found  in 
true  myopathy.  Possibly,  the  state  of  the  nerve  elements  is  one  of  delayed 
development. 

Pathology. — The  condition  is  ascribed  by  Oppenheimer  to  retarded 
muscular  development  and  functional  derangement  of  the  anterior  cornua  ; 
by  Bing  to  arrested  development  of  the  medullo-cerebellar  tracts  ;  and  by 
Baudouin  to  a  defect  in  the  peripheral  neuron.  It  has  also  been  ascribed 
to  defect  in  the  thymus,  and  regarded  as  akin  to  myxcedema. 

Course. — It  appears  to  be  non-progressive  and  improvement  may  be 
hoped  for.  The  upper  extremities  recover  before  the  lower  ones,  and  the 
'less  affected  flexor  muscles  before  the  extensors.  The  knee  jerks  may 
return  after  prolonged  absence.  There  is  grave  liability  to  fatal  bronchitis 
if  the  thoracic  muscles  are  involved. 

It  must  be  diagnosed  from  rickets,  infantile  palsy,  and  myopathies. 
A  case  described  by  Guthrie  under  the  name  of  "  rachitis  pseudo-paralytica 
hypotonia  muscularis  "  was  probably  of  this  type.  It  may  exist  in  a  mild 
-degree  as  "  double  jointedness."  The  treatment  consists  in  massage, 
faradism,  baths,  and  the  administration  of  arsenic  and  strychnia.  Faradism 
produces  the  most  rapid  improvement. 


CFFAPTER   lvi 

SPASMODIC    FUNCTIONAL    NEUROSES. 

•Convulsions  —  Epilepsy  —  Tetany  —  Laryngospasm  —  Myoclonus  —  Habit 
Spasm —  Tics —  Nodding  Spasm —  Head   Banging —  Nystagmus. 

A  condition  of  galvanic  hyper-excitability  of  the  peripheral  nerves, 
-associated  with  a  tendency  to  convulsions  and  muscular  twitchings, 
occurs  in  children,  especially  infants.  It  has  been  named  the  tetanoid 
condition,  Spasmophilia  or  the  spasmophilic  diathesis.  It  was  first  found  in 
tetany,  and  may  be  present  in  laryngospasm  and  eclampsia.  The  child  is 
usually  rachitic.  This  diathesis  is  more  or  less  hereditary.  Apart  from  the 
above-mentioned  diseases,  it  is  most  frequent  from  November  to  April 
and  at  its  maximum  from  February  to  April.  The  common  age  is  6-18 
months.  Fits  and  laryngospasm  are  most  frequent  from  the  fourth  to  the 
twenty-fourth  month  and  tetany  from  the  fourth  to  the  thirty-sixth 
month.     All  these  affections  may  occur  at  a  later  age. 

It  has  been  ascribed  to  haemorrhage  into  the  parathyroids  (von  Pirquet) 
and  to  some  unknown  metabolic  disturbance  dependent  on  the  food 
supply,  usually  cow's  milk.  Whey  is  said  to  be  equally  injurious.  It  is  rare 
in  the  breast-fed  and  often  ceases  on  a  diet  of  breast-milk.  According  to 
Gregor  it  can  be  cured  by  starvation  and  a  liberal  water  supply.  It  occurs 
in  both  fat  babies  and  in  lean  ones  with  alimentary  troubles.  Probably 
it  is  due  to  a  toxin  of  intestinal  origin.  The  characteristic  electrical 
reactions  are  that  K  0  C  is  below  5  ma.  and  that  K  0  C  >  A  C  C. 

Convulsions. — Syn.  :  Eclampsia. — A  convulsion  is  a  "  motor  dis- 
charge "  which  gives  rise  to  an  involuntary  purposeless  muscular  spasm  of 
temporary  duration,  as  opposed  to  the  constant  muscular  spasm  resulting 
in  permanent  contracture.  In  generalised  convulsions  the  spasms  are 
tonic  and  clonic,  and  are  usually  accompanied  by  other  symptoms  : — 
namely,  a  cry,  more  or  less  profound  loss  of  consciousness,  upward  and 
•convergent  squint,  loss  of  control  over  the  sphincters,  and  drowsiness, 
stupor  or  coma.  Gowers  has  pointed  out  that  convulsions  are  far  nearer 
normal  action  than  their  startling  character  suggests.  Nerve-structures 
hold  a  vast  amount  of  latent  energy  in  perfect  readiness  for  instant  relief, 
as  is  well  seen  in  the  sudden  movements  of  a  startled  animal.  The  pre- 
disposing cause  is  an  individual  instability  or  an  exaggeration  of  the  normal 
instability  of  the  nervous  system  in  early  life. 


736  Chapter  LVI. 

Pathology. — The  actual  mode  of  production  is  an  involuntary  discharge 
of  nerve  impulses  from  the  nerve  cells  in  motor  areas  of  the  brain.  Such  a 
discharge  is  caused  by  direct  irritation  of  the  motor  cells,  by  stimuli  trans- 
mitted from  other  parts  of  the  brain,  or  by  reflex  irritation  from  other- 
parts  of  the  body.  Sudden  normal  stimuli,  e.g.  light,  sound,  smell  or  touch, 
may  cause  a  convulsion  if  the  centra]  nervous  system  is  enfeebled  or 
imperfectly  developed.  At  birth  some  structures  are  perfect  while  others, 
have  to  undergo  considerable  developmental  change.  Nerve  structures, 
lower  in  function,  such  as  the  reflex  centres  and  motor  tracts,  are  developed 
before  the  higher  ones.  Hughlings  Jackson  regards  the  central  nervous. 
system  as  containing  sensori-motor  cells  grouped  in  3  tiers,  all  parts  of  the 
body  being  represented  in  each  tier.  In  infancy  the  upper  and  middle  tiers, 
are  not  fully  developed,  and  the  lowest  one  is  in  a  state  of  unstable  equili- 
brium and  liable  to  respond  unduly  to  exaggerated  physiological  stimuli. 
According  to  this  theory  petit  mat  depends  on  irritation  of  the  frontal  and 
occipital  regions  of  the  cortex  ;  Jacksonian  epilepsy,  on  a  lesion  in  the 
Rolandic  area  or  middle  tier ;  and  laryngospasm,  spasmodic  asthma* 
vomiting  and  possibly  rigors,  on  irritation  in  the  pons,  bulb  and  cord. 

The  early  predominance  of  the  lower  centres  is  slowly  reduced  into- 
subjection  as  the  higher  controlling  centres  develop.  The  reflex  activities 
of  these  lower  centres  are  therefore  unduly  prominent  in  infancy,  are  under 
inefficient  control,  and  react  with  abnormal  violence  to  slight  stimuli. 

Defects,  such  as  occur  in  imbeciles  and  allied  cases,  and  delay  of  develop- 
ment from  interference  with  nutrition,  affect  the  higher  undeveloped 
centres  to  a  much  greater  extent  than  those  structurally  and  functionally 
perfect. 

All  disorders  of  nutrition,  e.g.  rickets,  and  all  causes  leading  to  mal- 
nutrition result  in  the  persistence  of,  or  a  return  to,  the  infantile  state  with 
its  imperfect  control  over  the  lower  nerve-centres.  The  whole  nervous, 
system  is  affected,  and  convulsions  readily  occur  and  are  almost  invariably 
generalised.  Localised  or  unilateral  convulsions  are  commonly  due  to 
local  cerebral  causes.  If  due  to  an  apparently  generalised  cause,  the 
unilateral  character  can  be  explained  by  an  unequal  instability  of  the 
different  motor  cells,  or  an  unequal  distribution  of  the  exciting  factor  by 
reason  of  circulatory  or  lymphatic  inequalities. 

Experimental  results  are  not  of  much  pathological  value.  Con- 
vulsions have  been  produced  in  rabbits  by  suddenly  cutting  off  the  blood 
supply  to  the  brain,  by  mechanical  irritation  of  the  floor  of  the  fourth 
ventricle,  and  by  lesions  of  the  sciatic  nerve  but  not  of  the  brachial  plexus  in 
pigeons  and  guinea  pigs.  Fits  have  been  ascribed  to  vascular  anaemia, 
such  as  follows  severe  haemorrhage  ;  and  to  vascular  engorgement  of  the 
brain  and  its  membranes,  a  condition  frequently  found  after  death,  and 
possibly  a  result,  not  the  cause.  Engorgement  of  the  right  side  of  the 
heart  and  the  lungs  may  be  present  as  a  result  of  the  asphyxia  rather  than  . 


Spasmodic  Functional   Neuroses.  737 

the  cause  of  tlie  fit.  Convulsions  in  the  course  of  whooping  cough  are  due 
to  vascular  engorgement,  thrombosis,  or  haemorrhage.  There  is  rarely  any 
evidence  of  causation  after  death  except  in  cases  of  gross  organic  disease. 

Classification. — On  pathological  grounds  convulsions  are  divisible 
into  groups  according  to  their  dependence  on  defective  inhibition  and 
reflex  irritability,  auto-intoxication,  epilepsy,  rickets,  and  spasmophilia. 
Eclampsia  infantum,  as  a  spasmophilia,  must  piesent  the  signs  thereof 
between  the  attacks,  no  fever,  and  no  evidence  of  disease  or  toxaemia. 
On  anatomical  grounds  they  are  classified  into  : — (1)  those  in  idiotic  or 
imbecile  children  ;  (2)  those  in  children  with  hemiplegia  or  secondary 
contractures  ;  and  (3)  cases  in  which  there  is  no  organic  nerve  lesion, 
including  eclampsia  oi  external  fits,  and  spasm  of  the  glottis  or  internal 
fits. 

Inward  convulsions  is  a  term  often  used  for  attacks  of  temporary  pallor 
and  apparently  momentary  unconsciousness.  The  child  is  still  and  rather 
stiff,  moans  and  grins,  with  upturned  eyes,  clenched  fists  and  thumbs 
flexed  in  the  palms.  The  legs  may  be  drawn  up  at  frequent  intervals.  These 
may  be  mild  attacks  of  laryngospasm  and  are  sometimes  called  "  holding 
breath  spasms."  Occasionally  they  are  slight  syncopal  attacks,  due  to  colic 
or  pressure  of  a  dilated  stomach  on  the  heart,  and  less  often  truly  epileptic. 

Agonal  convulsions  are  convulsive  movements  occurring  just  before  or 
at  the  time  of  death  and  simply  a  mode  of  dying.  It  is  due  to  the  frequency 
of  convulsive  movements  of  this  type  that  fits  are  regarded  as  common  in 
infancy.  Screaming  convulsions  are  violent  screaming  attacks  in  infancy 
due  to  pain,  usually  colic,  occasionally  organic  brain  disease.  Sometimes 
they  indicate  mental  deficiency. 

Etiology. — Idiopathic  fits  are  those  for  which  there  is  no  apparent  cause, 
and  possibly  epileptic.  Symptomatic  fits  are  due  to  cerebral  causes,  reflex, 
toxic,  asphyxial,  or  circulatory  in  origin,  or  are  a  mode  of  dying.  The  more 
carefully  fits  are  investigated  in  infancy,  the  rarer  is  the  diagnosis  made  of 
an  idiopathic  origin.  Toxic  causes,  e.g.  fevers,  uraemia,  food  toxins,  poisons, 
alcohol  and  narcotics,  are  often  difficult  to  recognise. 

The  predisposing  factors,  those  which  produce  instability  or  irri- 
tability of  the  nervous  system,  are  inherited  or  acquired.  Slight  causes 
will  produce  fits  in  the  predisposed.  The  predisposing  factors  dependent 
on  age  and  development  are  common  to  all  infants,  yet  only  a  small 
proportion  have  fits.  If  the  exciting  cause  can  be  discovered,  the  results 
of  treatment  are  more  likely  to  be  satisfactory. 

Heredity. — A  family  history  of  organic  or  functional  nervous  disease, 
a  neurotic  temperament,  insanity,  suicide,  immorality  or  excessive  drinking, 
renders  an  infant  more  liable  to  fits.  In  some  families  all  or  most  of  the 
children  suffer  from  infantile  convulsions.  Undue  prominence  has  been 
given  to  heredity  on  account  of  its  influence  on  the  production  of  epilepsy. 

3  B 


738  Chapter  LVI. 

In  a  great  many  instances  the  children  of  such  parentage  do  not  have  fits 
in  infancy.  Even  when  they  do,  it  is  possible  that  the  underlying  cause 
may  be  found  in  the  mode  of  feeding  rather  than  in  the  family  history. 
Heredity  has  extremely  little  influence  per  se  during  the  first  3  years  of  life. 
I  could  only  obtain  a  family  history  of  epilepsy,  suicide  or  insanity  in  5  out  of 
200  successive  cases.  It  is  possible  that  alcoholism  in  the  mother  may  affect 
the  child  through  the  fcetal  circulation.  That  an  alcoholic  father  can  exert 
much  influence  on  the  germ  plasm  is  most  unlikely.  If  one  or  both  parents 
are  alcoholic,  other  factors  are  present  which  impair  the  nutrition  of  the 
child.  There  may  be  gastric  disturbance  in  the  mother  leading  to  dele- 
terious changes  in  the  milk,  insufficient  food  and  clothing,  and  chronic 
or  occasional  neglect  of  the  child.  These  factors  are  quite  enough  to  account 
for  the  fits,  without  ascribing  them  to  the  hereditary  influence  of  alcohol. 
Tuberculosis  and  other  diseases  of  malnutrition  in  the  parents  exert  a 
predisposing  influence  in  that  the  child  may  be  delicate  at  birth.  Provided 
the  parents  are  healthy  little  attention  need  be  paid  to  consanguinity  or 
great  difference  in  their  respective  ages. 

Age. — Most  fits  occur  before  the  completion  of  the  first  dentition.  Out 
of  300  successive  cases  44  began  in  the  first  6  months,  52  in  the  second 
6  months,  76  in  the  second  year,  and  44  in  the  third  year.  No  less  than 
216  were  under  3  years,  27  in  their  fourth  year,  and  the  remainder  under 
12  years.  From  the  fifth  to  the  twelfth  year  there  is  little  difference  in  the 
yearly  age-incidence.  In  those  who  have  already  suffered,  there  is  a 
slightly  increased  liability  at  the  onset  of  the  second  dentition. 

Undue  importance  has  been  attributed  to  rickets.  Neither  its  bone 
changes  nor  craniotabes  explain  the  convulsive  phenomena.  These  are 
really  due  to  the  dietetic  and  other  conditions  which  give  rise  to  the 
xickets.  The  frequent  coincidence  of  rickets  and  fits  is  because  rickets 
develops  at  the  age  when  the  child  is  likely  to  have  unsuitable  food.  Fits 
are  not  much  more  common  in  the  second  than  in  the  first  6  months  of  life, 
and  rather  more  frequent  during  the  first  than  the  second  year,  when  rickets 
is  most  marked.  It  must  be  regarded  as  a  predisposing  cause,  mainly  on 
account  of  its  complications  and  partly  because  it  impairs  the  nutrition 
of  the  nervous  tissues. 

The  cerebral  causes  are  organic  diseases  of  the  central  nervous  system 
such  as  concussion,  meningitis,  encephalitis  and  sclerosis  ;  haemorrhage, 
thrombosis  and  embolism ;  porencephalus,  microcephalus  and  hydro- 
cephalus ;  tumour,  abscess  and  parasitic  growths.  The  affections  leading 
to  cerebral  hemiplegia  are  the  most  common.  Fright  is  a  definite  exciting 
cause  in  a  few  children. 

Asphyxia  explains  some  cases  in  which  there  is  interference  with 
respiration.  The  venous  blood  directly  irritates  the  motor  cells,  e.g. 
cyanosis  in  the  newborn  and  cerebral  congestion  during  whooping  cough. 


Spasmodic  Functional   Neuroses.  739 

Possibly  some  of  the  fits  in  whooping  cough  and  hydrocephalus  are  due  to 
•changes  in  cerebral  pressure. 

Fever  may  be  ushered  in  by,  or  associated  with  fits,  though  they  are 
Tare  at  the  onset  of  specific  fevers,  unless  the  child  has  had  them  before. 
They  may  occur  in  any  specific  febrile  infection,  general  infective  disorders, 
throat  affections  and  even  herpes  ;  through  the  action  of  the  toxins  or 
micro-organisms,  rather  than  the  height  of  the  fever.  Occasionally  they  are 
•due  to  hyperpyrexia  or  heat-stroke.  Toxcemic  conditions  include  fevers, 
uraemia,  burns,  blisters,  and  food  poisoning.  Uraemic  fits  have  been  recorded 
in  the  first  month  of  life.  The  importance  of  food  poisoning  cannot  be 
•overrated.  In  many  instances  the  cause  is  not  a  mechanical  one  but  lies 
in  the  absorption  of  intermediate  products  of  protein  digestion,  or  some 
toxin,  produced  in  the  food  before  or  aftei  ingestion,  acting  directly  on  the 
•central  nervous  system.  Poisons  such  as  lead,  alcohol  and  narcotics  are 
•occasionally  to  blame.  In  country  districts  poisonous  berries  and  fungi  are 
not  infrequent  causes. 

Gastro-intestinal  disturbance,  inducing  colic,  is  very  common  in  infancy. 
The  younger  the  child  the  more  probably  is  some  indigestible  article  of  food 
■the  cause  of  the  convulsion.  Under  6  months  of  age  the  attack  is  frequently 
•due  to  cow's  milk,  boiled  bread  and  starchy  food,  especially  proprietary 
foods  consisting  mainly  of  starch.  In  older  children  I  have  seen  convulsions 
•due  to  pork,  bacon,  haddock,  bread  and  cheese,  peas,  currants,  cherries, 
strawberries  and  other  indigestible  foods.  The  influence  of  diet  decreases 
as  age  advances.  Thus,  the  attack  was  ascribed  to  dietetic  causes  alone  in 
22  out  of  31  infants  under  6  months  of  age,  in  10  out  of  30  in  the  second 
half  of  the  first  year,  and  in  only  8  out  of  32  in  the  second  year  of  life.  A 
typical  and  severe  instance  was  that  of  an  infant  brought  up  from  birth  on 
•cow's  milk  and  Mellin's  food.  Fits  began  on  the  seventh  day.  On  a  diet 
•of  humanised  milk  they  ceased  for  a  week,  and  then  recommenced  at  the 
xate  of  20-30  a  day.  Bromides  and  belladonna  proved  useless.  At  9  weeks 
of  age  a  modified  milk  mixture  was  ordered,  containing  only  0-5  per  cent,  of 
protein.    The  fits  immediately  ceased  and  did  not  recur. 

Other  sources  of  reflex  irritation  are  dentition  (p.  225),  worms  (p.  311), 
foreign  bodies  in  various  orifices,  chiefly  the  ear  and  nose  ;  boils  in  the 
•external  auditory  meatus  and  diseases  of  the  middle  ear  ;  inflammatory 
affections  of  the  nose  and  throat,  polypi  and  adenoids  ;  a  tight  phimosis, 
irritation  from  retained  smegma  and  balanitis  ;  severe  injury  to  cranial  or 
spinal  nerves,  sudden  and  severe  pain  in  any  part  of  the  body,  burns,  renal 
•or  intestinal  colic,  intestinal  strangulation  and  retention  of  urine.  Errors 
•of  refraction  and  astigmatism,  over-pressure  at  school,  examinations,  anxiety, 
fright,  shock,  masturbation  and  menstrual  disorders  have  all  been  blamed. 
Some  of  the  causes  mentioned  may  be  partly  reflex  and  partly  toxic  in  their 
action.  There  is  little  doubt  that  too  much  importance  is  attached  to 
Teflex  causes.    That  a  reflex  source  of  irritation  is  present,  is  no  proof  that 


740  Chapter  LVI. 

it  is  the  exciting  factor.  I  have  never  known  phimosis,  for  instance,  induce 
a  fit,  although  it  is  invariably  mentioned  in  text  books  as  a  cause.  Fits  have 
coincided  regularly  with  teething  and  have  recurred  at  the  onset  of  the 
second  dentition.  None  of  the  various  factors  is  in  my  experience  of  much 
importance  as  an  exciting  cause  in  comparison  with  those  dependent  on 
diet.  Mere  overloading  of  the  stomach  is  a  trivial  factor.  The  fit  usually 
comes  on  when  the  food  has  passed  into  the  intestine.  Occasionally  it  is 
due  to  mechanical  irritation  of  the  pylorus  by  indigestible  food. 

Symptoms. — Premonitory  signs  are  generally  absent.  A  certain 
amount  of  importance  can  be  attached  to  restlessness,  anxious  fades, 
twitching  of  the  muscles  of  the  face  or  eyelids,  screwing  up  the  mouth,  and 
screaming  attacks.  All  these  may  be  due  to  emotion,  flatulence,  colic  or 
teething.  Signs  of  nervous  irritability  and  gastric  or  intestinal  disturbance 
must  be  regarded  as  warnings. 

The  onset  is  generally  sudden.  In  a  mild  attack  the  face  turns  pale,  the 
eyes  are  fixed  and  up-turned,  breathing  shallow,  and  a  certain  amount  of 
rigidity  supervenes.  Then  the  child  takes  a  deep  breath  and  comes  round. 
In  severe  attacks  there  are  sudden  pallor,  unconsciousness,  tonic  spasms, 
clonic  spasms,  irregular  breathing,  cyanosis  and  sweating,  followed  by 
subsidence  of  the  spasms,  relaxation  and  return  to  consciousness.  The 
muscular  twitchings  begin  in  the  facial  or  ocular  muscles,  or  in  the  limbs, 
and  rapidly  involve  the  whole  body.  The  facial  spasm  causes  violent 
contortion  of  the  features,  hideous  grimaces.  The  head  is  retracted,  the 
back  arched  ;  the  elbows  flexed,  wrists  bent,  hands  clenched  and  thumbs- 
in-turned  ;  the  legs  rigidly  extended.  General  tonic  spasms  of  the  limbs- 
ensue.  A  slight  froth  collects  on  the  lips  and  clammy  sweat  on  the  fore- 
head. The  child  is  unconscious,  with  wide-open  eyes  and  immobile  pupils. 
Breathing  is  shallow,  feeble  and  often  spasmodic.  The  pulse  is  weak, 
frequent  and  perhaps  irregular.  Soon  the  face  reddens,  the  lips  become 
bluish  ;  mucus  collects  in  the  throat  and  produces  "  the  rattles  "  ;  and  the 
bladder  and  rectum  may  be  emptied,  though  the  actual  secretion  of  urine 
is  suspended  or  scanty.  Gradually  the  tonic  spasms  are  replaced  by  clonic 
ones,  which  soon  cease,  and  the  child  falls  asleep.  The  cyanosis  is  due  to 
inefficient  breathing  and  obstruction  to  the  free  entry  of  air  into  the  lungs. 
by  falling  back  of  the  base  of  the  tongue. 

The  actual  duration  varies  from  a  few  seconds  to  several  hours.  A  mild 
attack  is  soon  over  and  the  child  seems  normal  in  a  few  minutes.  In  the 
prolonged  cases,  the  status  eclampticus,  the  spasms  may  persist  throughout 
but  more  often  there  are  periods  of  relaxation  and  exacerbation.  After  an 
attack  there  is  considerable  prostration,  muscular  relaxation,  and  sometimes, 
temporary  paralysis  of  one  or  more  limbs.  Death  is  unusual,  unless  there 
is  organic  brain  disease  or  a  profound  toxeemic  exciting  cause.  Even  a  mild 
fit  may  prove  fatal  in  a  very  young  infant. 


Spasmodic  Functional   Neuroses.  741 

Sequels  are  rare,  except  temporary  loss  of  power,  aphasia,  and  mental 
<1  ulness.  Cases  of  amaurosis  have  followed  frequent  fits,  with  stupor  or 
coma  for  some  hours  or  days.  This  is  sometimes  called  "  Post- eclamptic 
Blindness,"  and  has  been  ascribed  to  exhaustion  or  anesthesia  of  the 
visual  cortical  centre,  due  to  the  fits.  Out  of  1 1  collected  cases  under  3  years, 
S  were  under  18  months,  an  age  when  basal  meningitis  is  most  common. 
In  some  of  them  the  persistence  of  hemiplegia  was  suggestive  of  organic 
•cerebral  disease.     The  sight  is  usually  regained. 

Diagnosis. — There  is  no  difficulty  in  recognising  fits  that  are  actually 
occurring  but  a  diagnosis  based  on  the  history  of  the  case  is  unreliable  in 
slight  attacks.  A  mild  fit  may  be  mistaken  for  syncope,  and  attacks  of 
iaryngospasm,  faintness  or  colic  ascribed  to  fits.  Even  the  movements  of 
thigh-friction  are  sometimes  called  fits.  Age  has  an  important  bearing  on 
the  diagnosis  of  the  cause.  Eclampsia  neonatorum  is  due  to  injury  at  birth, 
•cyanosis  or  sepsis.  Fits  beginning  after  the  second  week  of  life  are  rarely 
•due  to  injury  at  birth.  In  the  pre-dentition  period  the  common  causes  are 
diet,  meningitis  and  otitis.  Diet  exerts  a  potent  influence  during  the  first 
•dentition  and  rickets  is  often  present.  Subsequently,  up  to  the  second 
dentition  colic  and  toxaemia  are  the  most  important  causes.  Alimentary 
disturbance  or  the  ingestion  of  unsuitable  food  may  be  ascertained  by  inquiry 
•and  examination.  Always  ask  what  food  the  child  has  had  during  the 
previous  24  hours  and  inspect  the  vomit  and  stools,  if  any.  Fever  is  a  sign 
•of  acute  disease  or  severe  food  poisoning.  The  cause  of  the  fever  may  not 
be  certain  for  a  few  days.  In  some  cases  there  is  obviously  asphyxia  or  a 
•disease  likely  to  cause  asphyxia.  In  doubtful  cases  look  for  albuminuria. 
A  unilateral  distribution  occurs  in  Jacksonian  epilepsy  ;  prolonged  un- 
consciousness, if  there  is  an  organic  cerebral  cause  ;  and  petit  mal  in  serious 
■cerebral  defect.  Epilepsy  cannot  be  diagnosed  with  certainty  during 
infancy.  Stuporous  sleep  after  a  mild  fit  is  suggestive.  The  presence  of  a 
•definite  morbid  cause  is  in  favour  of  eclampsia  but,  though  the  fits  at  first 
are  eclamptic,  they  may  pass  into  true  epilepsy  without  any  clear  dividing 
line.  Occasionally  multiple  fits  occur  for  which  no  cause  can  be  ascertained. 
Eclamptic  fits  due  to  spasmophilia  may  occur  up  to  the  eighth  year  of  age 
and  can  only  be  distinguished  from  epilepsy  by  the  evidence  of  spas- 
mophilia between  the  attacks. 

Prognosis. — The  danger  of  a  single  convulsion  or  multiple  attack 
is  much  overrated.  Only  in  the  very  young,  the  very  rachitic  or  the 
profoundly  marasmic  is  death  probable  as  the  immediate  result.  Recovery 
ni.sued  in  the  case  of  a  child  who  was  collapsed,  sweating  freely,  with 
•dilated  pupils  and  no  corneal  reflex,  pulse  156,  respirations  72,  T.  103-105°  F. 
The  convulsions  had  been  going  on  for  12  hours  and  were  due  to  cerebro- 
spinal meningitis.  The  prognosis  depends  on  the  cause,  the  duration,  the 
-age  and  the  family  history.  Fits  due  to  cerebral  disease  are  the  least 
•amenable  to  treatment,  and  the  prognosis  is  that  of  the  primary  affection. 


742  Chapter  LVI. 

In  other  cases  the  older  the  child  the  less  likely  is  the  attack  to  prove* 
fatal.  In  late  stages  of  fevers  the  outlook  is  serious  for  the  nervous  system 
is  affected  by  toxins.  Ursemic  fits  are  not  necessarily  fatal  although  the' 
child  may  be  only  kept  alive  by  artificial  respiration  for  several  hours. 
If  the  fit  is  of  gastro-intestinal  origin,  the  child  may  never  have  another,, 
provided  it  is  properly  dieted.  During  an  attack  the  prognosis  increases- 
in  gravity  with  the  duration,  the  degree  of  asphyxia  and  general  prostration, 
the  feebleness  of  the  pulse,  and  the  depth  of  the  coma.  The  outlook  of 
status  eclamptieus  is  bad.  The  longer  the  interval  between  successive  fits- 
the  better  is  the  prospect,  for  drugs  and  other  measures  have  a  chance  to- 
exert  their  effects. 

Excluding  organic  causes  the  prognosis  is  good  as  regards  recurrence 
but  varies  directly  as  the  hereditary  predisposition.  The  probability  of 
epilepsy  is  least  when  there  is  a  definite  cause.  Infantile  fits  may  be  limited 
to  a  single  attack  ;  may  be  multiple  and  cease  in  a  few  months  ;  may  be- 
continued  into  life-long  epilepsy  ;  or  may  cease  and  recur  after  puberty 
or  later  in  life.  The  primary  fit  and  the  residual  state  of  the  nervous- 
tissues,  with  its  tendency  to  recurrent  explosive  discharges,  are  greatly 
influenced  by  heredity.  Usually  the  tendency  to  fits  dies  out  as  the 
higher  nerve  centres  acquire  control  over  the  lower  ones. 

Except  in  cases  where  the  fits  are  very  frequent,  or  very  severe,  and 
persist  for  a  number  of  years  it  is  uncommon  for  them  to  produce  any  effect 
on  intelligence.  After  multiple  fits  a  baby  may  remain  drowsy  and  stupid 
for  weeks  and  yet  recover.  Moral  and  general  character  are  more  likely  to' 
be  affected  than  intelligence.  The  child  becomes  mischievous,  destructive,, 
irritable,  bad-tempered,  and  perhaps  a  moral  lunatic.  The  psychical  defects- 
may  be  due  to  maldevelopment  or  changes  in  the  brain,  which  are  the  cause 
of  the  fits.  Local  convulsions  are  more  likely  than  genera]  ones  to  be  due 
to  organic  brain  disease.  If  no  cause  can  be  found  and  the  fits  are  frequent,, 
the  prognosis  is  bad  as  regards  life  and  subsequent  mental  development- 
It  is  advisable  to  be  reticent  in  foretelling  evil,  in  laying  stress  on  bad 
family  history  and  in  diagnosing  amentia.  Enlarge  on  the  favourable- 
features  of  the  case  and  the  benefits  of  care  and  attention. 

Epilepsy. — The  epileptic  fit  is  a  type  of  convulsions  of  unknown 
pathology.  According  to  Gowers  10  per  cent,  of  the  cases  begin  in  infancy.. 
The  slight  fits  of  infancy  may  pass  into  petit  mal  without  the  change  being 
recognised.  A  diagnosis  of  epilepsy  was  made  in  55  out  of  300  cases  of  fits- 
in  children  under  12  years  old  : — 15  of  them  had  fits  during  the  first  2  years- 
of  life  ;  2  of  these  were  more  or  less  imbecile,  and  in  6  others  there  was  a 
family  history  of  mental  affections.  In  only  13  out  of  the  55  was  there  a 
history  of  family  predisposition.  The  earliest  age,  at  which  epilepsy  was- 
diagnosed,  was  6  months  and  the  subsequent  course  proved  the  diagnosis- 
correct.  In  44  out  of  84  cases  between  the  ages  of  3  and  12  years  the  fits- 
were  regarded  as  epileptic. 


Spasmodic   Functional   Neuroses.  743 

The  etiology  is  similar  to  that  of  infantile  convulsions  and  includes  all 
cerebral  causes,  congenital  and  acquired.  A  meningeal  haemorrhage  at  birth 
may  be  slight,  produce  little  or  no  apparent  damage,  and  only  fits  in  child- 
hood or  later  life.  Too  much  importance  is  attached  to  infantile  convulsions. 
If  eclampsia  is  a  spasmophilia  and  epilepsy  is  not,  there  is  small  probability 
of  the  transference  of  one  into  the  other.  Statistics  are  of  little  value. 
Fletcher  Beach  states  that  hereditary  taint  is  present  in  more  than  one- 
third  of  the  cases  in  the  form  of  epilepsy,  insanity,  eccentricity  or  chronic 
neuralgia.  Spratling  found  a  family  history  of  epilepsy,  alcoholism, 
tuberculosis  or  insanity  in  over  50  per  cent,  of  1100  cases.  True  hereditary 
epilepsy  is  more  frequently  transmitted  through  the  mother  than  the  father, 
and  may  skip  a  generation.  The  chief  exciting  causes  are  alimentary 
disturbance  and  toxaemia.  The  foundation  of  the  attack  may  be  laid  in 
school  life  or  earlier,  by  unsuitable  meals,  constipation,  or  an  excessive 
nitrogenous  diet  which  unduly  stimulates  the  nervous  system. 

Idiopathic  Epilepsy  assumes  various  forms.  The  name  is  given  to  those 
cases  in  which  there  is  no  apparent  cause  and  no  definite  organic  change. 
It  begins  at  6-15  years  of  age.  Cases  starting  in  earlier  life  are  likely  to 
be  symptomatic  or  secondary.  The  patients  are  usually  dull,  stupid  and 
unemotional,  but  in  good  health.  The  symptoms  are  much  the  same  as  in 
adults.  A  fit  may  be  preceded  for  hours  or  days  by  irritability,  excitabilit}-, 
depression,  headache,  giddiness  or  digestive  disturbance.  A  definite  aura 
is  ascertained  with  difficulty  in  young  children  and  is  absent  if  consciousness 
is  quickly  lost.  It  may  be  motor,  sensory,  or  psychical  in  character.  A 
motor  spasm  or  twitching  usually  starts  in  the  thumb  and  spreads  upward. 
Tingling  or  numbness  may  have  a  similar  distribution.  Epigastric  dis- 
comfort, nausea  or  vomiting  is  the  most  common  visceral  aura.  Vertigo, 
fear,  hallucinations  and  illusions  occasionally  occur,  and  sometimes  auditory, 
visual,  olfactory  or  gustatory  aura?.  A  girl,  9  years  old,  stated  that  an  ugly 
bearded  black  man  seized  her  by  the  right  upper  arm  and  cut  her  head  off. 
A  14-year  old  boy  felt  thirsty  before  the  fits.  In  nocturnal  epilepsy  the  fits 
only  occur  during  sleep,  and  the  diagnosis  depends  on  involuntary  micturition 
or  defecation  and  drowsiness  in  the  morning.  Perhaps  the  tongue  is  bitten 
and  small  ecchymoses  may  be  found  in  the  skin. 

Haul  Mai  is  characterised  by  loss  of  consciousness,  tonic  spasms  up 
to  forty  seconds  duration,  clonic  spasms  with  lateral  deviation  of  the  head 
and  eyes  for  perhaps  2  minutes,  and  complete  stupor.  The  child  may  utter 
a  sudden  cry  at  the  onset.  Either  the  tonic  or  clonic  spasm  may  be  absent. 
The  child  recovers  in  about  a  quarter  of  an  hour,  or  may  not  fully  regain 
consciousness  for  about  an  hour  and  is  then  very  irritable.  Temporary 
paralysis  and  aphasia,  automatism,  mania,  hallucinations  and  illusions  are 
occasional  sequels.  Cyanosis,  foaming,  and  loss  of  knee  jerks  are  present  in 
the  period  of  unconsciousness  ;  in  the  stage  of  clonic  spasms  the  knee  jerks 
are  exaggerated  and  the  tongue  may  be  bitten.     The  sphincters  become 


744  Chapter  L  VI. 

relaxed  and  there  is  general  flaccidity.  This  may  be  followed  by  temporary 
con3ciousness  and  vomiting,  or  end  in  stuporous  sleep  and  perhaps  intense 
headache  on  waking.  Subsequent  examination  may  reveal  punctate 
ecchymoses,  spots  like  flea-bites,  on  the  neck  and  shoulders,  injected 
conjunctivae,  a  bitten  tongue  and  bronchi  filled  with  froth.  Between  the 
fits  there  are  noted  bodily  and  mental  exhaustion,  and  gradual  deteriora- 
tion in  character.  The  child  becomes  silly,  quarrelsome,  spiteful,  violent 
or  imbecile. 

Petit  Mai  is  associated  with  intractable  epilepsy  and  may  precede  it  by 
a  number  of  years.  Consciousness  is  lost,  impaired  or  clouded  ;  the  patient 
may  respond  to  orders.  Convulsions  are  absent,  or  rudimentary  and 
atypical.  There  may  be  a  momentary  pause  during  speaking  ;  faintness 
and  mental  confusion  ;  pallor,  fixation  of  the  eyes,  dilated  pupils  and 
dazed  look ;  an  aura  with  transient  unconsciousness  ;  or  momentary 
giddiness  with  short  loss  of  consciousness  during  which  the  child  may  fall 
and  have  slight  tonic  spasms  and  enuresis.  In  rare  instances  it  takes  the  form 
of  apparently  a  mere  trick,  e.g.  slow  rotation  of  the  head,  localised  t  witchings, 
and  nodding  or  procursive  epilepsy.    The  pupils  are  dilated  and  fixed. 

Procursive  Epilepsy  is  peculiar  to  childhood  and  youth.  It  causes 
involuntary  movement  forward,  generally  a  loud  cry,  unconsciousness,  and 
seldom  an  aura.  It  may  last  for  many  years  before  merging  into  ordinary 
epilepsy.  It  is  usually  associated  with  a  sclerotic  cerebral  lesion  but  may 
occur  without  demonstrable  alteration  in  the  nerve  centres.  It  is  often 
complicated  by  moral  insanity. 

Ambulatory  Epilepsy  is  rare  in  childhood ;  so  too  psychic  epilepsy,  in 
the  form  of  aurae  and  maniacal  excitement  or  depression.  It  may  alternate 
with  fits.  Automatic  actions  and  a  maniacal  state  may  initiate,  take  the 
place  of,  or  follow  a  fit.  A  girl,  aged  4  years,  had  a  mild  fit  and  remained 
in  a  very  excitable  state  threatening  to  "  end  "  herself,  cut  off  her  nose, 
etc.  Dreamy  mental  states  may  take  the  place  of  petit  mal  or  occur  in 
conjunction  with  epilepsy.    They  are  often  merely  due  to  brain  exhaustion. 

JacJcsonian  Epilepsy  depends  on  a  unilateral  local  cerebral  lesion.  The 
spasm  begins  locally,  and  may  remain  limited  or  terminate  in  general  con- 
vulsions. It  usually  begins  in  the  hand  or  face.  If  bilateral,  one  side  is 
affected  first  and  most.  The  past  history  is  very  important.  Most  cases 
are  associated  with  hemiplegia  and  begin  with  a  severe  convulsion  during 
the  first  3  years  of  life,  lasting  on  and  off  for  several  hours,  or  perhaps  a 
single  fit.  The  unilateral  character  may  be  present  at  the  onset.  The  first 
attack  often  comes  on  during  an  acute  fever,  whooping  cough,  the  pros- 
tration of  severe  illness,  or  after  injury.  Congenital  defects  of  the  brain 
account  for  a  certain  number.  The  initial  fit  or  series  of  fits  may  be  followed 
by  recurrence  for  a  month  or  two,  or  after  an  interval  of  a  few  years.  Complete 
continuity  is  not  very  common.  The  subsequent  fits  are  apparently  due  to 
sclerosis.     Indications  of  cerebral  palsy  may  be  present  in  the  form  of 


Spasmodic  Functional   Neuroses.  745 

asymmetry  of  the  face  and  skull,  slight  difference  in  the  size  of  the  limbs, 
possibly  a  short  leg  or  scoliosis,  left-handedness  and  mental  backwardness. 

Diagnosis. — In  true  epilepsy  the  first  fit  is  short  and  like  the  succeeding 
ones.  Both  convulsions  and  unconsciousness  may  be  absent.  In  secondary 
epilepsy  the  first  fit  is  often  very  prolonged  and  indicative  of  the  toxsemic 
or  infective  cerebral  disease.  Subsequent  attacks  become  shorter  and  more 
like  true  epilepsy.  Many  fits  may  follow  quickly  after  the  first,  whereas  in 
true  epilepsy  the  intervals  are  prolonged.  Secondary  epilepsy  is  little 
influenced  by  bromides  ;  and  the  patients  are  often  excitable  and  emotional. 
The  blood  shows  no  changes  in  pure  epilepsy  ;  in  other  forms  there  may  be 
leucocytosis  and  eosinophilia  at  the  time  of  the  fits,  suggestive  of  a  toxsemic 
origin. 

Prognosis. — Epilepsy  shortens  life.  Death  occurs  from  status  epilep- 
ticus  in  25,  pulmonary  phthisis  in  25,  and  heart  disease  in  10  per  cent.,  and 
in  the  remainder  from  pneumonia  and  other  lung  affections,  gastro- 
intestinal derangements  and  malnutrition.  Very  few  die  from  asphyxia  or 
injury  during  a  fit.  Recovery  takes  place  in  less  than  10  per  cent.  It  may 
occur  though  the  fits  are  very  numerous.  Thus  a  boy,  4  years  old,  had 
many  fits  for  9  months,  even  273  in  10  days.  No  cause  was  found  and  the 
fits  entirely  ceased,  leaving  no  ill  effects.  Mental  enfeeblement  and  dementia 
come  on  eventually  in  most  cases.  Petit  mal  and  nocturnal  epilepsy  are  the 
least  amenable  to  treatment.  In  view  of  the  grave  prognosis  and  the  fact 
that  some  oases  follow  eclampsia,  it  is  of  the  utmost  importance  to  prevent 
infantile  convulsions  and  their  recurrence. 

Treatment. —  Of  Infantile  Convulsions. — When  summoned  to  a  child 
in  a  fit  the  doctor  should  take  with  him  chlorofoim,  chloral  hydrate  solution 
of  known  strength  and,  though  less  necessary,  amyl  nitrite,  solution  of 
morphia  and  a  hypodermic  syringe.  As  soon  as  the  fit  starts  the  child  should 
be  laid  down,  with  the  head  a  little  raised  and  the  clothes  loosened  or 
removed.  He  must  be  kept  quiet  and  not  disturbed  more  than  necessary. 
A  hot  or  mustard  bath,  or  a  mustard  pack,  relieves  colic  and  may  reduce 
congestion  of  the  brain  by  dilating  the  vessels  of  the  skin.  Apply  cold  to  the 
head  at  the  same  time.  If  there  is  high  fever,  cool  the  bath  down  to  60°  F. 
The  bath  should  not  be  given  for  fits  due  to  syncope  or  collapse  of  the  lung. 
Give  inhalations  of  chloroform  to  control  the  spasms  until  other  measures 
can  exert  their  effect. 

Empty  the  lower  bowel  by  an  enema  of  glycerine,  salt  solution,  or 
sodium  sulphate  dr.  1-4  in  water  5-10  oz.  After  the  bowels  have  acted, 
or  even  before  in  bad  cases,  give  a  rectal  injection  of  chloral  hydrate grs.  5-10, 
according  to  the  age.  It  can  be  repeated  within  an  hour,  if  necessary. 
'Children  stand  chloral  well.  If  it  is  not  retained,  give  an  injection  of 
morphia  gr.  aV/o  and  atropine  gr.  ^-ho,  to  a  child  of  |-2  years  of  age. 
This  may  also  be  repeated  in  an  hour's  time.  It  is  safer  to  rely  on  chloral 
-and  to  give  chloroform  inhalations  until  the  chloral  begins  to  act.    If  there 


746  Chapter  LVI. 

is  unsuitable  food  in  the  stomach,  it  may  be  evacuated  by  lavage  or 
vomiting,  induced  by  tickling  the  fauces  with  a  feather.  Emetics  are  not 
advisable.  Usually  irritant  food  has  passed  through  the  pylorus  before  the 
fit  occurs.    Oxygen  gas  is  useful  in  cases  of  cyanosis. 

As  soon  as  the  child  can  swallow,  give  a  dose  of  calomel  to  empty  the 
intestines  and  relieve  cerebral  congestion.  Lancing  the  gums  and  leeches 
are  useful  in  cerebral  congestion  caused  by  asphyxia.  Abundant  urination 
may  be  looked  on  as  a  critical  phenomenon  announcing  the  speedy  ter- 
mination of  the  fit.  Active  treatment  can  then  be  discontinued.  For 
idiopathic  multiple  fits  give  chloral  grs.  1-2,  or  more,  every  2  hours  until  the 
fits  have  ceased  for  24-48  hours  and  the  baby  is  almost  too  drowsy  to  swallow- 
Great  care  in  feeding  is  necessary  or  inhalation  pneumonia  may  be  set  up. 
Leave  the  drug  off  gradually. 

After  the  attack  the  child  must  be  kept  quiet  for  a  few  days,  on  a  light 
diet,  the  bowels  carefully  regulated,  and  moderate  doses  of  bromide  given- 
During  sleep  the  room  must  be  well  ventilated,  the  feet  warm  and  the  head 
raised.  All  sources  of  reflex  irritation  should  be  attended  to,  and  any 
disease  present  efficiently  treated.  On  account  of  the  frequent  presence  of 
rickets  cod-liver  oil,  malt  and  iron  are  the  most  useful  drugs  for  the  pre- 
vention of  infantile  convulsions.  With  improved  nutrition  the  central 
nervous  system  becomes  less  liable  to  explosive  disturbance. 

Treatment  of  Epilepsy. — Insane,  feeble-minded  or  imbecile  epileptics 
should  be  kept  in  asylums  or  epileptic  colonies.  An  intelligent  epileptic- 
can  be  brought  up  at  home  in  the  country,  and  live  the  life  of  a  healthy 
animal.  Regular  sleep,  routine  life,  open  air  and  exercise  are  essential.. 
An  efficient  and  valuable  education  can  be  obtained  from  the  objects  of 
country  life.  School-life  is  permissible,  if  the  fits  are  mild  and  infrequent 
and  the  child  mentally  sound.  Over-exertion,  mental  and  physical,  worry 
and  excitement  must  be  avoided.  Boys,  who  have  to  earn  their  living,  should 
be  brought  up  to  country  pursuits  or  some  outdoor  occupation,  involving 
more  or  less  physical  labour  and  no  dangerous  positions  or  exposure  to  great- 
heat.  Careful  attention  must  be  paid  to  the  intestinal  tract,  constipation 
remedied,  and  intestinal  antiseptics  given  if  necessary.  The  diet  should  be 
plain,  unseasoned,  limited  in  amount,  and  contain  little  meat  and  little- 
salt.  Bread  can  be  made  with  bromide  of  soda  (Bromopan).  Alcohol,  tea,, 
coffee,  meat  extracts  and  other  stimulants  must  be  avoided.  As  antiseptics 
give  borax  and  /3-naphthol  grs.  15  daily,  or  salol  grs.  10  in  5  oz.  of  water,, 
night  and  morning.  Many  fits  are  toxic  in  origin  and  can  be  prevented  by  an 
occasional  blue  pill  and  black  draught. 

Bromides,  up  to  drs.  3  daily,  given  night  and  morning,  and  combined 
with  salt  starvation,  should  be  continued  for  2  years  in  bad  cases.  The 
addition  of  opium  is  sometimes  useful.  Borax,  belladonna,  salts  of  zincr 
and  valerianates  are  the  next  best  drugs.  Pot.  iod.  is  sometimes  usefuL 
For  fits  on  rising,  give  a  light  meal  and  medicine  an  hour  beforehand- 


Spasmodic   Functional   Neuroses.  747" 

Treat  nocturnal  fits  with  bromide  and  borax,  and  seek  for  asphyxial  causes.. 
Or  give  a  nightly  dose  of  bromide,  nux  vomica  and  digitalis.  Give  valerian 
if  there  is  any  hysteria  ;  belladonna  for  vasomotor  aurse  ;  bromides  for 
sensory  aurse  ;  morphia  for  motor  aurae  ;  and  cannabis  indica  for  psychical 
auras  and  persistent  headache.  Of  the  bromides  the  strontium  salt  is  the 
least  likely  to  cause  rashes.  Bromide  is  particularly  useful  in  combination 
with  phenazone.  Nux  vomica  can  be  added  to  prevent  depression,  digitalis 
if  the  heart  is  weak,  and  citrate  of  iron  and  ammonia  if  there  is  anaemia.. 
Urethane  may  be  efficacious  when  bromides  fail.  Trephining  sometimes- 
relieves  Jacksonian  epilepsy. 

The  status  epilepticus  may  be  induced  by  constipation,  feverish  attacks,, 
insolation,  alcohol  or  the  sudden  withdrawal  of  bromide.  Death  results  from 
asphyxia,  due  to  prolonged  respiratory  spasm  or  entrance  of  food  into  the 
larynx,  septic  pneumonia  or  intracranial  haemorrhage.  It  is  treated  by 
large  doses  of  chloral  per  rectum,  or  tr.  opii  with  an  equal  quantity  of 
tr.  strophanthi  if  the  heart  is  weak  ;  chloroform  inhalations,  with  oxygen 
if  there  is  asphyxia  ;  a  cold  pack,  if  there  is  high  fever  ;  or  hyoscine  sub- 
cutem.    Venesection  is  rarely  needed. 

Tetany. — Syn.  :  Tetanilla. — This  was  first  described  by  Steinheim  of 
Altona  in  1830,  and  named  "  tetanie  "  by  Corvisart  in  1852.  It  is  a  spasm 
of  the  muscles  which  especially  affects  the  extremities,  notably  the  hands 
and  feet.  The  spasm  is  tonic  in  character  ;  continuous,  intermittent  or 
paroxysmal ;  almost  invariably  symmetrical,  though  occasionally  limited 
to  one  limb.  It  is  of  uncertain  duration,  persists  during  sleep,  and  is  not 
associated  with  loss  of  consciousness  or  impaired  intelligence.  It  is  not 
due  to  organic  nerve  lesions,  though  it  has  been  recorded  in  connection, 
with  cerebellar  tumour. 

Etiology. — The  geographical  distribution  varies  with  climatic  conditions 
and  the  amount  of  attention  devoted  to  childish  ailments.  It  is  most 
frequent  between  November  and  April.  Cold  is  a  predisposing  and  an 
exciting  factor.  Griffith  found  only  50  cases,  38  in  children,  reported  in 
America  (1895).  Family  predisposition  may  be  disregarded.  In  some 
families  the  children  seem  more  liable  than  in  others.  I  have  known  it  occur 
in  2  brothers. 

It  is  infrequent  before  the  fourth  month  and  after  the  third  year,  and 
most  common  in  the  first  2  years  of  life,  especially  from  6-18  months,  when 
rickets  is  prevalent  and  children  are  often  badly  fed.  Out  of  14  successive 
cases  7  were  in  the  first,  5  in  the  second,  and  2  in  the  third  year  of  life  ;  10 
of  them  were  males.  During  the  early  yeavs  of  life  males  are  much  more- 
susceptible  but  at  a  later  age  the  females  preponderate. 

Rickets  is  present  in  quite  half  the  cases  but  tetany  can  occur  with  little 
or  no  evidence  of  it.  Gastric  and  enteric  disorders  are  common  exciting 
causes,  probably  through  toxaemia,  though  occasionally  refiexly  as  in 
painful  pyloric  spasm.    Tetany  occurs  in  dilatation  of  the  stomach  in  adults,. 


748  Chapter  L  VI. 

.and  in  infants  may  be  due  to  dilatation  from  overfeeding,  rickets,  febrile 
diseases,  pneumonia,  and  congenital  hypertrophy  of  the  pylorus.  A  dilated 
stomach  is  a  chronic  disorder.  It  is  the  chronic  alimentary  disturbances 
which  are  associated  with  tetany,  rather  than  acute  attacks  in  which  toxins 
.are  rapidly  eliminated.  It  has  been  reported  in  cases  of  dilated  colon  ; 
disappearing  after  irrigation  but  reappearing  on  accumulation  of  the 
faecal  material. 

Pathology. — It  is  due  to  hyper-excitability  of  the  nerve  cells  in  the  bulb 
and  anterior  cornua,  of  the  nerves  and  of  the  muscles,  due  to  toxaemia. 
Nutritional  and  functional  damage  of  the  nerve  cells  in  the  cord  is  shown 
by  the  muscular  weakness  and  atrophy  sometimes  present.  The  electrical 
reactions  indicate  that  the  upper  neuron  is  not  affected  by  the  toxin.  Eickets 
may  interfere  with  its  development  and  power  of  control  over  the  lower 
neuron.  The  cranial  nerves  are  sometimes  affected  ;  facial  irritability  is 
■common  and  squint  may  develop.  Bilateral  symmetry  and  the  uniform 
•character  of  the  spasm  indicate  a  spinal  affection.  Irregular  distribution  is 
due  to  special  susceptibility  of  certain  nerve  cells  or  unequal  dissemination 
of  the  poison. 

The  poison  is  derived  from  the  products  of  bacterial  activity  or 
imperfect  digestion.  Toxic  bodies  have  been  isolated  from  the  stomach 
but  so  far  tetany  has  not  been  produced  experimentally.  It  is  curious  that 
"tetany  may  be  induced  or  exaggerated  by  lavage  of  the  stomach  in  cases  of 
congenital  pyloric  stenosis.  Stoeltzner  suggests  that  tetany  is  due  to 
■excess  of  lime  salts,  which  are  5  times  as  abundant  in  cow's  milk  as  in 
human  milk.  He  states  that  the  addition  of  chloride  or  acetate  of  lime  to  the 
food  exaggerates  the  symptoms.  The  association  of  rickets  he  explains  as 
■due  to  excess  of  lime  salts  in  the  blood,  because  of  deficient  bone  formation. 
On  the  other  hand  it  has  been  ascribed  to  deficiency  of  lime.  Silvestre 
states  that  the  brain  contains  less  lime  than  normal.  There  is  no  reliable 
■evidence  that  any  component  part  of  pure  milk  is  the  primary  cause. 
Only  one  of  my  cases  was  breast-fed.  The  others  were  having  a  diet  of 
cow's  milk  or  condensed  milk,  and  usually  other  articles  of  food  sufficient 
to  cause  intestinal  derangement.  Kussmaul's  theory  that  it  is  due  to  de- 
hydration of  the  body,  especially  the  muscles  and  nerves,  can  hardly  be  said 
to  hold  water.  Its  relationship  to  the  parathyroids  is  considered  on  p.  208. 
The  most  probable  explanation  is  that  it  is  due  to  an  intestinal  toxin  acting 
■on  nerve  cells  whose  nutrition  is  impaired  by  rickets  or  other  causes. 

Symptoms. — The  spasm  may  come  on  quite  suddenly,  perhaps  during 
an  attack  of  laryngospasm  or  general  convulsions.  Usually  it  develops 
slowly,  in  the  course  of  some  alimentary  complaint  or  during  convalescence. 
Thus  a  boy,  aged  14  weeks,  had  hsernorrhagic  oedema,  probably  angioneurotic 
in  origin,  and  secondary  colitis.  When  convalescent  and  eating  well  he 
•developed  typical  tetany  which  lasted  3  days.  Older  children  may  complain 
■of  premonitory  symptoms  such  as  headache,  malaise,  and  burning,  tingling, 
numbness  or  formication. 


Spasmodic   Functional   Neuroses.  749* 

The  spasm  is  sometimes  only  present  on  waking  from  sleep.    It  begins 
at  the  periphery  and  spreads  upward.     The  hands  are  first  affected,  and 
assume  the  position  known  as  "  the  gynaecological  or  obstetrical  hand  " 
or  "  the  hand  of  the  accoucheur."    The  fingers  are  in  the  attitude  of  holding 
a  pen,  partially  flexed  at  the  metacarpo-phalangeal  and  fully  extended  at 
the  other  joints,  with  their  tips  approximated.    The  thumb  is  fully  extended 
and  adducted,  its  tip  applied  to  the  palmar  surface  of  the  terminal  phalanx 
of  the  first  or  second  finger  ;    or  it  may  be  flexed  across  the  palm.     The 
inner  and  outer  borders  of  the  palms  are  approximated,  hollowing  the 
palm.    The  wrists  are  immobile,  flexed,  tense  and  shiny,  perhaps  red,  and 
drawn  towards  the  ulnar  side.    The  forearm  is  semi-pronated  and  flexed  at 
the  elbow,  and  the  arm  is  adducted.     The  feet  are  rigid  in  the  position  of 
equino-varus,  with  inversion  of  the  sole  and  approximation  of  its  inner  and 
outer  borders.    The  sole  is  contracted  longitudinally  and  becomes  markedly 
concave,  with  a  median  furrow.    The  toes  are  extremely  flexed  and  overlap,, 
or   are  flexed   at  the   metatarso-phalangeal  and   extended   at  the   other 
joints ;    or    the    big    toe    is  hyperextended   and    the   other   toes    flexed. 
The  dorsum  of  the  foot  is  tense,  shiny,   and  perhaps  red.      Both  hands- 
and  feet  may  be  a  little  swollen  with  cedema,  and  this  swelling  may  be 
the  first  sign. 

Commonly  the  hands  alone  are  affected.  Next  in  frequency  come 
the  feet.  Other  muscles  of  the  limbs  may  be  involved.  The  legs  and 
thighs  are  sometimes  flexed  ;  or  the  adductors  may  be  so  strongly  con- 
tracted as  to  cause  crossing  of  the  legs.  Spasm  of  the  neck  and  back 
muscle  produces  retraction  of  the  head,  rigidity  of  the  neck  and  opisthotonos. 
Dyspnoea  may  result  from  spasm  of  the  thoracic  muscles.  Wrinkled  brow, 
pouting  lips,  squint,  trismus  and  risus  sardonicus  are  sometimes  present. 
Difficulty  in  swallowing  and  pupillary  rigidity  have  been  noted.  The 
abdominal  muscles,  bladder,  diaphragm  and  indeed  every  muscle  of  the 
body  may  be  involved.  In  2  cases  I  have  seen  marked  tremor  of  the  head 
and  neck,  and  in  1  of  them  the  hands  and  arms  were  similarly  affected. 
ParsesthesiaB  and  tenderness  in  the  limbs  may  be  present.  Pain,  due  to  the 
cramp-like  spasms  or  to  passive  extension  of  the  muscles,  induces  sudden 
cries. 

Tetany  does  not  cause  fever.  If  present  it  is  due  to  the  intestinal  con- 
dition or  some  complication.  Variable  appetite,  more  or  less  vomiting,  and 
loose  undigested  stools  are  almost  constant.  In  only  one  case  were  the 
stools  normal.  The  knee  jerks  are  variable.  Albuminuria  is  not  infrequent. 
Drowsiness  or  semi-coma  may  be  present  and  a  sign  of  toxaemia.  The  special 
signs  known  as  Trousseau's  phenomenon,  Chvostek's  sign  and  Erb's  sign 
(p.  617)  are  often  present.  Carpopedal  spasm  or  "  Arthrogryposis,"  is  a 
variety  in  which  the  fist  is  clenched,  with  the  thumb  in-turned  and  flexed  and 
the  fingers  flexed  over  it.  The  toes  are  flexed  and  the  big  toe  sometimes 
abducted  and  hyperextended  and  the  heel  drawn  up.  This  variety  of  spasm 
is  seen  in  other  affections,  notably  eclampsia.    In  another  type  the  thumbs 


750  Chapter  L  V  I. 

are  similarly  flexed  and  in-turned,  and  the  fingers  flexed  at  the  metacarpo- 
phalangeal joints  and  hyperextended  at  the  other  joints. 

The  chief  complications  are  laryngospasm,  convulsions,  enteritis, 
bronchitis  and  broncho-pneumonia. 

The  diagnosis  is  based  on  the  character  of  the  spasm.  "Latent" 
tetany  is  associated  with  rickets,  alimentary  disturbance,  laryngospasm, 
•convulsions  and  the  various  accessory  phenomena.  Occasionally  the  spasm 
is  typical  in  one  attack  and  carpopedal  in  subsequent  attacks.  The  latter 
type  of  spasm  may  occur  in  cerebral  sclerosis,  sometimes  with  fine  tremors 
and  convulsive  movements  of  the  arm. 

Pseudo-tetanus  occupies  an  intermediate  position  between  tetany  and 
tetanus.  Escherich  has  described  under  the  name  of  "  pseudo-tetanus  of 
the  newborn  "  a  condition  of  opisthotonos  and  recurrent  arrest  of  breathing. 
It  is  sometimes  called  "  acute  recurring  respiratory  failure."  Pseudo- 
tetanus  has  been  recorded  in  a  few  children  between  4  and  10  years  of  age, 
nearly  all  boys.  The  muscles  of  the  jaw,  neck,  back  and  legs,  are  affected 
by  persistent  chronic  spasm  ;  the  masseters  and  muscles  of  the  back  being 
•chiefly  involved.  In  this  respect  it  resembles  tetanus,  and  probably  many 
•cases  of  idiopathic  tetanus  ending  in  recovery  are  of  this  type.  It  is  usually 
abrupt  in  onset  but  the  symptoms  quickly  assume  a  milder  type.  Stiffness 
of  the  legs,  rigidity  of  the  jaws,  trismus,  opisthotonos  and  rigidity  of  the 
extremities  are  present.  The  muscles  of  the  trunk,  neck  and  legs  are  power- 
fully contracted  and  stand  out  prominently,  as  hard  as  marble  or  rigid  as 
wood.  Acute  muscular  spasms  are  mild,  infrequent,  and  may  be  induced 
by  cold,  noise,  handling  and  emotion.  The  arms,  hands  and  eyes  are  usually 
unaffected.  Knee  jerks  are  active.  Relaxation  is  incomplete  while  at  rest 
and  asleep.  Violent  attacks  of  laryngospasm  and  cyanosis,  diaphragmatic 
spasm  and  dyspncea  may  occur.  The  patient  is  not  emotional  or  nervous  ; 
remains  cheerful  and  comfortable  in  spite  of  the  unnatural  attitude  ;  and 
recovers  gradually  in  from  1-6  weeks.  There  is  no  spasmophilic  over- 
excitability  and  tetanus  antitoxin  is  of  no  value.  Chloral,  bromides  and 
morphia  are  the  most  useful  drugs. 

Prognosis. — Tetany  varies  in  duration  and  severity.  It  may  last  for 
hours  or  persist  for  months,  usually  only  2  or  3  days.  It  may  be  mild, 
painless  and  continuous,  or  severe  and  paroxysmal.  In  infants  it  is  usually 
of  the  first  type  and  present  while  asleep.  Paroxysms  may  last  a  few  minutes 
or  for  24  hours.  The  intermittent  or  paroxysmal  type  is  the  one  most  often 
seen  in  the  rachitic.  It  runs  an  acute  or  subacute  course  with  short  and 
painful  cramps,  increased  mechanical  and  electrical  reactions,  and  a 
tendency  to  recur  on  slight  provocation.  One  child  had  an  attack  in  her 
third  year,  which  persisted  on  and  off  for  3  months,  and  3  more  attacks  in 
the  next  4  years.  The  disease  is  not  fatal  in  itself  and  the  prognosis  is  that  of 
the  cause.  It  is  unfavourable  in  marasmus,  prolonged  diarrhoea,  bronchitis, 
broncho-pneumonia,   and  oedema  of  the  lungs.     Tremor  and  attacks  of 


Spasmodic  Functional  Neuroses.  751 

dyspnoea  are  bad  signs.  Drowsiness  and  semi-coma  indicate  severe  toxaemia. 
There  is  always  the  liability  to  death  from  laryngospasm  or  convulsions  and 
.a  tendency  to  recurrence. 

Treatment. — It  can  be  prevented  by  attention  to  the  general  health, 
warmth,  proper  clothing  and  diet.  When  present,  the  underlying  cause 
must  be  treated.  For  alimentary  troubles  give  calomel,  alkalies,  HCL, 
bismuth,  benzo-naphthol,  etc.  ;  and  diet  the  child  carefully.  Chloral  and 
hot  baths  are  the  most  efficacious  methods  of  relieving  the  spasm,  and 
bromides  are  of  some  value.  Eest  in  bed,  dark  room  and  complete  quiet 
.are  necessary  in  bad  cases.  Treat  the  rachitic  condition  when  the  attack 
is  mild,  the  digestion  good,  and  the  patient  convalescent.  Lavage  and 
irrigation  of  the  colon  are  occasionally  required. 

Laryngospasm. — Syn.  :  Laryngismus  Stridulus- — Spasmodic  Croup — 
Spurious  or  False  Croup — Cerebral  Croup — Child  Crowing — Inward 
Convulsions — Glottic  Spasm — Holding  Breath  Spasms. — This  is  a  form  of 
local  convulsion,  characterised  by  spasmodic  closure  of  the  glottis,  due  to 
spasm  of  the  adductor  muscles  or  inco-ordination  of  the  muscles  of  the 
larynx.  In  severe  cases  other  muscles  of  respiration  and  of  deglutition  are 
involved.  The  typical  symptom  is  a  peculiar  crowing  sound  on  inspiration, 
following  a  period  of  apneea.  Occasionally  the  glottis  escapes,  and  the 
:spasm  is  limited  to  the  diaphragm  and  external  muscles  of  expiration  ;  in 
"these  there  is  no  crowing.  The  crow  is  due  to  inspiration  through  a  narrow 
glottis. 

Etiology. — The  affection  is  most  common  in  families  with  a  neurotic 
taint.  Males  are  said  to  be  twice  as  liable  as  females,  but  in  my  experience 
they  only  slightly  preponderate,  in  the  proportion  of  5-4.  It  is  most 
frequent  between  6  and  18  months  of  age.  It  is  decidedly  uncommon  after 
"the  first  dentition.  About  90  per  cent,  of  the  cases  occur  before  the  milk 
teeth  are  fully  erupted.  The  attacks  are  most  common  in  the  first  5  months 
•of  the  year,  at  any  rate  in  London.  Barlow,  from  observations  on  Man- 
chester children,  found  that  70  out  of  114  cases  occurred  from  October  to 
February.  The  connection  with  rickets  is  the  most  marked  etiological 
factor,  for  this  disease  is  almost  invariably  present.  It  is  frequently 
associated  with  tetany  also  and  usually  presents  the  signs  of  spasmophilia. 
Some  cases  occur  in  healthy  infants  in  the  first  2  weeks  of  life,  and  appear 
due  to  adenoids  or  to  post-nasal  catarrh  grafted  on  adenoid  hyperplasia  ; 
the  frequency  and  severity  of  the  attacks  varying  directly  as  the  degree  of 
nasal  discomfort.  Exciting  causes  are  a  draught  of  cold  air  while  asleep, 
tickling  the  throat  or  external  ear,  an  elongated  uvula,  any  interference 
with  normal  respiration,  overdistension  of  the  stomach,  laughter  and 
•emotion.  Thus  the  predisposing  causes  are  rickets  and  increased  excita- 
bility of  the  nervous  system,  and  reflex  irritation,  alimentary  or  pharyngeal, 
is  the  chief  exciting  cause. 


752  Chapter  LVI. 

Pathology. — It  has  been  ascribed  to  craniotabes,  through  pressure  on 
the  softened  occiput.  Occasionally  attacks  can  be  produced  by  pressure 
on  the  softened  parts,  but  on  the  other  hand  many  occur  when  the  child 
is  sitting  and  when  there  is  no  craniotabes.  There  is  no  evidence  that  it  is 
due  to  pressure  of  an  enlarged  thymus  or  mediastinal  gland.  There  is 
distinct  evidence  that  catarrhal  conditions  of  the  pharynx  or  larynx,  and 
that  the  entrance  of  saliva,  mucus  or  milk  into  the  glottis  may  produce  an 
attack.  Most  probably  it  is  due  to  the  action  of  deficiently  aerated  blood  on 
the  respiratory  centre,  and  for  this  reason  the  attacks  are  most  common 
at  night  in  children  continually  breathing  impure  air.  The  important  facts 
to  bear  in  mind  are  the  connection  with  rickets  and  craniotabes  ;  the 
general  malnutrition  often  present ;  the  malnutrition  of  the  blood  and 
nerve  centres  ;  the  liability  of  the  nervous  system  in  infants  to  spasmodic 
affections  ;  and  the  connection  of  other  nervous  phenomena  with  the 
rachitic  condition.  In  fatal  cases  there  is  no  constant  lesion.  The  epi- 
glottis is  sometimes  impacted  and  the  mucous  membrane  of  the  larynx 
congested. 

Symptoms. — Usually  the  child  is  supposed  to  be  in  perfect  health,  but 
sometimes  there  is  an  antecedent  history  of  fretfulness  and  irritability.. 
The  attack  comes  on  at  night  and  awakens  the  child  from  sleep.  It  may- 
occur  in  the  daytime,  during  sleep  or  even  when  awake.  It  may  come  on 
while  suckling  and  recur  at  each  attempt  to  nurse.  In  a  typical  case  the 
child  awakes  suddenly  about  midnight,  makes  a  few  attempts  at  respiration,. 
a  long  crowing  or  whistling  inspiration,  and  then  the  sounds  cease  from 
complete  closure  of  the  glottis.  At  first  he  is  pale  or  slightly  flushed. 
The  face  has  an  anxious  expression  and  gradually  becomes  blue  or  livid,, 
especially  about  the  lips.  The  eyes  are  wide-open  and  staring,  or  rolled 
upward  and  outward.  The  head  is  thrown  back,  the  body  rigid,  and  in 
severe  cases  there  are  clonic  facial  spasms,  cyanosis  and  marked  opistho- 
tonos. Carpo-pedal  contractions  are  often  present.  If  old  enough  the  child 
sits  up  in  the  cot,  is  restless,  throws  itself  about  from  side  to  side,  and  is. 
evidently  very  frightened.  The  pulse  is  small,  perhaps  almost  impercep- 
tible. The  fontanelle  bulges  from  venous  engorgement.  After  the  spasm  of 
the  glottis  has  lasted  for  a  few  seconds,  it  ends  suddenly  with  relaxation 
and  a  long  crowing  inspiration.  The  child  then  bursts  out  crying,  vomits. 
or  has  a  fit  of  coughing,  and  falls  asleep  from  exhaustion.  In  mild  attacks. 
the  child  rolls  up  the  eyes,  crows,  may  flex  the  thumbs  in  the  palms 
and  recovers  in  a  few  moments.  It  then  bursts  out  crying  or  has  a  fit 
of  temper.  The  attack  may  be  mistaken  for  a  mere  exhibition  of  temper, 
if  the  symptoms  of  the  latter  are  well  marked  while  the  attack  is  merely 
momentary. 

In  very  young  infants  the  attack  may  come  on  silently  with  no  pre- 
liminary crow.  The  spasm  affects  the  diaphragm  and  respiratory  muscles, 
except  the  glottis.     The  body  may  remain  limp,  motionless  and  without. 


Spasmodic  Functional   Neuroses.  753 

respiratory  effort,  while  the  face  grows  darker  and  darker  for  a  few  seconds  ; 
or  there  may  be  a  general  rigidity  with  in-turned  thumbs. 

The  duration  is  variable,  usually  a  few  seconds  ;  and  even  in  attacks 
in  which  the  child  appears  on  the  verge  of  dissolution  it  probably  does  not 
last  more  than  a  minute.  Occasionally  the  spasms  recur  so  rapidly  that 
for  many  hours  the  child  passes  from  one  into  another,  a  condition  like 
that  of  status  eclampticus.  Usually  the  child  seems  quite  well  after  an 
attack  and  drops  off  to  sleep.  Next  day  it  seems  in  perfect  health,  but  at 
night,  often  exactly  at  the  same  time,  the  same  cycle  of  events  is  repeated. 
There  may  be  only  one  attack,  or  recurrence  may  take  place  for  months 
whenever  an  exciting  cause  is  present.  Several  paroxysms  may  occur 
in  the  same  night,  or  even  hourly  by  night  and  day,  and  occasionally  more 
frequently. 

Diagnosis. — The  sudden  onset,  especially  if  at  night,  the  characteristic 
crow,  carpopedal  contractions,  rickets,  good  health  between  the  attacks, 
and  the  absence  of  fever  or  constitutional  disturbance  are  sufficient  to  base 
a  diagnosis  upon.  Catarrhal  affections  of  the  larynx,  retro-pharyngeal 
abscess  and  congenital  laryngeal  stridor  must  be  excluded.  "  Holding- 
breath  "  may  be  due  to  mere  anger.  Syncopal  attacks  without  crowing 
may  be  mistaken  for  minor  epilepsy.  The  glottic  spasm  occasionally  occurs 
in  organic  brain  disease. 

Prognosis. — The  outlook  is  favourable  under  suitable  treatment 
but  there  is  always  the  liability  to  recurrence  and  to  death  in  even  a  mild 
attack.  As  a  rule  the  more  frequent  the  attacks  the  milder  they  are  in 
character.  There  is  no  subsequent  hoarseness,  fever,  or  respiratory  trouble. 
It  is  a  cause  of  sudden  death  in  apparently  healthy  infants.  A  fatal  result 
may  be  due  to  the  epiglottis  becoming  wedged  in  the  chink  of  the  glottis 
and  not  released  when  the  spasm  relaxes,  or  may  result  from  expiratory 
apncea  due  to  severe  spasm  of  the  glottis,  diaphragm  and  respiratory 
muscles.  Should  a  spasm  pass  into  general  convulsions  and  unconsciousness 
the  child  is  more  likely  to  die.  The  usual  causes  of  death  are  suffocation, 
asthenia,  repeated  attacks,  pulmonary  collapse,  deglutition  spasm  and 
starvation. 

Treatment. — Mild  attacks  require  no  treatment  as  they  are  merely 
momentary.  In  more  severe  ones  the  child  should  be  raised  to  a  sitting 
posture  and  may  be  carried  about,  but  should  not  be  allowed  to  lie  down. 
The  room  must  be  well  ventilated  and  no  undue  crowding  about  the  patient 
permittee].  A  sponge  or  flannel  wrung  out  in  hot  water  and  applied  to  the 
throat  may  abort  the  attack.  For  immediate  relief  hook  the  epiglottis 
forward  with  the  finger  ;  stimulate  the  conjunctiva  by  touching  it  with  the 
finger  ;  give  inhalations  of  chloroform,  ether,  amyl  nitrite,  smelling  salts 
or  acetic  acid  ;  apply  ice  to  the  larynx  or  epigastrium  ;  slap  the  face  or 
chest  with  the  end  of  a  towel  dipped  in  cold  water  or  pour  cold  water  on  the 
head  with  the  child  in  a  hot  bath.    Vomiting  may  be  induced  by  tickling  the 

3  c 


754  Chapter  LVI. 

fauces  with  a  feather  or  inserting  the  finger.  If  the  epiglottis  becomes 
impacted  it  must  be  at  once  released  by  the  finger.  Artificial  respiration 
should  be  taught  to  the  attendant  in  a  bad  case  and  should  be  adopted  for 
sudden  pallor,  dilatation  of  the  pupils,  and  cessation  of  struggling  and 
breathing. 

To  prevent  recurrence  treat  the  underlying  rachitic  condition  and  give 
bromide  in  doses  of  grs.  4-10  at  night,  or  in  smaller  doses  more  frequently 
if  the  attacks  occur  by  day.  Phenazone  at  bedtime  is  also  beneficial. 
Chloral,  trinitrin  and  opiates  are  sometimes  used,  but  it  is  rarely  necessary 
to  have  recourse  to  any  drugs  except  bromides  and  cod-liver  oil.  It  is  of 
importance  to  regulate  the  child's  diet  and  to  insist  on  the  hygienic  measures 
appropriate  in  rickets  ;  to  treat  post-nasal  catarrh  and  to  remove  adenoids 
if  present  ;  to  avoid  over-feeding,  keep  the  bowels  open,  and  insist  on  a 
plentiful  supply  of  fresh  air  by  day  and  night. 

Myoclonus. —  Syn. :  Myokymia  —  Paramyoclonus  Multiplex  —  Myo- 
clonus Epilepticus. — Children  of  a  neuropathic  or  alcoholic  heredity, 
at  5-15  years  of  age,  are  sometimes  affected  with  sudden  shock-like  con- 
tractions of  a  muscle  bundle  or  a  whole  muscle,  causing  fibrillary  twitching 
or  sudden  movement  of  a  limb.  It  never  affects  groups  of  muscles  and  is 
never  unilateral,  being  generally  symmetrical  and  often  isochronous.  Its 
effect  is  analogous  to  that  caused  by  a  single  induction  shock.  The  move- 
ments are  not  rhythmical  and  not  like  voluntary  ones.  They  last  for 
several  minutes.  The  ocular  muscles  are  never  attacked,  the  sphincters 
•are  unaffected,  and  the  face  often  escapes.  The  proximal  segments  of  the 
limbs  are  usually  the  most  involved.  The  superficial  reflexes  are  increased 
a,nd  the  deep  ones  are  variable.  There  is  no  atrophy,  no  change  in  electrical 
reactions,  and  no  abnormality  of  sensation.  The  movements  may  interfere 
with  volitional  movements,  cause  inability  to  dress,  and  affect  speech. 
They  generally  cease  during  sleep.  Slight  spasticity  may  exist  in  long- 
standing cases.  The  affection  is  slowly  progressive  for  a  time  and  then 
stationary  for  years.  Its  intractability  varies  with  its  duration.  A  few 
cases  are  fatal  within  a  few  months  ;  some  recover,  but  are  liable  to 
Tecurrence.  Epileptic  attacks  are  a  frequent  association.  Death  is  usually 
due  to  intercurrent  disease. 

No  explanation  has  been  found.  Probably  there  is  some  mischief  in  the 
motor  region,  for  it  is  associated  with  epilepsy  and  ceases  during  sleep. 
Myoclonus  may  occur  in  sclerosis  of  this  region.  The  diagnosis  depends  upon 
the  simple  shock-like  movements  in  symmetrical  muscles  on  opposite  sides, 
bearing  no  resemblance  to  voluntary  movements  and  destitute  of  rhythm. 
In  hysteria  the  movements  are  less  persistent  and  there  are  other  func- 
tional derangements.  In  gross  cerebral  disease  there  are  signs  of  cranial 
mischief.  Treatment  consists  in  maintenance  of  general  nutrition,  arsenic 
and  hydrotherapy. 


Spasmodic  Functional  Neuroses.  755 

Chorea  Eleclrica  of  Dubini  (1849). — Children  of  either  sex,  age  9-15, 
are  affected  with  sudden  muscular  contractions  of  the  neck  and  shoulder 
muscles.  The  cases  described  under  this  name  are  frequently  simple  habit 
spasm  or  habit  spasm  in  a  hysterical  subject.  A  few  are  associated  with 
petit  mal  or  Jachsonian  epilepsy,  and  due  to  a  grave  lesion  of  the  cortex  ; 
■others  are  identical  with  certain  cases  of  myoclonus.  In  the  disease  described 
by  Dubini  there  is  paresis,  atrophy,  loss  of  faradic  irritability,  and  con- 
vulsions which  may  be  unilateral.  There  may  be  high  fever  in  acute  cases. 
It  is  progressive  and  often  fatal.    No  constant  morbid  change  is  found. 

Habit  Spasm. — -Syn.  :  Tic — Co-ordinated  Tic — Tic  Convulsif — Habit 
Chorea — Mimic  or  Histrionic  Spasm. — A  tic  is  a  co-ordinated  purposive 
act  of  voluntary  type,  provoked  in  the  first  instance  by  an  external  cause  or 
an  idea  ;  repetition  leads  to  it  becoming  habitual,  and  finally  to  its  in- 
voluntary reproduction  without  cause  and  for  no  purpose,  at  the  same  time 
as  its  form,  intensity  and  frequency  are  exaggerated.  It  thus  assumes  the 
characters  of  a  convulsive  movement,  inopportune  and  excessive  ;  its 
execution  is  often  preceded  by  an  irresistible  impulse,  resisted  at  first  and 
then  overwhelming  and  followed  by  misery  at  giving  way  to  it,  its  suppres- 
sion associated  with  malaise.  The  effect  of  distraction  or  of  volitional 
effort  is  to  diminish  its  activity  ;  in  sleep  it  disappears.  It  occurs  in 
predisposed  individuals,  who  usually  show  other  indications  of  mental 
instability.  Such  is  the  description,  slightly  modified,  given  by  Meigs  and 
Feindel  (1908). 

"  Habit  spasms  "  is  not  a  good  name,  for  they  are  not  true  habits  and  a 
:spasm  cannot  be  controlled  by  an  act  of  will.  Guthrie  speaks  of  them  as 
motor  manifestations  of  psychical  unrest  or  cortical  instability.  In  a  way 
they  are  an  emotion  of  expression  ;  expressive  gestures,  preceded  by  a 
desire  to  perform  them  and  followed  by  a  feeling  of  satisfaction.  The 
•expression  varies  from  a  single  twitch  of  a  single  muscle  to  complicated 
■co-ordinated  movement. 

Simple  Tic. — The  movement  is  usually  only  of  one  kind,  stereotyped, 
and  commonly  involves  the  muscles  of  the  face,  especially  the  eyes  and 
mouth,  and  those  of  the  head  and  shoulders.  The  lower  limbs  are  much 
more  rarely  affected.  As  a  rule  it  is  unilateral  and  recurs  every  few  minutes, 
•occasionally  with  great  rapidity  one  after  another.  It  differs  from  chorea  in 
the  same  movement  being  constantly  repeated.  Sometimes  the  recurrent 
motions  are  not  identical.  They  are  restrained  and  much  more  limited  in 
extent  while  under  observation,  but  worse  afterwards,  more  or  less  control- 
lable, increased  by  excitement,  and  cease  during  sleep. 

Varieties. — There  are  numerous  varieties,  such  as  blepharospasm, 
nictitating  or  ocular  spasm,  due  to  spasmodic  contraction  of  the  orbicularis 
muscle  and  producing  winking,  blinking,  or  screwing  up  the  eyes  ;  some- 
times extending  to  other  muscles  of  the  face  or  involving  the  eyebrows  and 
•occipito-frontalis  muscle.    It  is  most  common  in  school  children  and  may 


756  Chapter  L  V  I. 

take  its  origin  in  hypermetropia  or  hypermetropic  astigmatism,  blepharitis, 
fissure  at  the  angle  of  the  lids,  ingrowing  hair,  and  affections  of  the  con- 
junctiva or  cornea.  If  due  to  a  phlyctenule  or  keratitis  the  spasm  is  gener- 
ally tonic  in  character.  A  true  spasmodic  squint  is  occasionally  seen.  In 
facial  spasm  most  of  the  muscles  of  one  side  of  the  face  are  involved  or  only 
the  zygomatics,  drawing  up  the  angle  of  the  mouth  on  the  affected  side. 
Other  varieties  are  shrugging  of  one  or  both  shoulders,  tossing  up  the  chin, 
lateral  movements  of  the  mouth,  elevation  of  the  upper  lip,  showing  the 
teeth  or  snarling,  nose  twitching,  nose  picking,  sniffing,  sucking,  licking,, 
yawning,  biting,  masticating,  grunting,  barking,  stamping  the  feet,  jerking,, 
hopping  and  leaping  ;   occasionally  echolalia  and  coprolalia. 

Etiology. — It  is  more  common  in  girls  than  boys,  and  in  neurotic  children 
or  those  of  neurotic  parentage.  The  patients  range  from  3  years  to  puberty,, 
usually  5-9  years.  They  are  generally  thin,  nervous,  excitable  children  of 
good  intelligence  ;  and  often  present  other  signs  of  nerve  instability,, 
e.g.  timidity,  somniloquence,  pavor,  somnambulism,  headaches,  enuresis,, 
debility  and  undue  emotionalism.  It  is  perhaps  a  symptom  of  psychasthenia. 
Bad  health  and  bad  hygienic  surroundings  are  predisposing  factors.  The 
chief  exciting  causes  are  mental  excitement  and  the  effects  of  education,, 
such  as  strain,  competition,  dread  of  failure,  fear  of  punishment,  teasing 
and  bullying.  A  few  cases  follow  fright  or  surgical  shock.  The  particular 
movement  may  depend  upon  some  peripheral  exciting  cause,  which  suggests, 
rather  than  produces  it.  It  is  then  maintained  because  of  the  neuropathic 
state.  Sometimes  it  is  a  pure  habit  or  family  peculiarity,  largely  dependent 
on  imitation  and  suggestion.  Such  a  habit  may  be  transmitted  from  an 
unknown  grandparent.  Mimic  or  histrionic  spasm  is  a  name  which  should 
be  reserved  for  epidemics  of  any  particular  type  in  several  children  of  the. 
same  family  or  at  the  same  school. 

The  spasm  may  persist  throughout  life.  The  prognosis  varies  with  the- 
age  of  the  child  and  duration  of  the  spasm.  Usually  it  subsides  gradually 
under  treatment,  if  not  too  much  attention  is  paid  to  it.  Frequently  the^ 
type  changes,  as  one  spasm  goes  another  comes. 

Convulsive  tic  is  simple  tic  in  a  severe  form  and  occasionally  combined 
with  explosive  utterances.  It  is  rather  more  common  in  males  and  usually 
begins  at  10-15  years  of  age.  The  spasm  is  less  restricted  to  a  simple  move- 
ment and  may  be  widely  distributed.  It  causes  grimaces,  pantomiming,, 
grotesque  attitudes  and  gestures,  and  sometimes  imitation  of  gestures. 
(Echokinesis). 

Psychical  tic  or  Gilles  de  la  Tourette's  disease  is  a  further  stage  of 
convulsive  tic,  with  no  motor  manifestations.  It  is  far  the  most  serious, 
variety,  and  possibly  due  to  organic  cerebral  mischief.  In  the  exclamatory 
tics  there  are  explosive  utterances,  articulate  or  inarticulate,  which  may 
take  the  form  of  echolalia  or  repetition  of  words  and  phrases,  coprolalia  or 
the  use  of  obscene  words  and  bad  language,  or  the  cry  of  some  animal. 


Spasmodic  Functional   Neuroses.  757 

In  another  form  there  are  fixed  ideas,  the  folic  dc  double  and  various  phobias. 
•Some  cases  are  characterised  by  impulsive  acts  and  in  others  there  is  general 
mental  impairment.  The  disease  usually  begins  at  10-15  years  of  age,  runs  a 
progressive  course  with  intermissions,  and  often  ends  in  insanity.  Recovery 
is  rare. 

The  Diagnosis. — Simple  habit  spasm  must  be  differentiated  from  the 
stereotyped  acts ;  various  spasms,  e.g.  of  the  face,  trismus,  spasmus 
nutans  and  torticollis ;  chorea,  tremors,  myoclonus  and  athetosis.  Hysterical 
spasm  is  worse  under  observation  and  may  be  cured  suddenly.  It  is  doubtful 
whether  one  is  justified  in  classifying  Simple  Tic  with  Psychical  Tic  and 
regarding  Convulsive  Tic  as  an  intermediate  stage,  although  apparently  it  is 
a  close  connecting  link.  Yet  on  the  one  hand  simple  tic  is  harmless, 
temporary,  unimportant  and  a  common  affection  ;  whereas  psychical  tic 
is  rare  and  of  very  grave  prognosis. 

Treatment. — Very  little  notice  should  be  taken  of  the  habit  and  it  is 
•essential  to  avoid  scolding  and  punishment.  A  system  of  encouragement 
and  rewards  may  assist  in  strengthening  the  will  power  and  diminishing  the 
"recurrence.  Any  peripheral  exciting  cause  present  should  be  cured.  For 
instance  zygomatic  spasm,  in  a  6-year  old  boy,  subsided  as  soon  as  a 
•decayed  molar  tooth  on  the  same  side  was  removed.  In  blepharospasm 
remedy  any  defect  of  vision.  Unsuitable  spectacles  may  give  rise  to  spasm, 
which  becomes  permanent  unless  the  use  of  them  is  stopped.  In  mild  cases 
^school  life  is  not  contra-indicated,  provided  the  child  gets  long  hours  of 
sleep,  is  not  teased  or  bullied,  and  is  not  overworked.  Frequently  a  change 
to  the  country  or  seaside  is  rapidly  curative.  A  certain  amount  of  benefit 
is  derived  from  movements  directed  to  preserving  immobility  and  replacing 
incorrect  ones  by  normal  ones.  For  this  purpose  the  selected  exercises  in 
gymnastics  should  be  done  under  supervision  and  in  front  of  a  long  mirror. 
It  is  rarely  necessary  to  do  more  than  prevent  eye-strain  and  overwork ; 
insist  on  good  general  hygiene,  fresh  air,  exercise  and  liberal  diet ;  and  give 
tonics  such  as  arsenic,  cod-liver  oil,  iron,  quinine  and  strychnia.  Bromides 
•and  valerianates  are  often  useful.  Psychical  tic  must  be  treated  as  a  nervous 
disease  liable  to  end  in  insanity.  This  involves  peace  and  quiet,  no  emotional 
•excitement,  no  mental  strain,  and  a  simple  country  life. 

Nodding  Spasm. — Syn.  :  Spasmus  Nutans  —  Head  Nodding,  Jerking 
■or  Shaking — Eclampsia  Nutans  or  Rotans — Gyrospasm. — This  affection 
is  characterised  by  movements  of  the  head  on  the  trunk,  commonly  asso- 
ciated with  nystagmus.  The  movements  vary  somewhat  in  different  cases. 
Usually  they  take  the  form  of  rotatory  nodding,  as  if  due  to  the  spasmodic 
■contraction  of  one  of  the  sterno-mastoid  muscles.  In  my  experience  the 
right  muscle  is  most  often  involved,  causing  the  head  to  be  drawn  downward 
to  the  right  shoulder  and  the  chin  to  be  pointed  toward  the  left.  Occasion- 
ally the  movements  are  pure  nodding  ones,  like  those  of  a  mandarin  doll, 
and  due  to  simultaneous  spasm  of  both  sterno-mastoids.     This  variety  is 


758  Chapter  L  VI. 

most  frequent  in  microcephalus.     Sometimes  the  head  is  simply  moved 
from  side  to  side. 

The  movements  are  not  constant,  but  maybe  remarkably  frequent  and 
almost  continuous.  They  are  increased  by  excitement  and  by  fixation  of  the 
eyes,  as  on  looking  at  a  bright  light.  They  cease  during  sleep  and  recum- 
bency, and  may  disappear  when  the  eyes  are  covered,  or  if  one  eye  alone  is 
covered  when  the  nystagmus  is  limited  to  that  eye.  Neither  face,  trunk  nor 
extremities  are  involved.  In  about  half  the  cases  the  head  is  held  in  a 
peculiar  way,  cocked  on  one  side,  thrown  backward  and  less  often  forward. 
The  child  sometimes  looks  at  objects  out  of  the  corners  of  the  eyes. 

Nystagmus  is  generally  present  in  one  or  both  eyes,  and  much  more  in 
one  than  the  other.  The  movements  are  very  rapid,  more  so  than  those  of 
the  head,  and  best  marked  when  the  eyes  are  fixed  or  the  head  is  held. 
They  are  usually  lateral,  4-6  a  second  and  of  short  range,  quivering,  twit- 
tering or  rolling.  Generally  they  are  horizontal  or  combined  with  some 
rotation.  They  are  not  constant  and  may  be  present  apart  from  the  head 
nodding.  Sometimes  they  are  only  induced  by  fixation  of  the  eyes,  by  re- 
straining the  movements  of  the  head,  placing  the  child  on  its  back,  or 
making  the  child  look  to  one  side.  On  conjugate  deviation  they  may  not  be 
present  when  the  deviation  takes  place  to  one  side  and  well  marked  when 
it  takes  place  to  the  other.  The  movements  of  the  head  and  eyes  are  often,, 
but  not  always,  in  the  same  direction.  Convulsive  movements  of  the  lids- 
are  not  infrequent  and  the  upper  ones  may  be  markedly  retracted.  Rarely 
there  is  spasmodic  convergent  or  divergent  squint. 

The  disease  is  exceptional  in  the  summer  and  is  most  common  in 
winter  and  spring,  possibly  from  want  of  light  through  living  in  dark  rooms. 
Either  the  head  nodding  or  nystagmus  may  begin  first ;  more  usually  they 
are  simultaneous  in  onset.  In  one  of  Gee's  cases  nystagmus  began  at 
4  weeks  and  the  head  movements  at  6  weeks.  The  usual  age  is  5-12  months, 
but  it  may  begin  at  18  months.  Males  and  females  are  equally  liable,  and 
more  than  one  child  in  a  family  may  be  affected.  There  is  no  definite 
connection  with  rickets  though  it  is  frequently  present.  Craniotabes  is 
almost  always  absent.  Dentition  cannot  be  regarded  as  a  cause  though  it 
may  aggravate  the  condition.  The  movements  may  appear  before  dentition 
begins.  These  babies  are  usually  precocious,  of  more  than  common  intelli- 
gence at  the  age  of  onset,  and  good-tempered.  Some  of  them  are  liable  to 
attacks  of  unconsciousness  or  possibly  vertigo. 

The  combination  of  head  jerking  and  nystagmus  suggests  that  the 
nuclei  of  the  spinal  accessory  and  upper  spinal  nerves  are  in  close  relation 
to  those  of  the  oculo-motor  nerves.  The  movements  are  rarely  confined  to 
the  sterno-mastoids  and  often  affect  the  muscles  which  rotate  the  head. 
In  many  the  rotatory  movements  are  the  most  marked.  Apparently  it  is  a 
derangement  of  co-ordination.  Normally  the  movements  of  the  head  and 
eyes  are  not  harmoniously  associated  until  about  the  fourth  month.     In 


Spasmodic  Functional  Neuroses.  759 

most  of  these  cases  the  patient  takes  notice  early,  develops  precocious 
movements,  and  is  liable  to  derangement  of  such,  movements.  If  this  is 
true,  the  defective  co-ordination  may  be  due  to  overstraining  the  eyes  to 
look  in  a  particular  direction,  aided  by  nutritional  weakness.  In  some 
respects  it  is  analogous  to  miner's  nystagmus. 

It  must  be  diagnosed  from  congenital  or  juvenile  nystagmus  due 
to  amblyopia,  a  central  macula  or  cataract ;  the  swaying  and  rolling 
movements  in  imbeciles  ;  and  from  eclampsia  nutans,  a  form  of  epilepsy 
in  which  there  is  a  series  of  rapid  nods  or  jerks  of  the  head,  with  vacant 
look  or  momentary  unconsciousness.  In  salaam  fits,  a  sub-variety  of 
eclampsia  nutans,  the  hands  are  placed  in  front  of  the  face,  palms  outwards, 
and  the  head  and  trunk  are  suddenly  bowed  down. 

The  prognosis  is  good.  All  get  well  and  there  is  no  liability  to  any 
nervous  disease  ;  if  such  is  present,  it  is  a  coincidence  rather  than  a  sequel. 
Many  recover  in  a  few  weeks  to  a  few  months,  and  it  rarely  lasts  more  than 
2  years.  Relapses  are  common.  The  nystagmus  persists  longer  than  the 
spasm. 

Treatment. — Attend  to  the  general  health.  The  movements  arc  harm- 
less and  unimportant.  No  special  drugs  are  required.  Phenazone  gr.  1, 
2-4  times  a  day,  may  do  good. 

Head  Banging  and  other  movements  such  as  head  rolling,  head  burying 
and  body  rocking,  occupy  an  intermediate  position  between  the  spasmodic 
nervous  affections  and  simple  bad  habits,  for  instance  thumb  biting,  pica  and 
masturbation.  For  some  inexplicable  reason  or  from  mere  temper  the 
child,  generally  an  infant,  beats  the  head  with  its  fists  or  bangs  it  against 
structures,  whether  hard  or  soft,  such  as  the  pillows  or  rails  of  the  cot,  the 
walls  or  the  floor.  Head  banging  may  alternate  with  some  of  the  other 
movements.  From  a  medico-legal  point  of  view  the  affection  is  important, 
as  the  banging  may  be  severe  enough  to  cause  abrasions  and  bruises. 

Most  often  it  occurs  as  the  child  is  going  to  sleep  but  it  may  take  place 
at  any  time  of  the  day  or  night.  It  resembles  epilepsy  in  the  tendency  of 
the  child  to  turn  on  the  face  before  the  attack  begins.  Sometimes  it  goes 
on  for  several  hours  or  even  all  night,  the  face  and  forehead  being  banged 
into  the  pillow  while  the  child  remains  fast  asleep.  In  a  6-year  old  boy  with 
acute  nephritis  the  habit  took  the  form  of  wrapping  the  head  up  in  a  sheet 
or  blanket  and  burying  it  in  the  pillow  or  bedding  (head  burying).  He 
was  dull,  lethargic,  with  drawling  speech,  and  decidedly  backward.  Double 
otorrhea  was  present. 

In  head  rolling  the  head  is  rolled  from  side  to  side  and  the  hair  gets  rubbed 
off  the  occiput.  The  movements  may  continue  in  sleep  and  are  painless. 
These  children  are  almost  invariably  under  2  years  of  age,  often  rachitic, 
and  frequently  have  middle  ear  trouble.  Sometimes  the  attack  seems  due  to 
dentition. 


760  Chapter  LVI. 

Body  rocking  is  anteroposterior  and  rarely  lateral.  It  takes  place  in 
a  sitting  posture  and  therefore  only  in  infants  who  can  sit  up,  and  may 
persist  in  sleep.  It  is  most  common  in  the  blind  and  mentally  defective, 
and  is  an  indication  of  an  eccentric  or  neurotic  temperament,  or  of 
imbecility. 

All  these  affections  have  been  found  associated  with  rickets,  ear  trouble, 
phimosis,  adherent  prepuce,  masturbation,  fits,  tuberculosis,  and  back- 
wardness or  actual  imbecility.  They  have  no  connection  with  nightmare, 
pavor  or  somnambulism.  Head  banging  must  not  be  confused  with  a  mere 
outbreak  of  temper  in  an  excitable  or  neurotic  child.  It  generally  begins 
before  the  end  of  the  first  dentition  and  may  persist  for  years.  It  has 
occurred  with  intracranial  tumour. 

Treatment  often  fails.  Attention  should  be  paid  to  the  digestion,  the 
general  condition  of  the  child  and  the  mental  state.  The  ears  must  be 
examined  and  local  sources  of  irritation  treated.  Bromides  and  phenazone 
are  sometimes  useful. 

Nystagmus. — The  involuntary  movements  of  the  eyeball,  known  as 
nystagmus,  assume  many  forms.  It  is  both  a  symptom  and  an  entity.  As  a 
family  peculiarity  it  has  been  recorded  in  2  and  3  generations  and  may  be 
■associated  with  head  nodding.  Sometimes  it  is  due  to  albinism.  These 
•children  have  light,  almost  white  hair  and  eyelashes,  pink  pupils  and  iris, 
and  photophobia.  It  has  been  described  by  Nettleship  as  occurring  in 
partial  albinism  with  imperfect  sight ;  a  condition  apt  to  run  in  families, 
affect  males  and  be  transmitted  by  females.  It  may  be  secondary  to 
cerebral  mischief,  e.g.  basal  meningitis  and  hydrocephalus ;  or  due  to  mental 
defects  and  cranial  peculiarities,  as  in  microcephalus  and  oxycephalus. 
Frequently  it  results  from  visual  defects  such  as  corneal  opacities,  con- 
genital cataract,  choroiditis  or  high  myopia.  The  movement  is  generally 
horizontal,  sometimes  vertical  or  rotatory,  and  occasionally  spasmodic, 
the  eyes  suddenly  converging  or  diverging. 


CHAPTER    LVII. 

NON-SPASMODIC    FUNCTIONAL    NEUROSES. 

Headache— Migraine—  Disorders   of   Sleep—  Nightmare— Somnambulism— 
Favor   Nocturnus — Pavor   Diurnus. 

Headache. — As  a  symptom  headache  occurs  in  most  febrile  conditions, 

-toxemias,  constitutional  states,  hygienic   errors,    nervous   disorders    and 

various  physical  defects.    It  is  not  always  possible  to  ascertain  the  exact 

•cause  and  often  more  than  one  is  implicated.     The  words  of  Juncker  still 

xemain  true  "  De  doloribus  capitis  ;    scandalo  medicorum,  difhculter  remo- 

vendo."     Headache  should  never  be  neglected  in  young  children.     It  is 

more  significant  in  them  than  in  older  people  and  may  indicate  the  onset 

of  acute  or  dangerous  disease.    It  is  acute  or  chronic.    Sometimes  it  takes 

the  form  of  "  paroxysmal  recurrent  headache  "  or  of  "  migraine."     The 

former  type  is  not  uncommon  in  children.    Bilateral  periodical  headaches 

cannot  be  differentiated  from  those  hemicranial  in  type.      Dolor  capitis, 

pain  due  to  changes  not  inside  the  cranium,  that  is  in  the  scalp  or  bones, 

must  be  excluded. 

Etiology.— The  chief  predisposing  causes  are  inherited  weakness  or 
instability  of  the  nervous  system,  the  gouty  and,  possibly,  the  rheumatic 
diathesis.  Children  of  neurotic  parentage,  or  themselves  neurotic,  are 
liable  to  headache  on  slight  provocation  such  as  excitement,  emotional 
disturbance,  and  active  brain  work. 

The  exciting  causes  are  impaired  general  health  and  anaemia,  leading 
to  malnutrition  of  the  nerve  cells  ;  alimentary  disorders,  through  the 
absorption  of  toxic  products  ;  deficient  aeration  of  the  blood,  toxaemia, 
uraemia,  and  the  toxic  effects  of  alcohol,  lead  and  other  metallic  poisons  ; 
eye-strain,  mental  arid  physical  overstrain,  and  excitement  or  emotion. 
The  headache  caused  by  a  vitiated  atmosphere  is  due  to  excess  of  CO,, 
■deficiency  of  oxygen,  and  the  absorption  of  deleterious  products  given  off 
from  the  lungs,  skin,  clothes,  etc,  of  others  present.  Deficient  oxygenation 
.accounts  for  headache  in  children  with  adenoids,  congestion  of  the  nasal 
mucosa  and  respiratory  affections. 

The  chief  organic  causes  are  meningitis,  cerebral  tumour  and  abscess, 
sunstroke,  injury,  and  syphilis.  It  is  often  difficult  to  get  a  histoiy  of 
injury  as  a  nurse  will  rarely  confess   that    she   has    dropped   the    child. 


762  Chapter  LVII. 

Provided  organic  disease  can  be  excluded,  it  will  be  found  that  toxaemic- 
causes  predominate,  chiefly  those  dependent  on  the  digestive  system. 

Classification. — Headaches  may  be  regarded  as  structural,  haemic  or 
nervous  in  origin.  In  the  structural  or  organic  headaches  there  is  usually 
increased  intracranial  pressure  and  the  pain  is  liable  to  keep  the  patient 
awake.  The  haemic  causes  include  anaemia,  hyperaemia,  fever,  and  all 
causes  of  toxaemia  and  auto-intoxication.  Nervous  headache  may  be  due 
to  brain  exhaustion  and  noise  ;  reflex,  usually  through  branches  of  the 
fifth  nerve,  e.g.  from  decayed  or  impacted  teeth,  errors  of  refraction,  otitis,, 
and  naso-pharyngeal  affections  ;   or  idiopathic,  e.g.  migraine. 

Symptoms. — In  the  very  young  there  is  dislike  of  light  and  noise,  con- 
stant putting  of  the  hand  to  the  head,  supporting  the  head  with  the  hands,, 
and  screaming  paroxysmally  or  when  the  head  is  moved.  The  intensity  of 
the  pain  varies  as  the  capacity  for  sensation  rather  than  with  the  primary 
cause.    It  is  greater  when  the  fontanelles  are  closed. 

Situation  and  Characters. — Localisation  is  a  doubtful  clue  to  pathology.. 
The  headache  of  fever  and  toxaemia  is  generalised  or  mainly  frontal.  Severe^ 
frontal  headache  with  rise  of  temperature  usually  indicates  the  onset  of  a 
specific  fever.  Such  headache  disappears  if  the  child  becomes  delirious, 
whereas  it  persists  if  due  to  organic  disease.  The  headache  of  meningitis 
is  a  fair  measure  of  the  severity  of  the  disease.  It  bears  no  proportion  to  the 
amount  of  fever,  is  more  constant  than  intense,  and  does  not  vary  with 
position.  Acute  headache  with  an  infrequent,  irregular  pulse  is  diagnostic- 
Acute  headache  without  vomiting  excludes  it.  But  headache,  intolerance- 
of  light,  vomiting  and  constipation  do  not  always  indicate  tuberculous- 
meningitis.    Roughly  the  causation,  based  on  localisation,  is  as  follows  : — 

Frontal. — Anaemia,  toxaemia,   eye-strain,   astigmatism,   naso-pharyngeal; 
affections,  over-growth. 

Vertical. — Anaemia,  hysteria,  epilepsy,  meningitis. 

Parietal. — Carious  teeth,  ear  troubles. 

Occipital. — Epilepsy,  meningitis,  eye-strain,  pharyngitis,  cervical  caries,, 
otitis  media,  decayed  molars,  cerebellar  disease. 

Supra-orbital  or  frontal. — Disease  of  the  nose  or  frontal  sinus. 

A  localised  headache  is  suggestive  of  tumour  or  abscess.  It  is  sometimes 
relieved  by  the  remedies  useful  in  simple  headache,  for  the  pain  is  due  to 
hyperaemia  or  irritation.  Possibly  the  pain  indicates  involvement  of  the 
meninges.  In  inflammation  of  the  tympanum,  middle  ear  or  Eustachian 
tube  the  pain  is  referred  to  the  external  ear  and  its  neighbourhood.  It  is- 
more  a  "  dolor  capitis  "  than  true  headache.  Mental  overstrain  is  often 
associated  with  phosphaturia. 

Toxosmic,  bilious  or  gastric  headache  generally  begins  in  the  morning, 
perhaps    because    of   the   comparative   inactivity    of    the    kidneys    and 


Non-Spasmodic   Functional    Neuroses.  763 

respiratory  system  during  sleep.    The  child  is  languid,  has  no  appetite  for 
breakfast,  and  exhibits  a  coated  tongue  and  indicanuria. 

Morning  headache,  frontal  in  distribution,  may  be  due  to  rapid  growth. 
It  is  most  common  in  rheumatic  and  neurotic  boys  at  9-12  years  of  age.  It 
is  aggravated  by  work,  decreased  by  rest.  The  headache  of  anaemia  and 
debility  is  relieved  by  recumbency  and  increased  by  the  upright  posture- 
Giddiness  and  nausea  are  produced  by  getting  up  suddenly. 

School  headache  is  due  to  vitiated  atmosphere,  mental  overstrain,  and 
errors  of  refraction.  Deficiency  of  animal  proteins  and  excess  of  carbo- 
hydrates in  the  diet  are  predisposing  causes.  If  due  to  fatigue  or  overwork 
it  comes  on  in  the  latter  part  of  the  day.  The  majority  of  children  do  not 
work  unduly  hard  at  school,  so  mental  strain  is  not  a  frequent  cause  of 
headache  and  breaking  down,  except  at  examination  periods. 

Migraine,  a  corruption  of  hemicrania,  occurs  in  periodical  or  quasi- 
periodical  attacks,  usually  early  in  the  day.  Hereditary  transmission 
or  a  family  history  of  headaches,  neuralgias,  gout  and  neurotic  affections,  is- 
often  present. 

H.  Neumann  gives  the  age  of  onset  of  43  cases  as  9  in  the  first,  21  in 
the  second,  and  13  in  the  third  5  years  of  life. 

The  prodromata  are  cloudiness  of  vision,  hemianopsia,  photopsia, 
teichopsia,  and  central  or  lateral  scotoma.  Sometimes  a  star  is  seen  near 
the  fixation  point,  zigzags,  Catherine  wheels,  or  a  fortification  spectrum,  which 
may  be  coloured.  Occasionally  an  aura,  like  an  epileptic  aura,  spreads  up 
the  arm.  It  is  much  more  prolonged  and  deliberate  in  it's  ascent,  and  is- 
followed  by  hemicrania,  and  perhaps  aphasia  for  some  hours,  much  more 
severe  than  in  minor  epilepsy.  Prodromata  last  for  a  fewT  minutes  to  half 
an  hour,  subsiding  as  the  pain  comes  on.  Pain  may  be  the  first  sign.  It  is. 
unilateral,  increases  in  severity  for  some  hours,  and  may  be  intense.  There 
is  no  unconsciousness  ;  no  shrieking,  as  in  meningitis  ;  and  it  subsides- 
gradually,  the  patient  then  falling  asleep.  Nausea  is  common,  vomiting 
infrequent.  Frequently  the  symptoms  consist  of  fever,  drowsiness, 
moderate  headache  and  vomiting.  They  may  simulate  meningitis.  The- 
pain  may  be  so  severe  as  to  cause  delirium  and  stupor,  and  suggest  post- 
epileptic mania.  A  boy,  aged  12,  was  subject  to  attacks  for  a  year.  The 
pain  was  in  the  right  frontal  region,  sufficiently  severe  to  make  him  cry  out 
and  light-headed,  and  associated  with  visual  hallucinations.  He  came  under 
treatment  for  chorea. 

The  symptoms  are  suggestive  of  primary  vasomotor  constriction  of  the- 
posterior  cerebral  artery  or  its  occipital  branch,  followed  by  dilatation. 
The  pain  can  be  relieved  by  compression  of  the  carotid.  During  the  stage- 
of  vaso-constriction  there  is  no  headache.  Occasionally  migraine  and 
epilepsy  alternate  in  the  same  patient,  and  migraine  may  cease  when 
epilepsy  develops.     This  is  a  rare  event.    Possibly  the  connection  depends- 


764  Chapter  L  VII. 

on  the  susceptibility  of  the  brain  in  childhood  to  irritation  and  convul- 
sions. The  pain  of  migraine  may  be  of  such  severity  as  to  cause  con- 
vulsions, which  may  eventually  result  in  epilepsy,  in  spite  of  the  gradual 
subsidence  of  the  attacks  of  migraine.  As  a  rule  epileptics  are  remarkably 
exempt  from  headaches. 

Paroxysmal  recurrent  headache,  frontal  or  occipital,  is  a  sub-variety 
of  migraine  although  it  is  not  unilateral.  They  are  both  recurrent,  due 
to  similar  causes,  separated  by  intervals  of  poor  health,  and  may  alternate 
in  the  same  child.  In  gouty  cases  the  child  may  be  quite  well  between  the 
attacks.  Severe  neuralgic  headaches  occur  in  dyspeptic  children  during 
the  second  dentition.  They  produce  intolerance  of  light,  nausea  and 
vomiting.  In  girls  they  may  recur  at  puberty  and  at  each  menstrual  period, 
with  some  gastric  disturbance  but  little  uterine  pain. 

Ophthalmic  Migraine. — Syn.  :  Periodic  Oculo-motor  Palsy — Transient 
Ophthalmoplegia  Externa — Recurrent  Palsy  of  the  Third  Nerve — Fleeting 
■or  Recurrent  Palsy  of  Ocular  Muscles. — This  begins  with  periodical  attacks 
of  hemicrania,  nausea  and  vomiting  ;  followed  by  oculo-motor  palsy  which 
■at  first  disappears  between  the  attacks  and  later  on  becomes  permanent. 
It  may  occur  in  infancy  and  old  age,  but  is  most  common  in  young  adults. 
Autopsies  have  shown  plastic  exudation  or  tuberculous  granulations  round 
the  trunk  of  the  third  nerve,  and  fibrochondroma  or  fibroma  of  the  nerve 
or  nerve  sheath. 

Treatment  of  Headache. — Procure  elimination  in  toxaemic  cases  by 
•calomel  or  grey  powder  ;  and  give  a  mixture  of  rhubarb  and  soda,  if  there 
is  any  digestive  trouble.  Attend  to  any  local  cause.  Do  not  overlook 
albuminuria  and  chronic  interstitial  nephritis.  For  migraine  prescribe 
complete  rest  and  quiet  in  a  warm,  darkened  room.  Inducing  vomiting 
may  cut  short  an  attack.  Cooling  lotions  to  the  scalp  and  a  mustard 
leaf,  or  even  a  leech,  over  the  mastoid,  may  do  good  ;  or  hot  fomentations 
■or  an  ice  bag.  Lower  general  blood  pressure  and  intracranial  pressure. 
Lumbar  puncture  might  be  tried  if  all  other  measures  failed  to  give  relief. 
It  is  often  used  in  cases  of  organic  cerebral  disease.  Trinitrin  is  useful,  with 
strychnia,  in  anaemic  headaches  and  migraine  ;  amy!  nitrite,  if  vasomotor 
spasm  is  indicated  by  pallor ;  ergot  and  strychnia,  if  there  is  general 
"vaso-dilatation.  Chloroform  inhalations,  valerian  and  camphor,  sal 
volatile,  ether  and  opiates  are  beneficial.  Iron  and  tonics  are  required  for 
the  headache  of  debility  and  overgrowth  ;  aspirin  and  sod.  bromid.  for 
rheumatic  neurotics  ;  and  in  all  cases  regulation  of  the  diet  and  mode  of  life 
in  accordance  with  the  causation  of  the  headaches. 

Sleep. — Sleep  is  a  regularly  recurring  function,  not  merely  cerebral. 
Goltz  removed  the  cerebrum  of  a  dog.  It  survived  1-|  years  and  showed 
Tegular  alternations  of  sleep.  Modifications  depend  on  exhaustion,  toxic 
substances  such  as  morphia,  cold  as  in  the  hibernation  of  animals  and 


Non-Spasmodic   Functional   Neuroses.  765- 

plants,  the  interruption  of  nerve  conducting  paths  in  cerebral  tumour,  and 
the  abolition  of  sensory  stimuli  in  cutaneous  anaesthesia. 

Many  growing  children  suffer  from  too  little  sleep,  none  from  too  much. 
A  child  needs  more  than  an  adult  for  its  vital  processes  are  much  more 
active  while  awake,  and  a  longer  interval  is  necessary  for  recuperation  as 
well  as  for  mechanical  rest  of  growing  structures.  At  puberty  and  in 
children  of  active  intelligence  sleep  is  most  essential.  The  stress  and  strain 
of  modern  life  must  be  prepared  for  by  training  in  habits  of  sleep,  by  ensuring 
proper  development  of  the  body  and  brain,  and  by  guarding  against  the 
effects  of  strain  in  school  life. 

The  newborn  babe  falls  asleep  after  its  bath  and  only  wakes  in  response 
to  sensations  of  hunger,  thirst,  cold,  wet  or  colic.  Its  wants  attended  to, 
it  falls  asleep  again.  If  labour  has  been  much  prolonged  sleep  may  approach 
semi-coma  for  1-2  days.  Actual  cerebral  injury  produces  fits  or  rigidity. 
During  the  first  24  hours  the  babe  is  almost  constantly  asleep.  In  the 
second  3  months  the  intelligence  develops  and  the  child  sleeps  less.  By 
the  fourth  month  it  may  remain  awake  for  a  few  hours  at  a  time  without 
injury,  but  should  still  sleep  for  18  out  of  24  hours.  In  the  second  year 
the  child  should  sleep  12-14  hours  at  night  and  about  2  hours  in  the  middle 
of  the  day.  By  the  fifth  year  the  day  sleep  may  be  omitted,  if  the  child 
has  the  same  hours  of  sleep  at  night. 

The  normal  attitude  is  on  the  side,  curled  up  in  the  infra-uterine 
position,  with  the  eyes  and  mouth  closed.  The  babe  should  be  trained  in 
habits  of  sleep  from  the  time  of  birth.  Quiet,  darkness,  warmth,  dryness  and 
suitable  diet  are  needed.  One  period  of  sleep  at  night  should  last  5-6  hours. 
After  the  sixth  month  this  should  be  prolonged  to  8-9  hours,  the  child  only 
being  fed  6  times  in  24  hours.  Allow  no  sleeping  at  the  breast  or  bottle,  no 
rubber  teat,  and  no  nursing  or  rocking.  Do  not  encourage  profound  silence 
in  the  room  or  house,  nor  sleeping  out  of  doors  at  the  expense  of  indoor  rest. 
Do  not  let  ventilation  be  sacrificed  to  darkness.  Do  not  encourage  special 
habits  for  the  production  of  sleep,  e.g.  sucking  the  thumb  or  a  corner  of  the 
sheet,  covering  up  the  face,  the  sitting  posture  or  lying  on  the  stomach. 
Wake  the  child  to  pass  water.  It  will  drop  off  to  sleep  again  at  once. 
After  the  first  2  years  of  life  sleep  is  much  more  profound. 

Excessive  sleepiness  is  occasionally  a  sign  of  imbecility  or  due  to  drugs. 
Paregoric  and  soothing  syrups  produce  constipation.  White  bryony,  sold 
in  the  form  of  white  globules,  causes  diarrhoea.  Drowsiness  is  a  sign  of  the 
onset  of  measles  and  other  illnesses,  and  may  be  extreme  in  cerebral  tumour. 
Some  neurotic  children  are  difficult  to  wake  up  in  the  morning  and  are 
not  mentally  active  for  several  hours. 

Wakefulness  is  abnormal.  In  infancy  it  is  a  disturbed  and  restless, 
sleep  rather  than  true  insomnia.  It  is  due  to  colic,  excess  or  insufficiency 
of  food,  night  feeding  and  bad  training.  Some  children  lie  awake  for  hours 
and  then  sleep  normally.     At  all  ages  it  may  be  caused  by  painful  or 


76G  Chapter  LVII. 

irritating  affections,  e.g.  teething,  toothache,  skin  irritation,  ear  troubles, 
cough,  abdominal  complaints,  adenoids  and  enlarged  tonsils,  etc.  Some- 
times it  is  due  to  too  little  or  too  much  clothing,  cold  feet,  heat,  insufficient 
ventilation,  palpitations,  febrile  attacks,  or  the  starting  pains  of  hip 
disease.  Neurotic  children  sleep  badly,  wake  at  the  least  noise,  and  are 
soothed  with  difficulty.  Eestlessness  and  insomnia  are  common  in  rickets, 
tetany,  laryngospasm,  head  banging,  anaemia  and  dyspepsia.  Over- 
stimulation, nervous  excitement  and  over-fatigue  are  common  causes. 
■Quite  half  the  cases  are  of  digestive  origin. 

Treat  the  cause,  if  discoverable.  In  other  cases  rely  on  wholesome 
Tegular  diet,  hygiene  and  exercise,  and  training.  Put  the  child  to  bed  at 
a  regular  time,  in  a  dark,  quiet  room.  The  nurse  or  mother  may  sit,  holding 
the  child's  hand,  and  sing  monotonous  tunes  in  a  low  voice.  If  the  child 
is  very  nervous  or  suffers  from  pavor,  allow  a  night  light  and  let  the  atten- 
dant sleep  in  the  same  room  or  an  adjacent  one  with  the  door  open.  A 
warm  bath  should  be  given  at  bedtime.  Give  no  food  during  the  night 
and  omit  supper,  if  there  is  any  pavor  or  digestive  trouble.  Bromides  are 
needed  for  pavor,  chloral  for  cough  and  laryngospasm,  and  opiates  for 
actual  pain;  chloral,  bromides,  codeia  or  trional  for  acute  febrile  disturbance. 

Sleep  at  School. — Usually  the  hours  of  sleep  are  too  limited  but  the  evil 
effects  are  counter-balanced  by  long  holidays.  Yet  many  children  suffer 
in  later  life  from  over-cerebral  activity  during  school  life  and  this  is 
undoubtedly  due  to  insufficient  sleep.  It  is  remarkable  what  a  number  of 
children,  regarded  as  exceptionally  brilliant  at  school,  prove  failures  as 
adults.  The  early  rising  and  morning  chapel,  followed  by  a  repetition 
lesson  before  breakfast,  are  by  no  means  advantageous  to  mental  and 
physical  development.     Individual  requirements  of  sleep  vary. 

Boarding-school  life  should  begin  at  8-10  years  of  age,  even  a  year 
•earlier  in  some  cases,  and  from  then  up  to  the  twelfth  year  the  child  should 
go  to  bed  at  8.30-9.0  p.m.,  and  get  up  at  7.30  a.m.  in  summer,  and  at  8.0  a.m. 
in  winter.  Allow  10J  hours  sleep  at  11  years  of  age  and  reduce  the  amount 
by  a  \  hour  yearly,  or  \  hour  every  2  years,  up  to  19  years  of  age.  From 
13-16  years  of  age  the  child  should  go  to  bed  at  9.0  p.m.  and  get  up  at  7.0 
a.m.  in  summer  and  \  hour  later  in  winter.  After  that  the  retiring  hour 
may  be  10  p.m.  It  is  absurd  to  suppose  that  habits  of  self-indulgence  are 
induced  by  long  hours  of  sleep.  Nature  is  a  reliable  guide  during  the  early 
years  of  life.  After  puberty  is  safely  over,  more  spartan  habits  may  be 
encouraged.  The  distinction  between  junior  and  senior  boys  must  be  based 
■on  age  and  not  on  mental  activity.  A  clever,  forward  boy  requires  as  much 
sleep  if  not  more  than  a  backward  one  of  the  same  age.  The  sleeping 
apartment  must  be  darkened,  so  that  the  child  is  not  awakened  by  light  in 
summer,  and  kept  quiet  by  suitable  discipline.  Boys  who  retire  at  a  later 
hour  should  not  occupy  the  same  apartments  as  those  who  are  already  in 
bed.     Insufficient  sleep  produces  a  tired  aspect,  mental  inefficiency,  retarded 


Non-Spasmodic   Functional   Neuroses.  767 

•growth  and  development,  sleepiness  and  inattention  at  lessons,  nightmare, 
somniloquence,  pavor  and  somnambulism.  It  must  not  be  forgotten  that 
growth  takes  place  while  in  bed.  Later  results  are  the  effects  of  cumulation 
and  may  not  be  evident  for  months  or  years.  They  are  indicated  by 
neurasthenia,  brain  fatigue  and  exhaustion,  inability  to  stand  strain,  head- 
aches, insomnia,  neuroses,  and  possibly  chorea  and  epilepsy. 

Nightmare. — Children  sometimes  scream  out  in  their  sleep  and  fre- 
quently wake  up  at  night  fiightened,  excited  or  terrified.  Dreams  may  be 
pleasant  or  unpleasant.  Nightmare,  somnambulism,  teeth  grinding,  pavor 
nocturnus  and  pavor  diurnus  are  all  more  or  less  allied.  There  is  no 
strict  dividing  line  and  the  same  child  may  suffer  from  all.  The  chief 
■etiological  factors  are  a  neurotic  heredity  and  predisposition,  ill-health, 
febrile  states,  the  various  causes  of  respiratory  obstruction  leading  to 
•deficient  oxygenation  of  the  blood,  poisons  such  as  lead,  belladonna, 
and  alcohol  at  bedtime,  and  gastro-intestinal  disturbance. 

Nightmare  is  a  dream  in  which  there  is  great  distress  in  consequence  of 
■a  feeling  of  inability  to  move  and  save  oneself  from  a  horrible  or  fatal 
situation.  The  dream  is  unpleasant  and  terrifying,  and  the  child  wakes  up 
frightened  and  excited.  The  mind  is  clear,  the  attendants  are  recognised, 
and  the  details  of  the  dream  are  often  remembered  next  day.  Nightmare 
may  occur  at  any  age.  There  may  be  several  attacks  during  the  same  night, 
in  the  same  or  a  different  form.  In  recurrent  attacks  on  subsequent  nights 
the  same  dream  may  be  repeated.  Asphyxial  and  gastric  causes  are  the 
■chief  factors  in  its  production.  Many  attacks  are  due  to  a  late  meal,  over- 
feeding at  night,  ill-digested  food  or  constipation  ;  others  depend  on 
.adenoids,  large  tonsils  or  nasal  obstruction  ;  and  possibly  a  few  are  due  to 
reflex  irritation.  The  type  of  dream  is  based  on  some  visual  or  auditory 
impression  during  the  waking  hours. 

Somnambulism  is  a  type  of  nightmare  of  similar  causation.  The  term 
includes  all  varieties  of  motor  action  during  sleep  and  is  not  limited  to 
■"  walking."  In  this  state  the  child  can  do  many  things  impossible  to  him 
while  awake,  such  as  climbing  and  walking  along  dangerous  parapets. 
Or  he  will  get  out  of  bed,  look  for  things  under  the  bed,  empty  or  rummage 
in  drawers,  open  windows,  walk  downstairs,  and  carry  out  almost  any  action, 
■even  dangerous  ones  to  other  people,  including  getting  a  knife  and  stabbing 
•another  child.  The  eyes  are  wide-open,  the  movements  deliberate  and 
purposive,  but  consciousness  is  in  abeyance  and  attendants  are  ignored 
■completely.  A  bright  light  or  sharp  order  will  send  the  subject  back  to  bed. 
Visual  hallucinations  are  exceptional.  A  7-year  old  boy  saw  "  things 
•crawling  on  the  wall."  Next  day  there  is  no  remembrance,  or  only  a  very 
faint  one,  of  the  occurrence.  Late  suppers  and  school  work  are  the  common 
exciting  causes.  These  children  should  be  fastened  in  bed  with  a  belt 
round  the  waist  and  a  ring  at  the  back.  ■  Pass  a  bandage  through  the  ring 
and  tie  it  under  the  bed. 


768  Chapter  LVII. 

Somniloquence,  or  "talking  in  sleep,''''  can  be  regarded  as  a  mild  form  of 
somnambulism.  Children,  on  first  going  to  school,  constantly  talk  over  their 
lessons,  especially  sums,  in  their  sleep.  In  a  severe  form  long  conversations. 
are  held  with  imaginary  people  and  the  condition  is  analogous  to  pavor. 

Teeth  grinding  is  similar  in  character.  It  is  apt  to  occur  in  infants, 
during  illness,  and  in  neurotic  and  imbecile  children.  Occasionally  it  is 
associated  with  other  motor  habits,  e.g.  the  child  "  scratches  his  stomach," 
"  worries  at  himself,"  "  turns  over  and  kicks  about."  In  this  respect  it  is. 
allied  to  head  burying  and  similar  complaints.  All  the  teeth  may  become 
bevelled  down  to  the  same  level. 

Pavor  Nocturnus  or  Night  Terror. — An  excellent  description  of  this, 
peculiarity  is  given  in  Lamb's  Essay  on  "  Witches  and  other  Night  Fears. '* 
It  is  a  type  of  sleep  disturbance  characterised  by  emotional  distress  or  a 
nightmare  exaggerated  by  the  neurotic  disposition  of  the  child.  Much 
attention  has  been  devoted  by  Guthrie  and  Coutts  to  a  differentiation 
between  nightmare  and  pavor.  Certainly  between  the  two  extremes  the 
difference  is  considerable,  but  there  are  so  many  intervening  degrees  of  the. 
same  states  that  on  the  whole  it  seems  advisable  to  regard  them  as 
similar  in  their  causation  and  mode  of  production,  though  perhaps  of 
different  prognostic  import.  In  one  sense  it  is  a  paroxysmal  neurosis  of 
the  higher  centres.  Emotional  distress,  hallucinations,  abeyance  of  con- 
sciousness and  lack  of  remembrance  next  day  are  the  chief  features. 

The  attack  comes  on  in  the  early  part  of  the  night,  an  hour  or  two 
after  going  to  sleep.  The  child  suddenly  starts  up  with  a  piercing  shriek 
and  is  found  sitting  up  in  bed,  standing  on  the  floor  or  hiding  in  some  part 
of  the  room,  in  a  state  of  terror  and  mental  confusion,  with  sometimes  a  sense 
of  suffocation.  Sometimes  he  is  very  pale.  He  may  scream  with  fright,  or 
cry  out  inarticulately  and  unintelligibly.  He  is  oblivious  of  his  surround- 
ings, does  not  recognise  his  nurse  though  he  may  cling  convulsively  to  her, 
and  has  hallucinations  of  vision,  rarely  of  hearing.  His  pupils  are  dilated, 
eyes  wide-open  and  staring,  the  body  trembling,  hands  clenched  or  moved 
as  if  in  self-defence,  and  he  sweats  freely.  A  vivid  description  was  given 
by  the  mother  of  a  5-year  old  boy  : — "  He  started  up  in  bed  with  a  piercing 
shriek  and  shouted  out,  '  The  devil  is  here  ;  take  the  knife  away  for  he  has. 
cut  her  head  off.'  His  eyes  were  like  saucers,  his  body  trembled  and  he 
was  all  of  a  sweat." 

The  terror  is  usually  undefined  and  does  not  vary  in  character.  Often 
it  takes  definite  shape  and  the  child  cries  out,  "Look,  look!"  "They  are 
coming!"  or  sees  "boys  and  horses  about  the  room,"  "worms  crawling  on 
the  pillow,"  "ugly  faces  with  masks  on,"  etc.,  due  to  visual  hallucinations. 
Sensory  disturbance  was  present  in  one  child  who  complained  that  "  dicky 
birds  were  biting  her  hands  and  feet."  Vertigo  is  not  infrequent  and  is., 
probably  auditory  in  origin. 


N on- Spasmodic   Functional   Neuroses.  769 

The  attack  lasts  a  few  minutes  to  an  hour.  Frequently  the  child  falls 
asleep  without  return  of  consciousness.  If  he  becomes  conscious,  he  may 
remain  frightened  and  under  the  delusion,  or  talk  of  the  hallucination  and 
later  ask  to  be  put  back  to  bed.  Profuse  micturition  or  defalcation  may  occur 
at  the  end  of,  or  even  during,  an  attack.  Usually  there  is  no  remembrance 
of  the  attack  next  day  ;  sometimes  a  faint  recollection  or  consciousness  of 
something  horrible  or  unpleasant.  The  child  shirks  talking  about  it  but 
may  describe  the  nature  of  the  hallucination,  if  his  confidence  is  gained. 
Except  in  febrile  states  there  is  rarely  more  than  one  attack  a  night. 
It  may  recur  every  night,  at  varying  intervals  or  quite  irregularly.  The 
hallucination  is  almost  always  the  same. 

Pavor  has  been  divided  into  (1)  Asphyxial  and  (2)  Primary  Cerebral 
types.  The  asphyxial  type  is  allied  to  nightmare  and  the  terror  is  sub- 
jective. The  attack  develops  slowly,  comes  on  an  hour  or  more  after 
falling  asleep,  and  is  characterised  by  a  feeling  of  suffocation,  mental 
confusion,  hallucinations,  amnesia  and  muscular  weakness  in  consequence 
of  the  asphyxia. 

The  muscular  debility  is  shown  by  the  inability  to  articulate  clearly 
and  the  clumsy  movements.  The  incidence  and  severity  of  these  attacks 
depend  on  the  degree  of  respiratory  obstruction.  Fright  and  hallucinations 
may  occur  in  any  disease  leading  to  deficient  oxygenation.  On  the  other 
hand,  in  many  instances  the  cause  appears  to  be  gastric  or  intestinal.  In 
such  cases  we  must  attribute  the  dyspnoea  and  sense  of  suffocation  to 
reflex  stimulation  of  the  vagus,  if  we  accept  the  asphyxial  view  of  their 
pathology. 

The  primary  cerebral  or  idiopathic  type  is  the  one  in  which  no  asphyxial 
or  alimentary  cause  is  discoverable,  and  a  definite  predisposing  factor  is 
present  in  the  shape  of  a  neurotic  or  alcoholic  parentage,  a  rheumatic 
diathesis,  or  past  infantile  convulsions.  These  children  are  neurasthenic  ; 
nervous,  irritable,  impressionable,  excitable  and  often  anaemic.  They  sleep 
lightly,  restlessly,  and  wake  easily.  The  terror  is  objective  and  due  to 
over-excitement  of  the  cerebral  cortex  in  a  nervous  child.  The  exciting  cause 
is  the  same  as  in  other  varieties  of  disordered  sleep,  viz.,  school  work, 
pantomimes,  dark  rooms,  variable  shadows,  gruesome  pictures  or  tales  cf 
ghosts.  In  normal  children  ghost  tales  and  horrors  do  not  induce  attacks  ; 
possibly  they  merely  formulate  the  vision  in  the  susceptible  child.  Occasion- 
ally the  attacks  are  due  to  fever,  tuberculous  meningitis,  or  head  injury. 

Etiology. — Pavor  is  most  common  in  the  fourth  year  of  life,  the  age 
when  adenoids  are  likely  to  produce  the  greatest  amount  of  respiratory 
obstruction  ;  fairly  frequent  up  to  beginning  of  the  seventh,  coincident 
with  the  commencement  of  school  life  ;  less  common  up  to  the  twelfth 
year  and  rare  subsequently.  In  half  the  cases  under  my  care  a  digestive 
cause  has  been  present.  The  digestive  disturbances,  consequent  on  carious 
teeth,  the  second    dentition    and    late    meals,   and  school  life  are  often 

3  D 


770  Chapter  LVII. 

combined.  It  is  frequently  found  that  more  than  one  factor  is  present.  The 
sex-incidence  is  3  females  to  2  males. 

Complications. — As  already  stated  all  forms  of  sleep  disturbance 
may  occur  in  the  same  child  at  different  times.  In  the  cerebral  type  of 
pavor  we  are  likely  to  find  the  usual  signs  of  neurasthenia,  especially  head- 
ache, palpitations  and  muscular  fatigue. 

Abnormally  bad  temper,  habit  spasm,  enuresis,  moral  insanity,  fits, 
hysteria,  migraine  and  insanity  may  be  present ;  but  the  pavor  should  then 
be  regarded  as  a  symptom  of  these  affections  and  not  these  looked  upon  as 
complications  of  pavor. 

Diagnosis. — Never  accept  a  case  of  pavor  as  primarily  cerebral  until 
all  other  causes  have  been  excluded.  Do  not  confuse  nightmare  with  pavor. 
Coutts  draws  a  striking  distinction,  unfortunately  not  always  confirmed 
in  practice,  but  frequently  of  great  use.  He  holds  that  in  pavor  the  child  sees 
visions,  in  nightmare  he  dreams  dreams.  Nightmare  may  occur  in  any 
child,  at  any  age,  in  several  attacks  during  the  same  night,  and  without 
grave  terror.  It  is  associated  with  ill-health,  with  recollection  of  the  nature 
of  the  dream,  and  with  recognition  of  the  nurse  and  surroundings.  Night 
terror  occurs  in  the  neurotic  or  in  children  with  a  family  history  of  neuroses, 
is  rare  after  12  years  of  age,  is  independent  of  ill-health,  and  usually  in 
single  attacks.  There  is  lack  of  consciousness  of  surroundings,  grave  terror 
and  emotional  distress,  and  no  recollection  of  the  attack  next  day.  The 
nature  of  the  vision  is  constant,  while  the  dream  in  nightmare  may  vary  and 
take  several  forms  in  the  same  night.  Pavor  is  distinguished  from  epilepsy 
by  the  absence  of  a  fit,  tongue  biting,  and  subsequent  stupor  or  intellectual 
torpor. 

Prognosis. — Sleep  disorders  are  commonly  symptomatic  and  the 
outlook  good.  Somnambulism  may  persist  in  those  of  neurotic  ancestry 
and  lead  to  fatal  accident.  The  predisposing  causes  of  cerebral  pavor  may 
produce  tics,  migraine,  neurasthenia,  hysteria,  epilepsy  and  insanity  in  later 
life.  Imbecility  or  severe  brain  disease  is  rarely  present.  Pavor  does  not 
predispose  to  epilepsy. 

Treatment. — Give  an  aperient,  attend  to  the  diet,  and  regulate  the 
mode  of  life.  Ventilate  the  sleeping  apartment  thoroughly,  allow  the  use 
of  a  night  light,  and  let  the  nurse  sleep  in  an  adjacent  room  with  the 
intervening  door  open.  Treat  local  causes  of  asphyxia  and  irritation. 
Permit  no  physical  or  mental  strain,  limiting  school  work  to  the  morning 
hours  ;  no  late  meals  and  no  parties. 

The  child  should  sleep  on  a  hard  mattress,  with  no  heavy  bed-clothes,  and 
have  a  bobbin  fixed  to  the  spine  to  keep  it  off  the  back.  Neurotic  children 
must  be  protected  from  unpleasant  sights  and  shocks,  ugly  pictures, 
gruesome  tales,  threats,  excitement,  and  some  of  the  appalling  toys  which 
are  wrongly  considered  suitable  for  children.  Attend  to  the  digestion, 
giving  a  mixture  of  rhubarb  and  soda,  and  keep  the  bowels  open.    Give  a 


Non-Spasmodic  Functional  Neuroses.  771 

•dose  of   bromide,   bromide   and   chloral,   or  phenazone   at   bedtime  ;     or 
bromides  or  plienazone  grs.  1-4  t.d.s.    Iron  is  needed  if  there  is  anaemia. 

Pavor  Diurnus. — This  is  a  day-terror  of  cerebral  origin,  which  may  be 
associated  with  or  replace  pavor  nocturnus.  In  some  cases  there  is  definite 
irritation,  e.g.  constipation,  worms  or  colitis.  There  is  a  sudden,  un- 
accountable attack  of  screaming  and  terror.  The  child  rushes  to  someone 
for  protection  and  cannot  be  pacified.  The  attack  may  come  on  in  the 
midst  of  play,  or  while  the  child  is  apparently  awake  though  possibly  in  a 
dreamy  state,  and  with  visual  or  auditory  hallucinations.  There  may 
be  dread  of  the  mother  or  nurse,  and  even  temporary  mania.  In  milder 
attacks  there  is  sudden  pallor,  sometimes  a  vacant  look,  but  no  loss  of 
consciousness.  They  last  from  a  few  seconds  to  15  minutes.  Attacks  may 
■occur  several  times  daily,  or  only  at  intervals  of  a  week  or  two.  In  young 
infants  they  may  take  the  form  of  paroxysmal  screaming  and  be  put  down 
to  bad  temper.  An  anaemic  dyspeptic  boy,  16  months  old,  had  frequent 
screaming  attacks  for  3  weeks.  They  were  of  sudden  onset  and  cessation, 
and  followed  by  much  trembling  for  10-15  minutes.  They  ceased  as  soon 
as  the  dyspeptic  state  was  cured. 

Day  terrors,  day  somnambulism  and  narcolepsy  may  be  associated. 
The  outlook  is  less  favourable  than  in  other  forms  of  pavor  for  they  appear 
to  indicate  a  high  degree  of  the  neurotic  disposition,  and  a  greater  liability 
to  neurosis  in  later  life. 


CHAPTER    LVIII. 

DISORDERS    OF    THE    HIGHER    FACULTIES. 

Neurotic  Children — Precocity —  Neurasthenia — P  sychasthenia —  Hysteria — 
Mental  Deficiency — Mongolism — Insanity — Speech  Defects —  Deaf- 
Mutism — Word- Deafness — Word- Blindness — Idioglossia — Stammering. 

Neurotic  Children.— The  neurotic  disposition  is  inherited.  It  can  be- 
modified  by  training  and  environment  but  not  wholly  eliminated.  This, 
peculiarity  of  the  nervous  system,  rather  than  the  normal  instability 
of  the  nerve  centres  in  early  life,  is  the  primary  cause  of  bad  habits  and 
neuroses.  The  chief  predisposing  factors  are  those  common  to  all  children ; 
viz.  defective  control  by  the  higher  over  the  lower  centres,  and  imperfect 
definition  of  the  motor  tracts  leading  to  inco-ordination  and  spasmodic- 
affections.  The  effects  on  the  nervous  system  of  malnutrition,  rickets,, 
alimentary  disorders,  rheumatism,  various  toxaemias  and  reflex  irritation,, 
are  partly  predisposing  and  partly  exciting  causes. 

These  children  are  subject  to  general  impairment  of  metabolism  and 
vitality.  Emotional  excitability  is  abnormally  keen,  easily  stimulated  and 
controlled  with  difficulty.  Whether  restrained  or  unrestrained,  it  is 
physically  and  mentally  exhausting.  It  may  develop  into  a  definite  neurosis- 
if  the  will  power  is  also  defective.  Guthrie  recognises  a  restrained  and  an 
unrestrained  emotional  type.  In  the  former  the  emotions  are  as  strongly 
controlled  as  they  are  felt.  Though  intelligent  and  observant  these 
children  are  so  reticent  that  they  are  thought  dull  and  stupid.  They  are 
sensitive,  shy  and  proud  ;  desirous  of  sympathy  and  affection  ;  possess- 
no  sense  of  humour  ;  are  brooding,  gloomy,  solitary  and  revengeful ;  and 
develop  abnormal  scruples  and  phobias.  Children  of  the  unrestrained' 
emotional  type  are  normally  or  unduly  intelligent,  timid,  high  spirited,, 
full  of  restless  energy  and  easily  discouraged.  They  are  impetuous, 
enthusiastic  but  wanting  in  judgment,  extraordinarily  vain,  with  a  saving; 
sense  of  humour,  and  do  not  always  take  themselves  seriously.  Thus,  in 
one  variety  there  is  emotional  stress  with  expression  thereof,  and  in  the 
other  stern  repression  of  the  signs  of  excessive  emotion.  Under  suitable 
conditions  hysteria  develops  in  the  unrestrained  and  neurasthenia  in  the 
restramed  type. 

Symptoms  in  Babies. — Hypersensitiveness  of  the  special  senses  is  the- 
chief  sign  of  a  neurotic  disposition.  The  baby  may  refuse  substitutes  for  the 


Disorders  of  the  Higher  Faculties.  773 

■breast,  rebel  against  slight  changes  in  the  diet  which  may  be  imperceptible 
to  the  adult,  express  repugnance  to  certain  flavours  and  disgust  at  the 
presence  of  the  least  particle  of  solid  or  gritty  matter.  This  objection  to 
solid  food  may  be  so  great  as  to  cause  nausea,  "  gagging,"  gargling  and 
vomiting,  and  prolonged  bottle-feeding.  Occasionally  it  depends  on  inco- 
ordination of  the  muscles  of  deglutition.  It  may  lead  to  idiosyncrasies  in 
food  and  drink,  and  the  desire  for  unsuitable  foods.  Hot  greasy  fat  and 
•cod-liver  oil  are  intensely  disliked  by  neurotics  of  the  unrestrained  type  ; 
and  the  necessary  amount  of  fat  must  be  given  in  the  form  of  butter, 
margarine,  cream,  dripping,  or  olive  oil  in  salads.  Pica  (p.  250)  is  not 
uncommon  in  the  first  year  of  life. 

Hypersensitiveness  to  light  is  indicated  by  the  unduly  early  acquire- 
ment of  normal  perception  and  alarm  at  the  sight  of  unaccustomed  objects 
and  people.  Co-ordination  of  the  ocular  muscles  is  established  in  the  third 
month,  but  a  precocious  child  may  follow  a  bright  light  and  turn  its  head 
as  early  as  the  sixth  day.  People  and  objects  are  recognised  in  the  sixth 
month.  Occasionally  there  is  abnormal  sensitiveness  to  colour,  and  the 
expression  of  alarm  at  red  or,  less  often,  yellow. 

In  the  first  24  hours  the  child  is  apparently  deaf.  In  2  weeks  it  appre- 
ciates loud  sounds,  and  in  two  months  it  recognises  the  direction  of 
•conveyance  of  sound  and  turns  toward  it.  Acuity  of  hearing  develops 
more  quickly  in  some  infants  and  they  may  awake  at  the  slightest  sound. 
Neurotic  babies  are  very  sensitive  to  loud  or  discordant  noises,  and  often 
frightened  thereby.  Such  sensitiveness  may  persist  and  be  a  cause  of  the 
timidity,  tearfulness  and  unsociability  of  some  children  at  noisy  parties. 
It  may  depend  on  the  musical  sense  and  be  stimulated  only  by  unmusical 
sounds.  Loud  noises  often  terrify  children.  The  sense  of  smell  may  be 
abnormal  and  certain  odours  may  produce  paroxysmal  asthma,  syncope, 
nausea  or  vomiting.  Cutaneous  hypersensitiveness  is  shown  in  the  tendency 
to  erythematous  and  urticarial  rashes.  The  irritation  of  tight  bands  or 
unsuitable  garments  may  cause  insomnia,  habit  spasm  and  other  disorders. 

Other  signs,  more  obvious  in  older  children,  are  fretting,  home-sickness, 
timidity,  fear,  morbid  apprehensions,  worry,  and  perversions  of  religious 
and  moral  emotions.  Day-dreaming  is  an  exaggeration  of  the  imaginative 
faculty  to  such  an  extent  that  the  dream  is  mistaken  for  reality.  It  may 
lead  to  romancing  or  lying.  Usually  the  dream  relates  to  the  child's  own 
personality.  Timidity  is  not  necessarily  cowardice.  It  may  depend  on 
imagination,  the  fantastic  shapes  evolved  from  lights  and  shadows  ;  on 
fear  of  reproach,  harsh  words,  anger  or  ridicule,  or  the  disgrace  of  corporal 
punishment ;  or  fear  of  the  unknown  or  of  impending  trouble.  Ridicule 
will  frequently  prevent  a  child  attempting  even  simple  feats  or  ordinary 
■book  tasks.  In  its  severest  form  the  child  is  afraid  of  ordinary  animals, 
•sights  and  sounds.  These  children  must  be  encouraged.  Their  confidence 
must  be  acquired,  night  lights  allowed,  and  their  fears  relieved  by  common 


774  Chapter  LVIII. 

sense  explanations  of  the  phenomena  causing  them.     Day-dreamers  must 
be  kept  occupied  with  work  or  play. 

Mental  or  Intellectual  Precocity  is  unduly  rapid  development,  relative- 
to  an  artificial  standard  applicable  to  children  of  the  same  race,  family,, 
sex,  age  and  environment.  Like  natural  ability  it  follows  the  laws  of 
variation  from  the  mean  and  is  not  necessarily  abnormal  or  pathological. 
The  variation  from  the  mean  may  take  place  in  other  directions  and 
result  in  imbecility,  criminality,  sexual  perversions  or  moral  insanity,  all 
of  which  may  occur  in  the  same  family  as  that  of  the  genius. 

True  precocity  is  a  variation  from  the  normal,  dependent  on  an  inborn 
or  hereditary  tendency  and  modified  by  environment.  It  must  be  dis- 
tinguished from  false  or  artificial  precocity,  due  to  external  influences,  over- 
pressure, town  life,  and  excessive  stimulation  of  the  mental  faculties- 
External  influences  modify  but  do  not  cause  true  precocity. 

Precocious  children  are  usually  the  first  or  last  of  large  families,  or 
born  of  parents  of  greatly  dissimilar  ages.  In  these  respects  precocity  is 
like  Mongolism.  Only  children  show  precocity  because  of  their  surroundings, 
being  constantly  in  the  society  of  their  elders  and  over-stimulated.  Over- 
grown children  are  liable  to  be  precocious,  through  being  dressed  in  accord- 
ance with  their  size  and  associating  with  older  companions.  Mental 
troubles  and  neuroses  are  frequent  during  the  period  of  rapid  growth  of  the 
brain,  from  1-7  years,  and  at  puberty,  and  are  rare  in  the  intervening  period- 
Care  should  be  taken  not  to  over-stimulate  the  brain  at  these  periods. 

Precocity  may  be  of  good  or  bad  omen.  It  does  not  imply  prematurity 
and  early  decline  of  the  intellectual  powers,  nor  is  it  incompatible  with  long 
life  and  prolonged  mental  ability.  The  idea  that  precocious  children  die 
young,  or  become  insane  because  of  their  precocity,  is  not  borne  out  by 
facts,  at  least  as  regards  the  truly  precocious  ones.  But  excessive  ability  of 
an  acquired  type  is  often  associated  with  defective  heredity  and  may  end  in 
dementia  preecox,  neurasthenia  or  hysteria.  Extraordinarily  clever  men 
have  generally  surpassed  ordinary  children  in  their  early  years.  This  is 
notably  the  case  among  artists  and  musicians,  while  mathematicians  and 
philosophers  are  of  later  development.  In  the  course  of  intellectual  growth 
sense  impressions,  mental  images  and  abstract  ideas  develop  successively. 
Genius  does  not  always  specialise  and  in  its  highest  form  (intellectus  univer- 
salis) includes  everything,  except  perhaps  music  and  art.  As  a  rule  the 
great  men  of  the  world  are  drawn  from  the  precocious  children,  but  fond 
mothers  can  console  themselves  by  the  fact  that  genius  is  not  always- 
recognised  in  early  life  and  the  supposed  dullard  is  sometimes  a  boy  of 
remarkable  originality.  Many  great  men  are  not  piecocious  in  childhood. 
Some  children  develop  much  later  than  others.  Yet,  as  a  rule,  the  greater 
the  ability  in  early  life  the  greater  is  the  prospect  of  distinction  in  later  life, 
provided  that  failure  does  not  ensue  from  lack  of  opportunity,  perseverance,. 


Disorders  of  the  Higher  Faculties.  775 

ambition  or  other  moral  qualities,  and  that  the  precocious  brain  is  not 
spoilt  by  overpressure  or  uncongenial  work. 

Mentally  diseased  children  may  be  precocious  and  precocity  may  be 
associated  with  delicacy,  though  by  no  means  frequently.  Constitutional 
weakness  is  not  uncommon  in  the  "  Wunderkinder  "  at  one  end  and  in 
imbeciles  at  the  other  end  of  the  scale.  Imbeciles  are  liable  to  tuberculosis. 
Delicacy  may  induce  artificial  precocity,  through  compelling  the  child  to  a 
less  active  life,  with  more  constant  stimulation  of  the  brain  by  reading  and 
adult  companionship.  It  is  generally  found  in  schools  that  the  taller 
children  of  the  same  age  are  in  the  higher  classes  and  that  dullards  are 
below  the  mean  height.  "Wunderkinder"  are  exceptional,  e.g.  calculating 
prodigies  and  those  with  extraordinary  memory,  musical  capacity,  excessive 
manual  skill  or  muscular  power,  mimetic  faculties,  etc.  Some  of  these  have 
normal  or  increased  genera]  mental  power,  while  others  (idiot  savants) 
are  mentally  deficient  and  usually  die  young.  A  minor  degree  of  brilliance 
in  one  direction  may  be  associated  with  dulness  in  others.  Precocity  and 
natural  ability  follow  the  same  laws  of  health  and  physical  development. 
Artificial  precocity  is  the  most  likely  to  be  worked  out  and  end  badly. 

Treatment. — True  precocity  may  be  encouraged  in  its  natural  bent  and 
should  not  be  thwarted,  as  long  as  there  is  no  excessive  stimulation. 
Artificial  precocity  must  be  repressed  and  the  child's  energies  directed 
into  other  channels  such  as  an  open-air  life,  games,  botany  and  the  study 
of  animal  life.  A  liberal  allowance  of  sleep  is  essential.  Erratic  precocity 
is  the  most  dangerous  and  requires  assiduous  care.  Aim  at  complete 
all  round  development  and  map  out  the  daily  routine  of  life.  Guard  against 
emotion  and  excitement.  Inculcate  physical,  mental  and  moral  discipline. 
Each  case  should  be  treated  on  its  merits,  and  delay  in  mental  development 
must  not  be  considered  a  drawback. 

Neurasthenia. — Neurasthenia,  psychasthenia  and  hysteria  can  be 
differentiated  from  each  other,  though  they  are  often  combined  and  present 
many  intermediate  forms.  They  may  occur  in  early  life,  especially 
about  puberty  and  in  early  adolescence,  but  are  more  frequent  at  later  ages. 
The  predisposing  cause  is  a  neurotic  heredity,  a  capacity  for  feeling  emotions, 
sensations  and  physical  stimuli  to  an  abnormal  degree  and  on  inadequate 
provocation  in  comparison  with  a  normal  child.  The  exciting  causes  are 
physical  and  psychical  depression  such  as  result  from  malnutrition,  the 
toxins  of  influenza  and  other  infections,  fear,  shocks,  injury,  lack  of  sleep, 
irregular  mode  of  life,  over-stimulation  of  the  brain  and  imagination,  family 
jars  and  quarrels,  and  undue  strain  on  the  emotions. 

Neurasthenia  is  a  state  of  irritable  feebleness  with  general  depression 
of  the  cerebrospinal  functions  ;  a  combination  of  irritability  and  exhaus- 
tibility  of  the  higher  cerebral  and  spinal  nerve  centres,  or  a  hypersensitive- 
ness  of  the  higher  centres  and  ready  exhaustion  of  physical  and  nervous 
energy.    Affected  infants  are  abnormally  easily  frightened,  startled  by  noise 


776  Chapter  LVIII. 

or  bright  light  and  utter  reflex  cries,  struggle  or  cry  violently  in  the  bath, 
are  constantly  wailing  and  sleep  lightly.  In  young  children  fear  of  strangers, 
animals  and  new  toys  is  the  most  marked  symptom. 

The  chief  symptoms  are  somatic  and  psychical.  Nutrition  is  impaired 
and  the  general  health  indifferent  or  bad.  The  main  objective  and  per- 
manent signs  are  exaggerated  deep  reflexes,  normal  or  deficient  corneal  and 
pharyngeal  reflexes,  variable  pupils,  tremor  of  the  eyelids  and  incomplete 
closure  on  shutting  the  eyes,  tremulous  hands,  cold  hands  and  feet,  hurried 
or  stammering  speech,  variability  in  the  pulse  rate,  vasomotor  troubles  and 
fleeting  erythema.  Downheartedness,  disinclination  to  play  or  work, 
restlessness,  rapid  fatigue,  and  undue  emotion  are  commonly  present. 
Other  symptoms  are  subjective  and  often  paroxysmal  in  character,  such  as 
headache,  syncope  on  fright  or  fatigue,  vomiting  on  waking  or  going  to 
school,  anorexia,  constipation,  enuresis,  frequent  micturition  and  stammering 
of  the  bladder,  palpitations  and  arrhythmia  ;  convulsive  and  alarming 
cough  with  cyanosis,  choking  and  vomiting,  simulating  pertussis  ;  exhi- 
bitions of  wild  rage,  convulsive  sobbing  or  laughter  ;  egotism  and  seJf- 
analysis.    Dreamy  states  take  the  place  of  hysterical  fits. 

Attacks  of  convulsive  rage  are  most  frequent  at  1-5  years  of  age. 
The  child  is  unable  to  cry  because  of  arrested  expiration,  due  to  spasm  of  the 
expiratory  muscles.  The  face  turns  pale,  body  rigid,  eyes  upward,  and  the 
child  falls  backward  unconscious.  At  the  onset  she  may  strike  out  wildly 
with  the  fists,  roll  on  the  floor  and  kick,  or  throw  herself  down  and  scream 
violently  in  the  public  street.  Sometimes  the  face  is  turgescent  and  bluish, 
the  whole  body  trembles,  and  the  child  suddenly  ceases  to  scream  and 
becomes  rigid,  with  the  mouth  wide-open,  and  comatose.  Then  the  spasm 
relaxes  and  a  loud  cry  is  uttered.  There  is  rarely  involuntary  micturition 
and  defalcation.  It  differs  from  the  expiratory  apncea  of  laryngospasm  in 
the  absence  of  inspiratory  stridor  and  of  galvanic  over-excitability.  The 
attack  can  often  be  stopped  by  punishment  or  threat  thereof  at  the  onset, 
that  is  as  soon  as  the  child  attempts  to  hold  the  breath,  and  can  be  shortened 
by  dashing  cold  water  in  the  face,  a  slight  smack  or  cutaneous  irritation. 

Neurasthenia  is  acquired  and  curable.  It  is  usually  gradual  in  onset 
and  chronic  in  course.  It  may  be  temporary,  and  cured  by  removal  of  the 
cause.  Sometimes  it  is  localised  in  one  special  symptom  and  difficult  of 
diagnosis,  or  it  may  be  an  early  stage  of  organic  nervous  disease.  The 
prognosis  depends  upon  the  heredity  and  environment. 

Psychasthenia  is  a  variety  of  neurasthenia  in  which  the  mental  symptoms 
predominate.  It  may  be  associated  with  unusual  intellectual  gifts,  defective 
intelligence,  or  lack  of  moral  sense.  It  chiefly  affects  timid,  impressionable 
children  ;  and  may  be  regarded  as  the  climax  of  hereditary  predisposition, 
having  its  basis  in  an  inherited  and  more  or  less  degenerate  nervous  con- 
stitution. Hence  it  can  never  be  regarded  as  completely  curable.  Usually 
it  comes  on  at  puberty  or  shortly  after,  but  may  begin  as  early  as  the 


Disorders  of  the  Higher  Faculties.  Ill 

•eighth  year.  Half  the  cases  are  under  20  years  old.  It  is  more  common  in 
females  and  there  is  often  no  apparent  exciting  cause. 

The  child  develops  morbid  scruples,  increasing  mental  uncertainty 
and  hesitation,  lack  of  initiative  power  or  acting  promptly,  auto-analysis, 
and  excessive  emotional  reactions.  Next  it  commences  imperious  strange 
acts  such  as  frequent  washing  of  the  hands,  aimless  rummaging,  and 
verification  of  unimportant  matters  (tics)  ;  or  stays  in  a  state  of  rumination 
•or  reverie. 

Finally,  it  develops  fixed  ideas,  persistent  obsessions  and  phobias. 
Uncontrollable  actions  depend  on  these  uncontrollable  ideas,  though  they 
-are  realised  by  the  patient  as  morbid.  The  will  is  enfeebled  and  irresolute,  the 
child  being  incapable  of  fixing  either  attention  or  energy.  In  manner  there 
is  eccentricity  and  in  action  clumsiness.  In  spirit  the  joyousness  of  youth 
is  replaced  by  melancholy  or  hypochondriasis. 

The  affection  may  take  several  years  to  develop  fully,  and  often  there 
•are  periods  of  remission.  The  child  may  know  when  an  attack  is  coming  on. 
She  becomes  flushed,  restless,  unable  to  keep  still,  jerky  and  agitated  ;  or 
occasionally  dull,  inert,  listless  and  mumbling. 

The  obsession  or  phobia  is  well  marked  and  assumes  various  types  in 
different  cases.  It  may  be  persistent  or  vary  in  different  attacks.  The  chief 
types  are  : — (1)  Doubt,  hunting  out  objects,  counting  and  naming ; 
{2)  Metaphysical  mania  or  exaggerated  scruples  of  cleanliness  and  exactness, 
giving  rise  to  uncontrollable  desire  to  wash  and  even  self-mutilation  ; 
(3)  Agoraphobia,  claustrophobia,  dread  of  travelling,  an  intense  desire  to 
roam,  truancy  and  running  away  from  school ;  (4)  Fear  of  light,  fire,  sharp 
•objects,  clothing,  dirt,  etc.;  (5)  Criminal  desires,  perhaps  theft ;  (6)  Sexual 
perversity  ;  (7)  The  alcohol  and  drug  habit ;  (8)  Self-accusation.  The 
•disease  is  progressive,  unless  treated  (p.  780),  and  liable  to  end  in  suicide 
during  depression,  hypochondriasis,  melancholia,  or  delusional  insanity. 

Hysteria. — In  this  we  find  a  lack  of  will  power,  combined  with  a 
process  of  self-suggestion  and  hypnosis  in  the  production  of  a  great  variety  of 
symptoms,  which  are  sometimes  extraordinarily  difficult  of  differentiation 
from  organic  disease.  It  is  a  mental  disease  of  the  "  unconscious  or  sub- 
conscious mind,"  an  aberration  of  the  cells  governing  function  and 
nutrition.  It  is  curable  by  and  produced  by  suggestion,  and  must  be 
•distinguished  from  imposture,  simulation,  malingering  and  organic  disease. 
A  normal  child  does  not  simulate  disease.  Accepting  this  view  we  must 
■consider  some  of  the  symptoms,  generally  regarded  as  hysterical,  as  signs  of 
added  neurasthenia.  True  hysterical  symptoms  depend  on  intellectual  or 
•emotional  psychic  causes.  The  hysterical  child  is  egotistical,  desires  im- 
portance and  attention  or  admiration,  is  emotional,  and  has  a  lively 
imagination.  Explosiveness  and  excitability  of  the  higher  nerve  centres 
are  combined  with  lack  of  control  over  emotional  display  and  subsequent 
■exhaustion.    It  is  a  cerebral,  not  a  cerebrospinal  affection.    The  symptoms 


778  Chapter  L  VIII. 

may  come  and  go  suddenly,  subside  rapidly  and  completely,  be  cured 
suddenly  after  a  duration  of  years,  are  dominated  by  mental  and  moral, 
influences,  and  are  compatible  with  perfect  physical  health  and  nutrition. 

Etiology. — The  predisposing  and  exciting  causes  are  the  same  as  in 
neurasthenia.  Apart  from  the  latent  condition  the  exciting  cause  is 
usually  quite  inadequate.  Susceptibility  is  greatly  influenced  by  training 
and  environment,  by  undue  fostering  of  the  emotional  side  and  by  over- 
indulgence. Association  with  neuropathic  and  capricious  parents,  and 
imitation,  are  important  causes.  It  is  as  common  among  the  poor  as  the 
rich,  in  isolated  rural  centres  as  in  towns,  and  at  any  period  of  the  year. 
It  usually  begins  at  8-12  years  of  age,  rarely  before  5  years,  but  may  occur 
as  early  as  3  years.  Most  of  the  cases  in  the  very  young  are  more  truly 
neurasthenia.  It  is  more  common  in  girls.  Boys  are  more  affected  in 
childhood  than  in  later  life  and  more  severely  than  girls.  It  is  more  difficult 
to  recognise  in  boys,  for  organic  disease  is  better  simulated  and  boys  play 
the  game  more  thoroughly,  being  afraid  of  being  found  out  or  laughed  at 
for  girlish  tricks. 

Symptoms. — The  onset  is  sudden,  with  full  development  of  symptoms 
which  are  usually  limited  to  one  and  that  exaggerated  in  type  ;  generally 
motor,  rarely  sensory.  Many  symptoms  arise  from  suggestion  or  imitation ;. 
or  are  due  to  auto-suggestion,  persisting  after  the  original  cause  has 
disappeared.  Certain  general  symptoms  may  be  present  as  well  as  the 
particular  one  that  attracts  attention,  but  hysterical  stigmata  are  rare  in 
the  very  young  for  the  child's  mind  is  simple,  and  less  common  in  older 
children  than  in  adults.    At  puberty  they  approach  the  adult  type. 

The  sensory  disturbances  include  anaesthetic  spots,  anaesthesia  of  the 
pharynx,  conjunctiva  and  skin,  hemi-ansesthesia,  or  a  sleeve-like  distri- 
bution on  one  limb  ;  hyper-aesthetic  areas  not  corresponding  wuth  any 
special  nerve  or  nerves,  and  hysterogenetic  zones  or  tender  points  ;  con- 
centric limitation  of  the  field  of  vision  ;  headache,  clavus  and  localised  pain  ; 
and  globus  hystericus.  Deafness,  deaf-mutism,  mutism  and  blindness  are 
rare.  Sometimes  there  is  aphonia  or  dysphonia,  which  is  absent  on 
coughing  and  singing.  The  speech  is  whispering  for  the  cords  are  imper- 
fectly approximated.  Dysphagia  may  be  present  in  neurotic  infants  about 
the  time  of  weaning  and  due  to  objectionable  food,  hurried  feeding  or 
nervousness.  In  older  children  there  may  be  vigorous  but  unavailing  attempts 
to  swallow. 

The  psychical  symptoms  take  the  form  of  putting  out  the  tongue  and 
spitting,  attacks  of  shouting  and  screaming,  exhibitions  of  anger  and  crying 
without  sufficient  cause,  apparent  fright,  in  which  the  hands  are  clenched, 
uncontrollable  laughter  or  giggling,  mimicry  of  animals,  stuporous 
states,  and  sexual  or  erotic  troubles. 

The  motor  symptoms  include  convulsions,  spasmodic  seizures  and 
contractures,  paralyses  and  tremors.    Some  relapses  in  chorea  are  hysterical.. 


Disorders  of  the   Higher  Faculties.  779" 

In  hysterical  convulsions  there  is  no  self-injury,  no  tongue  biting,  no 
sphincter  incompetence,  and  no  true  unconsciousness.  The  eyelids  are 
tightly  closed,  the  pupils  react,  and  the  movements  are  theatrical.  Astasia- 
abasia,  inability  to  walk  or  stand  but  ability  to  move  the  limbs  freely  in  bed,, 
may  follow  slight  injuries,  fright  or  confinement  to  bed  for  a  few  days. 
Paralysis  may  be  local  or  general  and  take  the  form  of  paraplegia,  mono- 
plegia or  hemiplegia.  Monoplegia  of  a  leg  is  the  most  common.  The 
knee  jerk  may  be  absent.  The  face  generally  escapes.  It  may  be  combined 
with  rigidity  or  flaccidity,  a  little  wasting  from  disuse,  and  possibly  mechani- 
cal oedema  in  a  dependent  limb.  Contractures  are  rare  under  puberty .. 
They  are  usually  more  painful  and  more  extreme  than  in  organic  disease, 
and  relax  during  sleep  and  under  anaesthesia.  They  may  simulate  tor- 
ticollis, cervical  caries,  scoliosis  or  hip  disease.  The  possibility  of  early 
disease  in  hysterical  subjects  must  not  be  overlooked.  The  plantar,  pharyn- 
geal and  superficial  reflexes  may  be  lost.  The  plantar  reflexes  are  never 
extensor,  and  the  deep  reflexes  are  normal  or  exaggerated.  There  is  no 
ankleclonus. 

Respiratory  symptoms  may  take  the  form  of  continuous  yawning,  slow 
and  deep  breathing,  dyspnoea,  orthopnoea,  and  barking  or  spasmodic 
cough.  Violent  stridor  and  asthmatic  attacks  may  occur,  if  the  child  has  had 
such  symptoms  before  from  organic  disease.  The  circulatory  symptoms 
are  palpitations,  tachycardia,  abnormal  pulsation  in  the  abdominal  aorta, 
and  carotids,  exaggerated  flushing  and  pallor,  and  dead  fingers. 

Symptoms  referable  to  the  digestive  tract  include  anorexia  nervosa,, 
polydipsia,  vomiting,  cardiospasm,  constipation,  persistent  diarrhoea, 
faecal  incontinence,  prolapsus  recti,  haernatemesis,  enterospasm,  and 
meteorism  due  to  swallowing  air  or  spasm  of  the  diaphragm. 

The  urinary  symptoms  include  anuria,  pollakiuria,  polyuria,  enuresis, 
retention,  and  possibly  albuminuria  and  haematuria.  The  skin  may  show 
vasomotor  irritability,  and  attacks  of  pallor  or  flushing,  the  pallor  being  due 
to  sudden  dilatation  of  the  splanchnic  area  ;  fugitive  patches  of  congestion, 
dermatographia  acroparaesthesiae  and  erythromelalgia  ;  and  exudative 
skin  eruptions,  e.g.  urticaria,  local  circumscribed  oedema,  angioneurotic 
oedema,  urticaria  factitia,  i.e.  produced  by  pressure,  and  serous  or 
haemorrhagic  effusions.  Almost  any  symptom  of  organic  disease  may 
be  noted. 

Diagnosis. — It  is  chiefly  important  not  to  overlook  organic  disease. 
Hysteria  is  comparatively  infrequent  in  children,  so  it  is  advisable  to  be 
cautious  in  attributing  symptoms  to  this  cause.  Occasionally  supposed 
hysterica]  symptoms  precede  by  years  the  evidence  of  organic  mischief, 
for  instance  cerebral  tumour. 

The  prognosis  is  favourable  as  regards  the  particular  symptom  and  the 
general  psychical  state,  provided  it  is  recognised  early  and  properly  treated. 
Otherwise  it  is  bad,  for  the  affection  becomes  rooted  in  the  child's  inner 


780  Chapter  LVIII. 

■consciousness.  The  outlook  is  most  favourable  in  the  imitation  hysteria 
which  breaks  out  in  schools. 

Treatment. — In  all  the  above  conditions  the  treatment  is  both  moral 
and  physical.  Separate  the  child  from  neurotic  parents  or  attendants. 
Encourage  it  to  exercise  will  and  self-control.  Auto-suggestion,  as  in 
christian  science,  is  of  great  value.  Direct  education  to  bridling  the  passions, 
-attaching  little  importance  to  trivialities,  and  taking  a  large  view  of  life. 
•Cultivate  unselfishness.  Provide  continuous  occupation  to  prevent  intro- 
spection and  self-indulgence.  Understanding,  tact,  sympathy  and  firm 
moral  support  must  be  afforded  by  the  physician.  Intentional  neglect  is 
■advisable  in  convulsive  affections,  and  indeed  for  most  symptoms.  Point 
out  the  baselessness  of  phobias  and  obsessions. 

Improve  the  nutrition  and  tone,  and  reduce  the  irritability,  of  the 
nervous  system  by  rest,  abundance  of  sleep,  isolation,  diet,  massage, 
•electricity,  hydrotherapy,  exercise  and  hypnotism.  Removal  from  the  old 
■surroundings  is  necessary  for  treatment  by  intentional  neglect.  Choose  a 
sanatorium  in  the  country  by  preference.  Keep  the  child  in  bed  at  first. 
Allow  no  alcohol.  Gavage  or  the  passage  of  a  stomach  tube  may  be  needed 
for  anorexia  nervosa.  Faradisation  of  the  abdomen  is  beneficial  in  psychic 
diarrhoea,  in  which  the  stools  are  normal  and  frequent.  Static  electricity 
is  best ;  galvanism  for  rigidity.  Measures  which  produce  a  strong  suggestive 
action  through  pain,  unpleasantness  or  mystery,  are  the  most  useful,  e.g. 
cold  douching,  gavage,  galvanism,  and  the  f  aradic  current  in  aphonia  and 
deaf-mutism.  Hypnotism  is  a  last  resort  for  the  worst  cases.  It  is  of 
doubtful  value  in  hysteria  and  neurasthenia,  and  useless  in  psychasthenia. 
Drug  treatment  consists  in  tonics  for  the  general  health  ;  bromides  and 
hypnotics  for  sleeplessness  ;  laudanum  and  purgatives  for  mental  anxiety 
■and  depression  ;  apomorphine  for  convulsions  ;  trinitrin,  pilocarpin  and 
•erythrol  tetranitrate  as  vaso-dilators  ;  ergot  as  a  vaso-constrictor  ;  calcium 
salts  for  eruptions  ;    and  assafcetida  and  valerian. 

Mental  Deficiency. — Backwardness,  feeble-mindedness,  imbecility  and 
idiocy  are  merely  differences  in  degree  of  mental  change.  A  backward 
child  has  the  mental  condition  of  one  younger  in  age.  An  idiot  cannot 
attend  and  does  not  react  to  impressions  from  without.  In  imbecility  the 
attention  can  be  attracted  but  not  fixed.  In  a  small  number  the  parents 
are  normal  and  the  child  merely  presents  deviations  from  the  noimal. 
In  the  remainder  one  or  both  parents  are  insane,  feeble-minded  or  physically 
degenerate.  Consanguinity  is  of  little  importance  unless  there  are  pre- 
disposing causes  in  the  family.  The  slighter  defects,  preventing  the  child 
being  taught  as  a  normal  child,  are  present  in  about  1  per  cent,  of  all 
children. 

Etiology. — In  about  one-third  there  is  a  family  history  of  idiocy, 
imbecility  or  some  form  of  insanity  ;  occasionally  a  history  of  intemperance 
or  immorality,    alone   or   associated   with   a   low   degree   of  intelligence, 


Disorders  of  the   Higher   Faculties.  781 

congenital  syphilis  or  tuberculosis.  Nine-tenths  of  the  cases  depend  on 
modifications  of  the  germ  cell  or  early  embryo.  Sometimes  the  hereditary 
defect  only  affects  the  male  children.  The  influence  of  the  age  of  the 
parents  is  shown  in  Mongolism.  The  older  the  mother,  the  more  likely  is 
mental  defect  to  be  present  in  the  child  or  to  follow  some  exciting  cause, 
especially  an  infectious  fever.  Cretinism  depends  on  athyroidea.  In 
Mongols  and  microcephalus  there  are  morphological  anomalies  but  no 
gross  cerebral  destruction.  Hydrocephalus  only  causes  mental  changes  in 
late  stages.  Idiocy  "  by  deprivation"  is  due  to  adenoids  and  deafness,  or  to 
ocular  causes  such  as  congenital  cataract,  hypermetropia  and  astigmatism. 
Paralytic  idiocy  depends  on  gross  cerebral  mischief.  It  is  associated  with 
paralyses  and  contractures,  and  includes  many  epileptic,  paralytic, 
syphilitic  and  traumatic  cases.  Recurrent  fits  cause  mental  deterioration 
and  usually  depend  on  past  encephalitis,  syphilis  or  birth  injury.  The 
various  cerebral  scleroses,  including  family  amaurotic  idiocy,  are  endo- 
genous or  depend  on  injury  at  birth  or  encephalitis.  Possibly  the  toxins 
of  infective  disorders,  gastro-enteritis,  chorea  and  rheumatism  are  exciting 
causes,  independently  of  encephalitis.  Malnutrition  is  a  potent  pre- 
disposing factor.  Post-natal  traumatism,  heat,  opium,  malaria,  fright  and 
shock  are  rare  causes,  unless  other  factors  are  present.  In  most  cases  there 
is  some  primary  constitutional  weakness  as  well  as  an  exciting  factor. 

According  to  Macpherson  (1904)  the  absence  of  certain  mental  faculties 
is  "  wholly  or  in  part  correlated  with  the  development  of  the  physical 
organisation,  especially  that  of  the  central  nervous  system,  and  it  is  rare 
to  meet  with  imperfect  structure  of  the  nervous  system  in  the  absence  of 
bodily  imperfections."  The  greater  the  mental  defect,  the  more  pro- 
nounced are  the  malformations. 

Stigmata  of  degeneration,  or  physical  defects  of  other  parts,  are  often 
present.  Similar  conditions  are  found  less  often  in  normal  children,  so  too 
much  stress  must  not  be  laid  upon  them.  They  merely  afford  presumptive 
evidence.  The  head  may  be  micro-,  macro-,  hydro-,  brachy-  or  dolicho- 
cephalic; asymmetrical;  present  an  abnormally  narrow  frontal  region,  poor 
or  absent  frontal  eminences  ;  or  show  irregular  bosses  of  syphilitic  or 
rachitic  origin.  The  face  is  asymmetrical.  The  ears  may  be  unduly  large 
and  prominent,  have  adherent  lobules,  or  show  irregularity  of  the  helix. 
A  highly-arched  or  V-shaped  palate  is  found  in  about  half  the  cases,  and  in 
only  one-fourth  of  normal  children.  Up  to  the  time  of  the  second  dentition 
there  is  no  difference  between  the  palates  of  the  sane  and  of  idiots.  Mentally 
defective  children  may  retain  the  infantile  form  of  palate  up  to  the  fifteenth 
year.  Hence  a  deformed  palate  can  only  be  regarded  as  one  of  a  number  of 
indications  of  imperfect  anatomical  development.  A  normal  palate  does 
not  prove  absence  of  degeneracy,  nor  does  an  abnormal  one  indicate  its 
presence.  Other  anatomical  stigmata  are  deformed  nasal  bones,  an  epi- 
canthicfold,  opacities  in  the  media,  high  errors  of  refraction,  badly  developed 


782  Chapter  LVIII. 

jaws  and  teeth,  prognathism,  narrow  naso-pharynx,  hare-lip,  transversely- 
fissured  tongue,  webbed  fingers  and  toes,  supernumerary  digits,  sluggish 
circulation,  congenital  morbus  cordis  and  early  puberty. 

There  is  delay  in  acquiring  the  erect  posture,  walking,  manual 
■dexterity,  speech  and  control  over  the  bladder. 

Abnormal  nerve  signs  are  noted  on  examination.  The  facial  expression 
is  lacking  in  intelligence,  the  mouth  open  and  the  forehead  wrinkled.  The 
tone  of  the  facial  muscles  is  poor,  and  there  is  defective  capacity  to  fix  the 
-eyes  and  attention.  The  limbs  lack  control  and  co-ordination,  the  fingers 
twitch,  and  there  is  constant  fidgets  (microkinesis).  The  response  to  stimuli 
is  slow.  Tremors,  athetosis,  spasticity  and  contractures  indicate  organic 
cerebral  mischief. 

Various  bad  habits  or  stereotypia,  such  as  pica,  sucking,  licking,  tongue- 
sucking,  lip-picking,  nail-biting,  head-scratching,  teeth-grinding,  head- 
banging,  etc.,  faecal  incontinence,  enuresis  and  masturbation  may  be 
present.  They  are  signs  of  nerve-instability,  except  in  some  cases  when  they 
-are  clearly  due  to  local  or  reflex  causes.  Nerve-storms,  of  the  type  des- 
cribed under  "  psychasthenia,"  may  occur,  notably  inexplicable  attacks  of 
screaming  or  violent  temper,  and  obsessions,  morbid  fears  or  moral  insanity 
may  be  present.  In  quite  one-third  the  heart's  action  is  feeble,  and  there 
may  be  bradycardia.  It  is  more  often  enlarged  than  undersized.  Murmurs, 
■especially  mitral  ones,  are  not  uncommon  and  the  pulse  may  be  irregular. 
These  children  are  more  often  delicate  and  liable  to  tuberculosis  than 
normal  children.  This  is  partly  due  to  defective  innervation  and  circulation, 
and  partly  to  less  care  by  others  and  less  competence  to  look  after 
themselves. 

Diagnosis. — Many  dull  children  show  none  of  the  above  defects  and 
many  who  do  show  them  are  by  no  means  feeble-minded.  In  infancy  the 
•diagnosis  is  very  difficult.  The  face  is  a  better  mirror  of  the  mind  than  in 
adults.  Its  expression  may  arouse  suspicion.  It  may  be  stupid,  fatuous, 
vacant,  sullen  or  apathetic,  or  the  child  may  smile  inanely,  grin  mono- 
tonously and  make  grimaces.  The  babe  may  recognise  neither  mother  nor 
nurse.  Lax  jaws,  pendulous  lips  and  slobbering  are  suspicious  signs. 
An  exceptionally  "  good,"  placid  baby,  vacantly  smiling  and  rarely  or 
never  crying,  is  generally  feeble-minded. 

In  the  presence  of  good  physical  development,  without  deformity 
or  contracture,  try  intellectual  and  physical  tests,  note  the  attitudes  and 
■demeanour,  enquire  as  to  conduct  and  mode  of  life,  the  date  at  which  the 
various  functions  were  acquired,  and  compare  the  power  of  reading, 
writing  and  doing  arithmetic  with  that  of  normal  children.  Note  the 
facial  aspect,  and  the  amount  and  duration  of  attention  paid  to  various 
objects  and  stimuli.  Note  the  presence  of  undue  self-consciousness, 
nervousness  or  fright,  or  unusual  lack  of  shyness.  Test  the  visual  and 
auditory  reactions.    If  they  are  normal,  there  is  often  only  a  mild  degree  of 


Disorders  of  the  Higher  Faculties.  783 

idiocy.  Test  sensation  to  pain  ;  to  heat  and  cold  ;  and  to  taste,  by  a 
2  per  cent,  solution  of  saccharin,  quinine  2  per  cent.,  HC1  2  per  cent, 
and  common  salt  5  per  cent.,  noting  the  effect  on  the  facial  and  oro-lingual 
expression.  All  these  reactions  may  be  modified  by  intercurrent  disease. 
Note  speech  defects  and  examine  the  reflexes. 

Prognosis. — If  nutrition  is  poor,  do  not  give  a  definite  diagnosis  or 
prognosis  until  it  improves.  Physical  weakness  and  lack  of  resisting  power 
are  common,  especially  in  Mongols  and  cretins.  Quite  50  per  cent,  die 
between  10  and  30  years,  and  few  live  over  40  years  of  age.  In  severe 
forms  the  child  is  unable  to  recognise  its  parents,  know  its  own  clothes, 
find  its  way  about  or  feed  itself.  Abstract  ideas  of  duty,  etc.,  are  absent. 
Emotional  faculties  are  fully  developed.  The  outlook  as  regards  mental 
•development  varies  with  the  type  and  degree.  Often  children  most  normal 
in  appearance  develop  the  worst ;  so,  too,  those  who  have  fits.  Mongols  can 
rarely  do  much  brain  work.  Cretins  develop  well,  if  put  under  thyroid  treat- 
ment from  the  first  year.  Organic  heart  disease  is  an  important  factor  in 
•causing  continued  deterioration.  It  is  impossible  to  be  certain  how  much 
improvement  will  take  place  in  any  particular  case.  Much  depends  on 
education. 

Training. — The  mental  processes  are  slow  and  difficult  to  control, 
and  the  mental  impressions  are  less  powerfully  fixed  and  less  co-ordinated 
for  future  use.  Teaching  must  be  objective.  Cultivate  attention  through 
the  sight  and  by  this  means  train  the  child  in  the  control  of  the  eye  muscles. 
The  muscular  sense  is  educated  through  finger  exercises,  movements  of  the 
hands  and  arms,  and  in  estimating  the  weight,  size  and  shape  of  objects. 
Other  muscles  of  the  body  must  be  also  trained.  Differences  in  temperature, 
weight  of  coins,  sounds  and  colours  are  useful  exercises.  Later,  teach  the 
•child  to  imitate  the  movements  of  the  teacher  in  writing  and  speaking.  Then 
pass  on  to  drawing,  modelling,  games  involving  counting  and  calculation  or 
the  sense  of  touch  and  accuracy  of  sight,  the  value  of  coins,  marching  and 
other  forms  of  drill.  Encourage  self-help  in  all  forms.  Teach  reading  and 
the  knowledge  of  figures  and  time.  In  early  stages  limit  education  to  one 
sense  at  a  time,  viz.  sight,  touch  and  hearing  successively.  Over-exercise 
is  injurious  to  backward  and  imbecile  children  because  of  the  heart  weakness. 
Amusements  and  simple  entertainments  are  necessary.  The  teacher  must 
live  with  the  child.  No  school  work  is  permissible  before  7  years  of 
age.  Development  generally  stops  at  16  years.  Attend  to  any  physical 
troubles,  such  as  adenoids,  eye  defects,  rickets,  contractures  and 
•deformities.  If  there  is  any  suspicion  of  cretinism,  give  thyroid 
extract.  If  there  is  no  cretinism,  it  produces  no  improvement 
•and  thyroidism  soon  ensues.  Training  of  muscles  and  brain  must  be 
steady  and  persistent. 

Mongolian  Idiocy. — This  is  a  variety  of  congenital  idiocy  in  which  the 
features  are  of  the  Mongol  or  Kalmuck  type.    The  appearance  of  the  eyes 


784  Chapter  LVIII. 

is  like  that  of  the  Chinese  and  Japanese.    From  3-5  per  cent,  of  all  idiots 
are  Mongols  and  they  present  a  remarkable  likeness  to  each  other. 

Etiology. — A  Mongolian  idiot  is  usually  the  last  child  of  a  large  and 
normal  family,  as  if  due  to  exhaustion  of  the  reproductive  power.  Generally 
the  mother  is  of  advanced  age.  Occasionally  it  is  the  product  of  the  union  of 
an  old  man  with  a  young  woman.  In  rare  instances  it  is  the  first  child  of 
young  parents.  Exceptionally  a  later  child  may  be  normal.  One  or  both 
of  twins  may  be  affected.  Mongolism  is  more  frequent  in  Great  Britain  than 
elsewhere.  It  is  doubtful  whether  it  occurs  among  the  Jews.  The  causation 
is  obscure.  Consanguinity,  ill-health  and  syphilis  cannot  be  regarded 
as  more  than  encouraging  factors.  Sutherland  obtained  a  family  history 
of  syphilis  in  14  out  of  25  cases  but  anti-syphilitic  remedies  are  useless. 
The  cerebellum,  pons  and  bulb  were  unduly  small  in  5  cases  examined  by 
A.  W.  Wilmarth.  Oberther  (1904)  found  meningo-encephalitis  in  3  cases, 
with  atrophy  and  chromatolysis  of  cells.  W.  B.  Hill  (1908)  noted  thinning 
of  the  cortex  and  rarefaction  of  nerve  cells,  especially  the  large  pyramidal 
cells.  Some  of  these  effects  may  be  sequels.  One  of  Oberther's  patients 
was  12  years  old  and  died  from  tuberculosis. 

Symptoms. — At  birth  the  child  is  small.  Growth  is  slow  and  at  1  year 
the  child  looks  like  a  6-month  old  baby.  The  stature  is  always  subnormal 
and  the  weight  about  one-fourth  of  the  normal.  The  head  is  small,  brachy- 
cephalic,  the  antero-posterior  diameter  being  equal  to  the  transverse,  and 
the  occiput  much  flattened.  This  has  been  ascribed  to  premature  ossifica- 
tion of  the  basilar  bones  or  defective  growth  of  the  structures  at  the  base  of 
the  brain.  It  is  probably  secondary  to  lack  of  development.  The  fon- 
tanelles  and  sutures  close  late.  The  hair  is  fine  and  abundant.  The  face  is 
small  and  rounded  ;  the  cheeks  round,  soft  and  chubby,  of  a  dirty  yellow 
or  ruddy  colour,  and  often  show  venous  congestion.  The  cartilaginous 
part  of  the  nose  is  broad,  the  alse  extruded  and  opening  in  an  upward 
direction,  the  nasal  bridge  flat  or  sunken,  and  the  tip  frequently  red  and 
retrousse.  The  ears  may  be  unduly  small.  The  palpebral  apertures  are 
almond-shaped,  small,  narrow  and  oblique,  sloping  upward  and  outward 
like  the  orbits.  Marked  epicanthic  folds  are  due  to  redundancy  of  skin  and 
give  an  appearance  of  increased  distance  between  the  oval,  tilted  eyes. 
Chronic  blepharitis  is  common.  Nystagmus  and  squint  are  often  present 
during  the  first  6  months,  possibly  due  to  refractive  errors.  There  is  no 
puckering  of  the  brows,  no  pumness  under  the  eyes,  and  no  fat  pads  above 
the  clavicles  as  seen  in  cretinism. 

The  lips  are  normal,  the  palate  often  high  and  narrow,  the  mouth  small 
and  usually  kept  open,  and  the  naso-pharynx  small.  Apparent  enlargement 
of  the  tongue  at  birth  is  either  due  to  abnormal  shortness  of  the  mouth, 
causing  a  normal  tongue  to  protrude,  or  there  may  be  actual  enlargement 
of  the  tongue.    Later  on  it  becomes  curiously  rough  and  fissured  transversely, 


Disorders  of  the  Higher  Faculties.  785 

raw  and  sodden,  with  swollen  papillie.  J.  Thomson  has  carefully  observed 
the  progress  in  these  cases  and  states  that  the  swelling  of  the  papillae 
begins  in  the  third  to  ninth,  occasionally  in  the  second  month,  and  the 
Assuring  in  the  second  to  sixth  year.  He  ascribes  the  condition  to  deficient 
resistance  of  the  lingual  mucosa  and  to  tongue-sucking,  present  in  59  out  of 
69  cases  and  possibly  overlooked  in  others.  The  upper  lip  is  often  sucked  in. 
The  character  of  the  tongue  depends  on  the  degree  and  duration  of  tongue- 
sucking.  Its  protrusion  is  not  constant  as  in  cretinism  and  may  be  absent 
during  sleep.  Dentition  is  delayed  and  the  teeth  ill-formed,  perhaps  widely 
separated.  The  voice  is  guttural  and  the  child  is  apt  to  crow  as  inlaryngo- 
spasm. 

The  hands  are  broad  and  square,  with  short,  squat,  blunt  fingers.  The 
thumbs  and  little  fingers  are  abnormally  short.  The  second  phalanx  of 
the  little  finger  is  unduly  small  and  the  finger  incurved  laterally.  The  fingers 
may  be  spread  out  widely,  the  main  en  trident.  The  ligaments  are  loose,  and 
the  mobility  of  the  joints  may  be  so  great  that  the  fingers  can  be  bent  back 
to  touch  the  aim.  The  muscles  are  hypotonic.  The  skin  is  smooth  and 
white  in  infancy  and  furfuraceous  later.  The  trunk  is  not  dwarfed.  The 
abdomen  is  generally  large  and  distended,  and  may  show  umbilical  hernia. 
The  genital  organs  are  small  and  cryptorchism  is  sometimes  present.  The 
pelvic  and  long  bones  are  smaller  than  normal,  and  the  bones  show  delayed 
ossification.  The  limbs  may  be  short  and  their  ligaments  unduly  lax.  The 
feet  are  flat  and  broad.  Muscular  power  is  feeble  and  walking  delayed. 
The  extremities  are  blue,  cold  and  clammy,  for  the  circulation  is  feeble. 
Sitting  cross-legged  is  a  favourite  attitude.  Knee  jerks  are  often  absent 
and  the  plantar  reflex  extensor.  Constipation  is  common  and  the  habits 
may  be  quite  cleanly. 

Congenital  morbus  cordis  and  other  defects  are  present  in  20  per  cent. 
(Sutherland).  Garrod  (1898)  drew  attention  to  the  frequency  of  the  heart 
mischief.  Hutchison  found  cardiac  defects,  often  of  the  septum,  in  5  out  of 
18  cases.  Other  deformities  are  spina  bifida,  club-foot,  imperforate  anus 
and  renal  cysts.  Mentally  there  is  nothing  noticeable  beyond  backwardness, 
less  marked  than  in  cretins.  They  are  "  good  "  babies,  giving  less  trouble 
than  normal  ones,  apathetic,  easy  to  manage  and  easily  amused,  and  will 
lie  for  hours  smiling  placidly,  babbling  unintelligently,  grimacing,  making 
curious  throaty  noises,  and  biting  the  fingers.  As  they  grow  older  they 
may  be  bright  and  lively,  fond  of  gestures,  music  and  dancing,  and  imitative. 
The  expression  is  fatuous  in  bad  cases.  They  are  liable  to  stammer  and  have 
difficulty  with  the  letter  S.  Sight  and  hearing  are  good.  They  are  some- 
times obstinate,  rarely  spiteful  or  mischievous,  and  never  erotic  or  vicious. 

Prognosis. — Most  of  them  die  under  3  years  and  almost  all  the  rest 
before  20  years  of  age.  Their  vital  power  is  small.  They  have  a  subnormal 
temperature,  are  very  sensitive  to  cold  and  bear  illness  badly.  Heart 
lesions  increase  the  gravity.     Death  results  from  diarrhoea,   bronchitis, 

3    E 


786  Chapter  LVIII. 

pneumonia,  phthisis  or  other  intercurrent  disease.  Phthisis  may  exist 
without  cough  or  difficulty  in  breathing.  If  they  live,  they  develop  into 
affectionate  imbeciles  and  are  never  able  to  look  after  themselves,  much 
less  earn  a  living.  Muscular  power  and  co-ordination  are  acquired  very 
slowly.  The  patient  cannot  walk  or  talk  before  the  sixth  year.  They  are 
capable  of  a  certain  amount  of  education,  but  remain  very  backward  and 
can  rarely  read  more  than  a  few  short  words. 

Treatment  is  unavailing.  A  few  have  improved  on  thyroid  medication. 
Training  is  the  same  as  that  suitable  for  the  feeble-minded. 

Moral  Insanity. — Psychical  defects  have  the  same  etiological  founda- 
tions as  mental  deficiency,  chiefly  a  family  history  of  epilepsy,  disorders 
of  the  intellect,  or  moral  degeneracy  as  shown  by  excessive  alcoholism  and 
immorality.  The  child  is  often  epileptic.  In  others  the  cause  may  be  the 
action  of  toxins,  injury  or  disease.  There  is  a  temporary  or  permanent 
defect  of  moral  control,  moral  consciousness  or  will  power.  Lack  of  moral 
training  is  a  potent  cause  in  the  delicate,  and  crippled.  The  most  common 
indication  of  imperfect  moral  control  is  uncontrollable  passion  on  trivial 
provocation.  Screaming  attacks  in  infants  may  be  of  this  nature  but  they 
are  more  often  due  to  physical  pain,  a  pin  in  the  clothes,  constipation  or  day- 
terrors.  Next  in  frequency  comes  a  nasty  spitefulness  or  cruelty,  shown  by 
playing  cruel  tricks  on  other  children,  pinching,  scratching,  biting,  banging, 
etc.,  and  by  cruelty  to  insects,  birds  and  animals.  Thus,  a  9-year  old  girl  had 
a  propensity  for  trying  to  drown  little  boys,  apparently  from  no  motive 
save  an  innate  instinct  of  murder.  She  had  always  been  wilful,  dis- 
obedient, mysterious  in  her  ways,  and  mentally  somewhat  dull,  and  was 
unduly  composed  during  her  trial  (  Daily  Express,  1903).  The  cruelty  may 
take  the  form  of  trying  to  smother  babies,  inserting  injurious  articles  into 
their  mouths,  or  setting  fire  to  the  bedding.  Pleasure  is  nearly  invariably 
shown  in  the  sufferings  of  the  victim.  A  boy  drowned  a  younger  boy  that 
he  "  might  see  the  little  devil  kick  in  water."  Pyromania  is  due  to  a  love 
of  seeing  fire  or  a  craze  for  excitement.  It  is  common  in  epileptics. 
Cruelty  may  arise  from  jealousy  and  not  be  pathological. 

Defective  moral  control  is  also  shown  by  exaggerated  jealousy,  diso- 
bedience, and  a  reckless  disregard  for  authority,  parental,  tutorial  or  legal, 
in  spite  of  punishment.  This  condition  leads  to  criminal  acts  and  conflict 
with  the  law  in  later  life.  Dishonesty,  stealing,  destructiveness,  wanton 
mischief,  absence  of  shyness  or  reserve,  shamelessness,  immodesty  leading 
to  indecent  exposure  and  open  masturbation,  sexual  precocity,  immorality 
and  perversions,  viciousness,  habitual  and  useless  lying  and  romancing 
are  all  at  times  present  in  different  cases.  The  child  rarely  has  a  true 
conception  of  right  and  wrong,  but  may  express  fear  of  punishment  and 
appreciate  its  effects.    Sorrow  is  rarely  felt  or  expressed  for  any  misdeed. 

All  these  symptoms  can  be  ascribed  to  the  animal  desire  for  self- 
gratification  independent  of  the  feelings  of  others.     A  weak  or  defective 


Disorders  oj  the  Higher  Faculties.  787 

will  is  indicative  of  weak  inhibitory  powers,  the  normal  state  of  infantile 
life.  This  is  shown  by  the  lack  of  control  over  the  emotions  of  laughing  and 
crying,  comparable  with  the  emotional  state  so  often  seen  in  chorea.  Some 
•of  the  signs  are  due  to  the  persistence  of  an  earlier  normal  state. 

Diagnosis. — It  is  important  to  recognise  that  these  psychical  states 
may  be  quite  independent  of  idiocy  or  disease,  and  due  to  delayed  develop- 
ment. The  normal  state  of  a  child  depends  on  age,  environment  and 
heredity.  At  5-6  years  it  should  show  consideration  for  others  and  at 
■8  years  have  definite  ideas  of  right  and  wrong.  In  other  cases  there  is  a 
morbid  loss  of  an  already  acquired  normal  psychical  state.  Untruthfulness 
may  be  due  to  timidity,  a  vivid  imagination,  the  invasion  of  specific 
fevers,  or  the  onset  of  organic  cerebral  mischief.  Spitefulness,  cruelty, 
lying  and  temper  are  all  common  in  neurotic  children  and  do  not  necessarily 
foreshadow  criminal  lunacy.  Dishonesty  is  normal  in  young  children  for 
the  gratification  of  appetite.  Hysteria  may  lead  to  it  from  the  desire  to 
obtain  gifts  for  some  object  of  worship.  The  remark  of  a  child  "  Does  oo 
.love  Dod  ?  Then  oo  shall  see  Dod,"  as  he  squashed  a  fly  on  the  window- 
pane,  can  hardly  be  regarded  as  a  symbol  of  moral  obliquity;  nor  the 
.administration  of  an  enema  to  a  toy  elephant  by  a  5-year  old  girl  as  a 
sign  of  indecency.  Moral  delinquencies  should  be  due  to  little  or  no 
provocation,  persistent,  and  unassociated  witk  ability  to  realise  the  wrong- 
fulness of  the  action  or  with  true  penitence. 

True  moral  defectives,  without  some  stigmata  of  degeneration,  form 
a  very  small  group.  Most  of  them  are  feeble-minded.  If  there  is  idiocy, 
the  defective  control  and  impairment  of  intellect  vary  directly  as  the 
•degree  of  idiocy.  Suggestive  additional  symptoms  may  be  present,  such  as 
an  abnormal  desire  for  solitude,  a  lack  of  natural  affection,  an  incapacity 
for  sustained  attention  or  a  defective  memory.  Exaggerated  emotions  are 
•due  to  defective  inhibitory  volition.  Deficient  moral  consciousness  may 
be  shown  by  apparently  complete  ignorance  of  the  bearings  of  the  various 
acts,  e.g.  passion,  violence,  cruelty  or  indecency.  Yet  with  all  these  the 
intellect  may  be  normal.  It  must  be  noted  that  moral  control  does  not 
vary  with  the  intellectual  capacity.  Sometimes  periods  of  defective 
•control  alternate  with  periods  of  a  normal  psychic  state. 

The  treatment  is  similar  to  that  of  the  weak-minded.  Parents  and 
guardians  must  be  impressed  with  the  risks  of  injury  to  self  and  others, 
the  effects  of  indecency  and  immorality,  and  the  liability  to  personal  and 
family  disgrace.  The  difficulties  of  education  are  great.  These  children 
must  not  be  sent  to  school,  for  they  are  almost  certain  to  be  expelled.  A 
new  school  or  a  change  in  surroundings  is  temporarily  beneficial,  but 
the  effects  are  of  short  duration.  The  influence  of  bad  literature, 
*c  penny  dreadfuls,"  is  potent  for  harm.  Those  most  dangerous  to  others 
are  the  ones  in  whom  moral  insanity  is  combined  with  intellectual  superiority. 


788  Chapter  L  VIII. 

High  class  criminals  may  be  of  this  type  and  should  be  permanently 
segregated.     There  is  always  a  possibility  of  improvement. 

Insanity. —  Acute  delirium  is  the  most  common  form  of  mental 
instability.  It  is  screaming,  muttering,  or  associated  with  terror,  hallu- 
cinations, usually  visual,  and  motor  explosions.  There  is  generally  fever. 
Mania  is  rare,  usually  of  short  duration  but  apt  to  recur.  Savage  has- 
reported  it  in  a  3-year  old  boy.  It  takes  the  form  of  extreme  elation, 
restlessness  and  variable  fancies.  Less  often  there  are  delusions,  suicidal 
impulses  and  depression  ;  or  continuous  weeping,  melancholia  and  religious- 
mania.  A  case  of  the  former  type,  in  a  5-year  old  girl,  came  under  my 
notice  as  a  sequel  of  epilepsy.  Child-insanity  is  often  associated  with 
changed  affections,  obstinacy,  anger,  violence,  unreasoning  terror, 
hallucinations,  blasphemous  and  indecent  language,  and  even  suicidal 
impulses.  Complete  rest  and  large  doses  of  bromide  are  necessary.  Folie 
periodique  has  been  reported  by  Magnier  in  a  girl,  12  years  old,  with 
suicidal  tendencies.     Eighty  per  cent,  of  the  cases  begin  under  25  years. 

Acute  mental  confusion  may  follow  fright,  injury,  prolonged  excite- 
ment and  fever,  notably  typhoid.  It  is  associated  with  delirium  and 
stupor.  The  prodromal  symptoms  are  restlessness,  dulness,  apathy,  wet 
and  dirty  habits,  and  perhaps  hallucinations.  It  is  more  allied  to  the 
delirium,  which  is  liable  to  occur  in  the  neurotic  from  slight  fever,  than 
to  true  insanity. 

Suicide  in  children  attending  school  is  uncommon  in  Great  Britain. 
Eulenburg  (1907)  states  that  there  were  1152  cases  in  Prussia  from  1880-1903, 
310  in  the  higher  schools  and"  colleges.  Mental  and  nervous  troubles  were 
present  in  10  per  cent.  ;  423  were  ascribed  to  punishment,  non-success- 
in  class  work,  or  removal  for  misconduct ;  no  cause  was  found  in  265  ; 
some  were  due  to  love  affairs  and  philosophical  studies.  It  is  most  apt 
to  occur  in  schools  for  backward  children,  from  excess  of  theoretical  work 
and  lack  of  out-door  exercise.  Suicidal  impulses  arise  in  neurotic  children 
from  ennui,  melancholy,  disappointment,  physical  pain,  a  desire  to  attract 
attention  or  be  regarded  as  of  importance,  and  from  ignorance  or  curiosity 
as  to  death  and  the  future.  They  are  rarely  carried  out  beyond  the  extent 
of  causing  illness. 

Dementia  Praecox  (Kraepelin),  or  acquired  imbecility  (Esquirol), 
begins  in  youth  or  early  adult  life.  "  Prsecox  "  means  that  it  is  "  untimely,"' 
before  its  time.  Dementia  is  an  unemotional  state,  one  of  pronounced 
inactivity.  It  implies  full  development  of  the  mental  powers  and  per- 
manent loss,  and  is  therefore  an  acquired  disease,  differing  from  "  amentia  " 
or  congenital  enfeeblement.  The  characteristic  feature  is  loss  of  memory. 
On  the  whole  "  Adolescent  Insanity  "  is  a  better  term  and  it  may  be 
divided  into  hebephrenia,  katatonia  and  paranoia,  sub-divisions  which  are 
closely  allied  and  overlap.     Dementia  preecox  is  an  unsatisfactory  title 


Disorders  of  the  Higher  Faculties.  789 

or  there  is  not  always  permanent  loss,  some  recover,  and  the  loss  of  memory 
is  not  invariably  a  prominent  feature. 

Hebephrenia  begins  with  hallucinations  and  delusions  which  tend  to 
disappear.  The  chief  symptoms  are  eccentricity,  jerky  mannerisms,  loss 
of  voluntary  attention  and  activity,  loss  of  interest,  apathy,  perhaps 
mutism,  and  sometimes  maniacal  excitement,  followed  by  depression  and 
permanent  mental  debility. 

In  Catatonia  there  are  hallucinations,  apathy,  loss  of  interest  and 
attention,  stereotyped  movements,  and  mutism,  merging  into  katatonic 
stupor  and  muscular  tension.  Paranoia  begins  with  unjustified  suspicions, 
rapid  development  of  unsystematised  delusions,  hallucinations  and 
delusions  of  persecution  and  grandeur,  which  tend  to  pass  off  as  the  mental 
estate  deteriorates.  Some  katatonic  stupor,  mannerisms  and  stereotvpy 
may  be  noted.  The  premonitory  signs  of  this  form  of  insanity  may  take  the 
form  of  simple  mental  deterioration,  a  few  indefinite  delusions,  neuras- 
thenic or  hysterical  symptoms.  Sometimes  there  are  abnormal  fears, 
great  indecision,  and  destructive  or  criminal  impulses.  At  puberty  these 
children  may  show  great  exaltation  or  depression  of  spirits,  with  intellectual 
precocity.  In  a  few  months  to  2  years  signs  of  mental  dulness  and  failure 
are  evident. 

The  early  symptoms  of  mental  disorders  are  : — hyperaesthesia,  anaes- 
thesia, hyperacusis  ;  insomnia  ;  disorders  of  perception,  viz.  illusions, 
.hallucinations  and  imperception ;  imperative  ideas  ;  disorders  of 
emotion,  memory  and  conduct ;  disorders  of  instinct,  viz.  lack  of  interest, 
excess  of  energy,  extravagance,  boastfulness,  excessive  eating,  sexuality 
and  the  collecting  mania  ;  and  delusions.  Fortunately  mental  disorders 
aie  comparatively  rare  in  children,  except  in  the  degenerate  class  of  mental 
■defectives  and  in  epileptics.  Nevertheless  the  infrequency  of  their  occur- 
rence is  an  insufficient  ground  for  omitting  reference  to  them  in  a  work  of 
this  nature,  for  they  are  liable  to  be  overlooked  in  the  early  stages.  Unfor- 
tunately treatment  is  rarely  beneficial,  except  in  acute  cases  in  which  chief 
reliance  must  be  placed  on  isolation,  rest,  liberal  diet  and  nursing.  The 
recognition  of  the  frequency  of  moral  insanity  and  the  dangers  of  over- 
stimulation of  the  mental  faculties  of  children,  especially  if  neurotic  or 
mentally  defective,  should  be  constantly  borne  in  mind  by  those  in  whose 
charge  they  are  placed  for  educational  purposes. 

Menstrual  psychoses  take  the  form  of  loquacity,  incessant  talking  and 
singing,  agitation,  and  hallucinations  of  sight  and  hearing.  They  are  of  the 
same  nature  as  adolescent  insanity,  the  attacks  occurring  during  men- 
struation and  subsiding  soon  after,  but  liable  to  recur. 

Speech  Defects. — Wyllie  (1892)  divides  the  stages  of  acquirement  of 
speech  into  : — (1)  Inarticulate  sounds,  at  first  instinctive  ;  crying,  laughing 
and  grunting ;  (2)  Facial  expression  and  gestures  ;  (3)  Babbling  and 
•crowing,  mimic  reading,  and  echolalia  or  "  parrot  talk  "  at  the  end  of  the 


790  Chapter  LVIII. 

first  year  ;  (4)  Intelligent  speech.  Girls  speak  2-3  months  before  boys. 
Delayed  speech  is  due  to  mental  delects,  backwardness  from  rickets  or  acute- 
illness,  or  defective  hearing.  Some  children  learn  much  later  than  others, 
without  there  being  any  abnormality.  Delay  beyond  the  third  year  of  life  is- 
suspicious,  and  such  children  must  be  examined  for  physical  or  mental, 
defect.  Yet  occasionally  speech  is  not  acquired  until  the  fifth  to  seventh 
year  and  is  quite  normal  in  later  life.  Ketarded  speech  delays  mental 
development. 

The  speech  centre  is  supposed  to  be  in  the  posterior  third  of  the  third 
left  frontal  convolution  (Broca).  It  is  bilateral  at  birth.  The  left  one 
normally  develops,  but  if  it  is  damaged  or  destroyed  in  early  life,  the  right 
centre  takes  on  its  functions.  Aphasia  in  the  first  4  years  of  life  is  soon 
recovered  from.  Wernicke's  region  consists  of  the  angular  gyrus,  the 
supramarginal  gyrus,  and  the  posterior  parts  of  the  first  two  temporo- 
sphenoidal  convolutions.  Obliteration  of  the  middle  cerebral  artery  causes 
destruction  of  both  these  regions,  so  the  types  of  aphasia  vary  with  the 
extent  and  localisation  of  the  obstruction.  Marie  (1906)  argues  that 
Wernicke's  region  is  the  true  speech  centre  ;  and  that  Broca's  region  has 
nothing  to  do  with  speech,  can  undergo  softening  without  causing  aphasia, 
and  may  be  quite  unaffected  in  typical  cases.  Although  it  is  affected  in  50 
per  cent.,  it  is  because  the  damage  is  due  to  obstruction  to  the  middle 
cerebral  artery. 

True  aphasia  implies  a  defect  in  the  ability  to  understand  language: 
In  the  motor  aphasia  of  Broca,  the  lesion  being  in  Broca's  convolution,  the 
patient  cannot  speak  but  can  understand.  In  the  sensory  aphasia  of 
Wernicke,  the  lesion  being  in  Wernicke's  region,  the  patient  speaks  more  or 
less  incoherently  but  cannot  understand  speech  (word-deafness)  or  written 
symbols  (word-blindness).  Marie  maintains  that  the  only  difference  in 
these  two  varieties  is  the  absence  of  the  power  of  speech  and  that  this  is 
due  to  anarthria,  from  damage  to  the  region  of  the  lenticular  nucleus. 
In  both  there  is  inability  to  read,  write,  and  understand  complicated 
questions.  Wernicke's  centre  is  an  intellectual  and  not  merely  a  sensory 
centre.  The  apparent  word-deafness  is  due  to  lack  of  comprehension,  not 
to  a  damaged  auditory  centre. 

Anarthria  is  a  true  motor  aphasia  in  which  the  child  cannot  speak  or 
is  only  able  to  utter  unintelligible  sounds,  although  able  to  understand, 
read  and  write.  The  lesion  causes  inco-ordination  and  is  subcortical,  in  or 
near  the  lenticular  nucleus  or  internal  capsule. 

Amnesic  aphasia  is  the  loss  of  memory  for  words  which  may  result 
from  severe  illness.  The  loss  depends  on  deficiency  of  ideas.  In  chorea 
this  loss  may  be  partly  motor.  It  can  be  called  "  functional  aphasia," 
and  may  follow  severe  fright.  Paraphasia  is  the  use  of  words  incorrectly 
or  without  meaning.     Barely  the  speech  defect  depends  on  congenital: 


Disorders  of  the  Higher  Faculties.  791 

absence  of  the  speech  centres  or  on  bilateral  damage  of  the  motor  areas 
for  the  lips  and  tongue  by  meningeal  haemorrhage. 

Congenital  Word-Deafness  is  very  rare,  independent  of  deafness  and 
mental  defect,  and  does  not  always  affect  musical  sounds.  It  is  due  to  some 
defect  in  the  auditory  centre,  which  is  said  to  be  in  the  superior  temporo- 
sphenoidal  convolution,  though  Marie  can  find  no  clinical  or  pathological 
evidence  in  favour  of  this  site.  The  most  recent  view  of  the  site  of  the 
auditory  centre  (Flechsig,  1908)  places  it  mainly  in  the  anterior  transverse 
temporal  gyrus  (Heschl's  convolution)  on  the  upper  or  Sylvian  surface  of 
the  temporal  lobe,  and  continuous  with  the  upper  temporal  convolution. 
In  a  girl,  11  years  old  (Macleod  Yearsley),  there  was  only  vowel  hearing  and 
echolalia.  She  was  intelligent  and  could  lip-read.  Later  the  echolalic 
motor  response  was  necessary  to  enable  her  to  understand  but  subsequently 
a  slow  reply  was  obtained  without. 

Congenital  Word-Blindness  is  more  frequent  in  boys  than  girls,  and  in 
the  lower  classes,  and  often  familial.  S.  Stephenson  found  5  females  and 
1  male  affected  in  3  generations  of  a  family.  It  was  transmitted  from  the 
second  to  the  third  generation  by  an  unaffected  female.  C.  J.  Thomas 
(1905)  estimated  that  it  was  present  to  a  considerable  degree  in  1  in  2000 
London  elementary  school  children.  The  first  case  was  described  by  Pringle 
Morgan  (1896).  Kussmaul  (1877)  used  and  explained  the  term  in  reference 
to  acquired  cases  due  to  disease  of  the  left  angular  gyrus.  Slight  degrees 
are  apt  to  be  overlooked  in  hospital  work.  The  affection  is  rarely  recognised 
under  7  years  of  age. 

It  is  a  congenital  defect  in  the  visual  memory  centre  for  words  and 
letters,  or  a  failure  in  co-ordinating  written  and  printed  symbols  with  the 
sounds  and  ideas  which  they  represent.  There  is  an  imperfect  relationship 
between  the  visual,  auditory  and  articulatory  centres.  It  is  a  word  and 
letter  blindness,  an  inability  to  read  (developmental  or  congenital  alexia), 
and  often  associated  with  a  variable  amount  of  word-deafness. 

These  children  are  intelligent,  and  simply  have  a  variable  degree  of 
difficulty  in  learning  their  letters  and  in  reading  either  printed  or  written 
words.  Often  there  is  no  difficulty  with  figures  and  rarely  the  reverse 
condition.  A  few  of  them  can  understand  on  reading,  but  are  unable  to 
read  aloud,  that  is,  there  is  no  true  word-blindness  but  a  motor  failure, 
not  in  speech  but  in  translating  visual  characters  into  audible  sounds. 
Ordinarily  the  visual  images  of  words  fail  to  be  stored  up.  The  difficulty 
is  usually  ascribed  to  stupidity,  mental  defect  or  error  of  sight.  Visual 
acuteness  and  the  fields  of  vision  are  normal ;  hypermetropia  is  common. 
Memory  is  good  and  the  boy  may  be  able  to  play  games  well.  One  child 
was  brilliant  and  became  an  excellent  surgeon.  These  children  do  not  read 
for  pleasure.  Some  can  read  slowly.  Recognition  of  arabic  numerals  is 
easily  acquired.    They  can  be  taught  orally  and  remember  words  by  sound. 


792  Chapter  LVIII. 

Diagnosis  is  easy.  Defective  vision  can  be  excluded,  for  the  child 
cannot  read  large  type  any  better  than  small.  Words  can  be  recognised  by 
spelling  them  out.  An  error  of  refraction  may  lead  to  the  defect  being 
overlooked.  Try  if  the  child  can  understand  spoken  words  and  remember 
them.    Spontaneous  speech  is  usually  limited. 

Treatment. — The  earlier  the  diagnosis  is  made  and  special  methods  of 
education  adopted,  the  better  and  quicker  is  the  improvement.  Increase  the 
child's  vocabulary  by  placing  him  under  conditions  where  he  hears  plenty 
of  talking,  reading  and  word-building.  Constant  repetition  of  visual 
impressions  is  needed,  so  lessons  must  be  short  and  frequent.  The  child 
cannot  be  taught  in  class  for  it  is  soon  discouraged.  Probably  the  right 
angular  gyrus  takes  up  the  function. 

Deaf-Mutism. — A  deaf-mute  is  not  necessarily  totally  deaf  and  dumb. 
Quite  half  of  them  have  some  hearing  power,  though  not  enough  to  enable 
them  to  acquire  speech.  Some  are  congenitally  deaf.  About  half  are  cases 
of  acquired  deafness,  complete  or  incomplete.  A  few  have  congenital  word- 
deafness.  Bezold  states  that  absolute  deafness  is  more  common  in  acquired 
than  congenital  cases.  If  it  occurs  in  infancy,  it  may  be  erroneously 
ascribed  to  a  congenital  defect.  A  deaf  child  is  necessarily  backward. 
Some  hear  a  little  on  one  side. 

Heredity  exerts  an  influence  to  the  extent  that  the  affection  is  most 
common  in  families  liable  to  "  hardness  of  hearing."  Deaf-mutes  do  not 
transmit  the  condition  to  their  children.  Consanguinity  and  debility  in  the 
parents  are  possible  causes.  Bond  (1905)  pointed  out  that  deaf- mutism 
commonly  affects  children  of  the  same  sex,  male  or  female,  in  the  particular 
family.  In  other  instances  the  children  are  twins  or  contiguous  births. 
Labyrinthine  anomalies  of  embryonal  origin  have  been  found  in  several 
cases. 

Deaf-mutism  may  develop  before  or  after  speech  has  been  acquired, 
and  may  occur  as  late  as  the  sixth  year.  After  that  speech  is  retained 
though  deafness  arises.  It  is  due  to  ear  mischief,  often  secondary  to 
adenoids  and  throat  affections,  nervous  diseases  and  injury.  Some  result 
from  labyrinthitis  hyperplastica  of  syphilitic  origin  but  the  bulk  are  due 
to  labyrinthitis  exudativa,  secondary  to  scarlatina,  measles,  other 
infections,  and  meningitis.  Otitis  media  may  also  be  present  in  either 
variety.    Rarely  it  is  due  to  prolonged  impaction  of  wax. 

Diagnosis. — A  normal  child  hears  in  the  second  month.  Deafness 
cannot  be  recognised  with  certainty  until  4-6  months  of  age,  perhaps  not 
until  1  year.  If  there  is  mild  idiocy,  it  is  difficult  to  differentiate  the 
dumbness  from  that  of  deafness. 

Treatment. — Prevention  consists  in  caie  of  the  throat  during  infective 
disorders.  Mercury,  pot.  iod.,  and  pilocarpine  may  be  useful  in  labyrin- 
thitis.    Once  the  affection  is  fully  acquired  the  child  should  be  taught 


Disorders  of  the  Higher  Faculties.  793 

lip-reading.  Teaching  must  be  begun  early,  continued  for  6-8  years,  and 
requires  great  perseverance.  After  this  the  child  can  be  taught  quite  well 
with  ordinary  children,  if  he  can  see  the  teacher's  face.  The  sign  and  manual 
system  takes  5  years  and  is  not  nearly  as  satisfactory.  It  is  a  hindrance  to 
proper  education  by  the  oral  system.  Lip-reading  is  better  for  intelligent 
children  and  indeed  for  any  child  capable  of  being  taught  at  all.  For  in- 
complete deafness  ear  trumpets  and  other  appliances,  and  special  schools 
and  teachers  are  required. 

Idioglossia  is  a  defect  of  hearing,  analogous  to  errors  of  refraction  in 
the  eye,  or  a  variety  of  word-deafness,  or  a  defect  of  articulation.  The 
child  is  voluble,  though  unintelligible,  and  talks  a  gibberish  of  its  own. 
It  is  intelligent,  not  deaf,  has  no  local  defect,  and  can  read  and  write 
normally.  Similar  speech  has  been  noted  in  Mexicans,  Italians  and  South 
Sea  Islanders.  It  is  sometimes  familial  and  associated  with  a  family 
history  of  insanity.  Occasionally  there  is  a  defect  in  visual  and  musical 
.sense,  and  in  the  power  of  concentrating  attention. 

Formerly  these  children  were  mistaken  for  deaf-mutes.  They  hear  well 
and  express  themselves  by  articulate  sounds,  but  the  sounds  are  unlike 
those  of  any  known  language,  and  their  speech  is  distorted  or  imperfectly 
pronounced.  The  same  sound  is  always  used  by  the  same  child  to  express 
the  same  word.  The  speech  is  somewhat  like  "  baby  "  English  and  may  be 
due  to  imperfect  training.  In  consequence  of  inability  to  utter  certain 
■consonants,  others,  usually  T,  D  or  N,  are  substituted.  It  must  be 
treated  by  oral  methods  as  in  deaf-mutism.  Normal  speech  is  almost 
always  acquired. 

Lolling  is  the  persistence  of  infantile  speech,  usually  due  to  defective 
intelligence.  It  is  an  aggravated  form  of  lisping.  Consonants  may  be 
transposed  and  syllables  or  words  dropped. 

Lisping  is  a  faulty  articulation  of  certain  consonants  or  substitution  of 
wrong  consonants,  the  result  of  local  defects  or  malposition  of  the  various 
•organs  employed  in  articulation.  It  is  normal  in  infancy  and  may  persist 
from  faulty  habit  or  imperfect  education  ;  or  may  begin  when  the  milk 
teeth  are  shed  and  become  habitual.  The  commonest  form  is  the  use  of 
Th  for  S.  In  paralysis  of  the  lips  the  labia]  consonants  P,  B,  and  M  are 
pronounced  as  F  and  V  ;  in  palsy  of  the  tongue  the  Unguals  L  and  S  are 
said  as  Y  and  Th  ;  in  palatal  palsy  M  replaces  P  and  B.  In  hare-lip  there 
is  difficulty  with  M,  P,  B,  F  and  W,  letters  absent  in  the  words  of  various 
American  tribes.  In  cleft-palate  the  voice  is  nasal  and  there  is  difficulty 
with  dental  and  palatal  sounds,  especially  T,  D,  S,  B,  L,  K,  G.  A  high 
palate  may  have  some  effect.  Frequently  W  or  L  is  used  for  R  ;  sometimes 
T  for  G  or  K  :   and  L  may  be  replaced  by  D,  T,  S,  J,  N,  Ng. 

Stammering  and  Stuttering. — Speech  depends  on  the  co-ordinated 
action  of  three  mechanisms  under  the  control  of  the  nervous  system. 
The  expiratory  muscles  supply  the  blast  of  air.    The  laryngeal  or  phonetic 


794  Chapter  LVIII. 

system  produces  vocalisation  by  approximation  and  tension  of  the  vocal 
cords.  The  oral,  buccal  or  articulatory  mechanism  consists  of  the  lips, 
tongue  and  soft  palate,  and  varies  the  size  and  shape  of  the  orifice  through 
which  the  air  passes  and  produces  words.  The  vocal  and  oral  mechanisms 
can  be  used  separately  but  are  co-ordinated  in  speech.  Any  one  of  these 
parts  may  be  at  fault.  As  a  rule  the  defect  is  in  the  management  of 
expiration  or  delay  in  laryngeal  action.  Thus  stammering  may  be  due  to 
spasm  of  the  respiratory  muscles  or  diaphragm,  failure  of  articulation,  or 
failure  of  co-ordination,  i.e.  of  nervous  control.  It  may  be  denned  as  an 
irregularly  intermittent  fault  of  speech,  a  spasmodic  neurosis.  It  is  a  want 
of  promptitude  in  vocalisation,  a  sudden  check  in  utterance,  or  rapid 
repetition  of  consonantal  or  vowel  sounds. 

Etiology. — Macleod  Yearsley  (1907)  in  a  series  of  800  cases  found  the 
percentage  causation  was  heredity  40,  association  and  mimicry  29,  shock 
and  fright  16,  illness  15.  Congenital  cases  are  rare.  They  are  due  to 
weakness  of  the  syllabic  co-ordinating  apparatus,  defects  in  the  air  passages- 
or  in  breathing.  It  is  uncommon  among  imbeciles  and  not  a  sign  of  weak- 
mindedness.  Temporary  cases  occur  during  teething,  pertussis,  etc.  If 
caused  by  fright,  it  may  be  choreic  in  character.  Faulty  education,  imita- 
tion and  habit  induce  or  maintain  it. 

A  neurotic  family  history  is  of  prime  import.  It  affects  4  boys  to  1  girl. 
It  is  rare  before  the  third  year  of  life  ;  except  in  a  mild  and  temporary 
form  until  speech  is  properly  acquired.  Three-fourths  of  the  cases  begin 
between  4  and  9  years  of  age,  and  10  per  cent,  after  12  years.  It  is  a 
serious  disability,  a  handicap  in  most  walks  of  life,  and  an  annoyance  to 
self  and  others. 

Varieties. — The  simplest  variety  is  a  difficulty  in  articulating  an 
initial  consonant  or  a  spasmodic  arrest  before  some  syllable.  The  arrest 
may  be  complete,  due  to  spasmodic  arrest  of  the  diaphragm  and  cessation  of 
breathing,  and  analogous  to  the  difficulty  of  utterance  during  violent 
passion.  Usually  it  affects  the  explosives,  which  are  not  vocalised  at  the 
proper  time.  Or  the  initial  consonant,  fricative  or  nasal  resonant,  is 
prolonged  because  the  breath  is  driven  out  feebly  and  inefficiently.  Or 
there  may  be  stuttering,  the  spasmodic  repetition  of  the  same  syllable,, 
with  shallow  and  badly  managed  breathing,  low  and  hurried  speech,  clipped 
and  slovenly  articulation.  More  severe  types  are  associated  with  : — (1) 
Sounds,  e.g.  inarticulate  whimpering  noises,  grunting,  whooping,  crowing 
or  interpolated  meaningless  words  ;  (2)  Movements,  e.g.  grimaces  or  severe 
facial  contortions,  fidgets  of  hands  or  feet,  motor  spasm  of  limbs,  biting  lips 
or  tongue,  slapping,  pinching,  kicking  or  stamping.  The  voice  is  laboured 
and  the  secretion  of  saliva  excessive. 

Physiological  Alphabet  (Wyllie). — Vowels — i,  e,  a,  o,  u  are  pronounced 
in  the  latin  manner  as  ee,  eh,  ah,  oh,  oo  ;  and  y  as  an  initial  is  closely  allied 


Disorders  of  the  Higher  Faculties.  795 

to  i,  and  w  to  u.     The  voiceless  oral  consonants  are  purely  buccal,  the 
others  contain  a  vocal  element. 

Voiceless  Oral.  Voiced  Oral.  Voiced  Nasal. 
Labials        ....  P  B,  W  M 

Labio-Dentals        . .  F  V 

Linguo-Dentals      . .  S  Z 

Ant.  Linguo-Palatals  Sh,  T  D,  L,  R  N 

Post.  Linguo-Palatals         K,  H,  Ch  G,  Y  Ng 

In  this  alphabet  C  =  SorK;  Q  =  Kw;  X  =  Ks.  Usually  in  stammering 
the  explosive  or  closure  consonants  B,  P,  D,  T,  K,  hard  G,  are  affected,  due 
to  spasmodic  closure  of  parts  of  the  air  passages  which  should  be  thrown 
open.  Or  the  fricatives,  the  continuous  consonants,  V,  F,  C,  S,  Sh,  W,  M, 
N,  are  affected,  through  fixation  of  the  parts  engaged  in  uttering  the  par- 
ticular sound.  Or  the  vowel  sounds  are  at  fault,  from  mismanagement  of 
breathing  or  glottic  spasm,  a  condition  followed  by  rapid  speech  until 
breathless. 

Every  letter  is  partly  laryngeal  and  partly  oral,  the  vowels  being  more 
purely  laryngeal  than  the  consonants.  In  closure  of  the  lips,  first  stop 
position,  the  letters  P,  B  and  M  can  be  uttered.  With  the  tip  of  the  tongue 
applied  to  the  hard  palate  behind  the  upper  teeth,  second  stop  position, 
T,  DandN  are  formed.  In  the  third  stop  position,  approximation  of  the 
back  of  the  tongue  to  the  soft  and  hard  palate,  K,  G  and  Ng  (in  wing) 
can  be  pronounced.  In  spasm  of  the  true  and  false  vocal  cords,  a  fourth 
stop  position,  vowel  sounds  are  inaudible.  The  labio-dental  and  linguo- 
dental  are  also  stop  positions.  In  uttering  nasal  resonants,  voiced  nasal 
consonants,  the  soft  palate  drops  and  air  escapes  through  the  nose.  If  there 
is  nasal  obstruction,  M  is  pronounced  like  B. 

Diagnosis. — Examine  the  child  by  means  of  the  test  sentences  recom- 
mended by  Wyllie.    They  represent  the  usual  order  of  difficulty  :— 

Vowels. — Eels  ail  amid  ocean  ooze. 

Voiced  Fricatives. — We  visit  the  Zulus  like  ramblers  yearly. 

Voiceless  Consonants. — Far  shores  seem  thinly  hazy. 

Nasal  Resonants. — My  nephew. 

Voiced  Explosives. — Best  gold  dust. 

Voiceless  Explosives. — Two  poor  comrades. 

The  difference  between  stammering  and  stuttering  is  more  easily 
recognised  than  defined.  A  stammer  is  absent  during  singing  and  declaim- 
ing, and  often  when  whispering.  It  is  mainly  a  defect  in  co-ordination  of  the 
respiratory  and  laryngeal  mechanisms,  with  inability  to  produce  articulate 
sounds.  Sometimes  there  is  a  malformation  of  the  speech  organs.  The 
eyes  may  roll  and  the  features  be  distorted.  An  abnormal  mental  and 
emotional  state  depends  on  lack  of  co-ordination  of  mental  and  vocal 


796  Chapter  LVIII. 

processes.  There  is  rarely  any  spasmodic  or  convulsive  action  of  the  vocal 
apparatus. 

Stuttering  is  cerebral  in  origin  and  oral  in  production.  There  is 
lack  of  nervous  control,  an  abnormal  mental  and  emotional  condition  which 
is  primary  and  combined  with  improper  respiration  and  vocalisation. 
This  induces  vicious  attempts  at  utterance,  and  painful  and  rapid  repetition 
of  the  initial  syllable.  Inability  to  produce  articulate  sounds  is  rare.  With 
stuttering  there  is  associated  an  overflow  of  the  cerebral  stimulus  to  the 
larynx,  etc.,  causing  congestion  of  the  face,  cyanosis,  spasmodic  and  abnormal 
breathing,  and  excited  physical  movements.  Van  Praagh  states  that  a 
stammerer  does  not  know  how,  a  stutterer  does  not  know  when  to  speak. 

Prognosis. — The  outlook  is  bad,  if  the  intellect  is  defective.  It  depends 
on  the  intelligence  and  co-operation  of  the  patient.  It  is  worse,  if  associated 
with  severe  spasmodic  movements.  Mild  cases  frequently  get  well  after 
puberty. 

Treatment. — In  teaching  children  to  speak  they  should  be  made 
gently  to  repeat  letters  and  words,  until  they  do  so  without  stumbling. 
Attend  to  the  general  health  and  guard  against  neurotic  tendencies. 
Encourage  self-confidence.  Teach  breathing  exercises  and  see  that  the 
air  passages  are  unobstructed  by  adenoids,  enlarged  tonsils  or  nasal  defect. 
Attend  to  any  defect  in  the  mouth. 

If  there  is  the  least  sign  of  stammering  begin  early  a  regular  and 
rigid  system  of  training,  after  the  onset  of  the  second  dentition,  although 
many  recover  spontaneously.  The  best  results  are  obtained  at  12-16  years 
of  age  because  the  child  can  appreciate  the  method  and  understand  its 
importance.  Throughout  life  the  patient,  in  bad  cases,  must  attend  to 
voice  production  for  relapse  is  common. 

First  teach  proper  breathing.  Encourage  abdominal  respiration  with 
attention  consciously  directed  to  it,  "  diaphragmatic  drill."  Then  teach 
prolonged  utterance  of  vowel  sounds,  aloud  and  in  whispers  ;  words  of  one 
syllable  beginning  with  (a)  vowel,  (b)  consonant ;  words  of  two  syllables 
and  more  ;  poetry,  prose  and  declamation.  The  child  should  vocalise 
strongly,  without  drawing  in  breath,  for  this  may  lead  to  inspiratory  or 
"  draw  back  "  phonation.  If  there  is  the  least  difficulty,  he  should  stop 
and  not  make  repeated  attempts  to  overcome  spasm.  Any  difficult  letter 
or  sound  must  be  practised  separately  and  all  consonants  clearly  enunciated. 
Speaking  must  not  be  attempted  until  the  lungs  are  fully  expanded.  The 
patient  should  keep  a  pebble  under  the  tongue,  to  prevent  it  cleaving  to 
the  floor  of  the  mouth,  or  a  piece  of  wood  between  the  teeth,  and  speak 
slowly  and  distinctly,  in  a  loud  full  voice,  prolonging  the  vowel  sounds  and 
beating  the  time  of  the  syllables  with  one  hand.  Attention  must  be 
directed  first  to  vocalisation  and  then  to  articulation.  Next  practise  reading 
aloud,  poetry  first  for  it  requires  more  voice,  in  a  large  room,  in  a  distant 
room  with  the  intervening  door  open  or  in  the  open  air,  without  shouting  or 


Disorders  of  the  Higher  Faculties.  797 

allowing  the  voice  to  drop  for  this  shows  that  the  chest  is  not  kept  full. 
Underline  defective  words  and  try  them  separately.  Intoning,  declamation 
and  singing  are  often  curative,  but  may  induce  a  sing-song  delivery.  Guard 
against  nervousness  and  excitement.  When  the  child  is  old  enough  he 
should  have  exercises  in  which  his  attention  is  directed  to  the  mechanical 
movements  in  voice  production,  e.g.  the  exact  position  of  the  tongue  and 
lips.  He  can  then  correct  his  stammer  by  placing  his  mechanism  in  proper 
order  and  thus  overcome  the  hesitation. 

These  children  must  not  go  to  school.  Bad  cases  must  be  sent  from 
home  and  put  under  the  charge  of  an  experienced  teacher,  best  of  all  under 
single  charge  and  not  with  others  similarly  affected.  Treatment  is 
individual  and  little  progress  can  be  seen  for  a  month  or  more. 

Yearsley  recommends  a  course  of  4  hours  daily,  6  days  a  week,  for 
6  weeks.  It  is  directed  to  the  cultivation  of  self-possession,  efficient  breath- 
ing and  proper  vocalisation.  Respiratory  exercises  teach  thoracic,  dia- 
phragmatic and  abdominal  breathing.  Vocal  gymnastics  are  directed  to 
practising  the  natural  articulation  of  vowels,  explosive  utterance,  rising  and 
falling  inflection,  and  prolonged  articulation  at  normal  tone.  The  third 
exercise  is  devoted  to  combined  vocalisation,  breathing,  and  physical  drill 
with  dumb-bells  at  80  movements  per  minute.  Finally  the  child  reads  and 
recites  in  company,  syllable  by  syllable.  Half-an-hour,  morning  and 
afternoon,  is  devoted  to  each  exercise.  It  requires  2  weeks  to  re-establish 
normal  use  of  the  speech  organs  ;  2  weeks  to  encourage  application  and 
test  ability  ;  and  2  weeks  for  training  to  deliver  written  speeches  and 
recite  slowly  and  deliberately. 


Chapter  LIX. 

THE    MUSCLES,    BONES    AND    JOINTS. 

Muscular  Dejects  —  Myositis  —  Myositis  Ossificans  —  Torticollis  — Lateral 
Curvature — SprengeVs  Deformity — Club-foot — Osteomyelitis  —  Dislo- 
cations— Pulled  Elbow —  Arthritis — Rheumatoid  Arthritis — Pulmonary 
Osteoarthopathy. 

Congenital  absence  of  muscles  may  be  partial  or  complete.  It  is  most 
common  in  the  pectorals,  and  next  in  the  trapezius,  serratus  magnus  and 
quadriceps  extensor  femoris.  Absence  of  the  ocular  muscles  may  depend 
■on  infantile  nuclear  atrophy.  Absence  of  the  pectorals  may  be  associated 
with  absence  of  one  or  more  ribs,  aplasia  of  the  sterno-mastoid  and  other 
muscles,  atrophied  skin,  defective  development  of  the  breast,  webbed 
fingers  and  webbing  of  the  arm  to  the  chest,  and  Sprengel's  deformity. 
It  is  rarely  bilateral.  Permanent  defect  is  not  nearly  as  disabling  as 
might  be  expected.  Unilateral  absence  has  been  recorded  in  about  70  cases 
(J.  Gr.  Forbes,  1907).  Usually  the  pectoralis  minor  is  absent  and  the  sternal 
portion  of  the  pectoralis  major,  the  clavicular  portion  being  hyper- 
irophied.  It  is  most  frequent  in  males  and  on  the  left  side,  and  is  no 
hindrance  to  laborious  work  or  athletics. 

The  causation  is  obscure.  Apparently  it  is  not  dependent  on  atavism, 
physical  deterioration,  or  arrested  development  of  nerve  or  vascular 
supply.  Possibly  it  is  due  to  intra-uterine  compression  of  the  upper 
limb  against  the  thorax,  preventing  development.  The  side  of  the  chest 
may  be  grooved  and  the  hand  and  arm  malformed.  This  grooving  is  seen 
sometimes  in  infancy  and  obliterated  by  growth  in  later  life.  Similarly, 
the  pressure  of  the  knee  on  the  abdominal  muscles  in  the  right  or  left 
hypochondrium  is  supposed  to  cause  atrophy  and  lead  to  ballooning  of  the 
abdomen.  More  probably  it  is  a  developmental  defect  for  other  deformities 
are  often  present. 

Congenital  deficiency  of  abdominal  muscles  is  generally  associated 
with  genito-urinary  changes,  but  exists  without,  e.g.  in  hernia  of  the  cord. 
These  rare  cases  are  almost  always  male  infants  with  no  phimosis  or  urethral 
obstruction.  The  muscles  of  the  anterior  abdominal  wall  are  absent  or  very 
atrophied,  the  lower  segments  being  most  affected.  The  wall  may  be 
composed  only  of  skin.  The  abdomen  is  distended  and  bulged  on  each  side. 
The  abdominal  organs  are  easily  palpated.  Distended  coils,  sometimes 
dilated  ureters,  are  visible  under  the  skin.    The  ureters  are  dilated  and  mav 


The  Muscles,   Bones  and   Joints.  799 

be  convoluted.  The  bladder  is  contracted  and  hypertrophied  ;  or  forms  a 
pyriform  tumour  extending,  when  full,  up  to  the  umbilicus.  The  urachus 
may  be  patent.  The  kidneys  aie  normal,  maikedly  unequal  in  size,  or 
fibrosed.  The  testes  are  undescended.  Occasionally  the  external  genitals 
are  duplicated.  The  spinal  cord  shows  no  special  characteristics.  Micro- 
scopically the  character  of  the  muscle  is  that  of  non-development  and  not  of 
•degeneration. 

The  most  probable  explanation  is  a  primary  defective  development  of  the 
abdominal  muscles,  which  consequently  render  no  assistance  to  the  descent 
of  the  bladder.  The  ureters  are  therefore  abnoimally  placed  and  become 
dilated,  through  partial  obstruction  from  abnormal  angle  of  entry  into  the 
bladder,  and  the  changes  in  the  kidneys  are  secondary.  Another  theory  is 
that  an  abnormal  blood  supply  produces  a  simultaneous  embryological 
defect  of  development.  A  more  improbable  view  is  that  the  abdominal 
•distension  and  atrophy  are  secondary  to  primary  dilatation  of  the  bladder. 

Myositis. — Simple  myositis  is  due  to  injury,  microbial  infection  or 
adjacent  inflammation.  It  may  complicate  rheumatism,  gonorrhoea, 
scarlatina,  typhoid,  paratyphoid  and  other  fevers.  In  the  rectus  abdominus 
it  is  most  frequent  as  a  result  of  fever  or  injury.  It  causes  local  tenderness, 
pain,  swelling  and  perhaps  redness,  and  may  end  in  suppuration. 

Polymyositis  is  primary  or  due  to  trichinae.  Occasionally  it  is  asso- 
ciated with  cutaneous  oedema,  haemorrhage  into  the  skin  and  mucous 
membrane,  or  erythema  multiformse.  It  gives  rise  to  malaise,  fever,  anor- 
exia, vomiting,  headache  and  pain  in  the  limbs.  GMema  begins  in  the 
eyelids  and  face,  and  spreads  rapidly  all  over.  The  muscles  of  the  face 
become  rigid,  board-like  and  very  painful.  The  other  muscles  become 
involved,  especially  those  of  the  extremities,  feel  hard  and  doughy,  and 
are  very  painful.  The  deep  reflexes  are  abolished  and  there  is  inability  to 
move.  The  course  of  the  fever  is  like  that  of  typhoid.  Sometimes  there 
is  albuminuria.  Some  cases  are  subacute  or  chronic  in  course,  with 
exacerbations.  The  disease  is  usually  mild  in  children  and  gets  well  in  a  few 
weeks.  It  may  last  for  months,  or  end  fatally  from  involvement  of  the 
muscles  of  deglutition,  respiration,  and  the  heart.  The  treatment  is  purely 
symptomatic. 

Myositis  fibrosa  is  a  rare  variety  of  interstitial  inflammation  and 
secondary  muscular  atrophy.  The  abdominal  muscles  become  extremely 
hard  and  the  limbs  contracted. 

Myositis  ossificans  is  a  local  calcification,  secondary  to  inflammation 
•of  the  muscles  (e.g.  rider's  bone)  or  adjacent  parts.  It  may  be  secondary 
to  phlebitis  or  adenitis,  the  exudate  into  the  muscle  undergoing  calcification. 
The  process  is  analogous  to  that  in  tuberculous  glands,  hydatid  cysts  and 
trichinous  muscle. 

Myositis  ossificans  progressiva  is  a  constitutional  liability  to  bony 
deposit.     It  was  first  reported  by  Freke  in  1740.     There  are  now  about 


800  Chapter  L  I X. 

100  cases  on  record.  It  is  not  hereditary,  but  has  been  reported  in  father 
and  son  by  Burton  Fanning.  It  affects  5  males  to  1  female.  It  usually 
begins  at  2-4  years  of  age,  sometimes  not  until  the  eighth  to  sixteenth  year. 
Out  of  51  collected  cases  (Lorenz)  11  were  under  1  year,  16  between  1  and  5,. 
and  15  between  5  and  15  years.  It  may  be  started  by  injury  and  is  in  this 
respect  allied  to  "  rider's  bone." 

It  especially  affects  the  muscles  of  the  neck,  shoulders,  back,  upper 
arms  and  the  rectus  abdominis  ;  sometimes  chiefly  the  pectorals  and 
biceps.  Later  the  thigh,  lower  arm  and  leg  muscles  are  involved.  Even 
the  intercostals,  masseters,  temporals  and  platysma  myoides  may  be 
affected.  Occasionally  it  has  started  in  the  muscles  of  the  face,  but  these 
usually  escape.  The  muscles  of  the  tongue,  glottis,  diaphragm  and  heart 
are  never  involved. 

It  sometimes  begins  with  fever,  pain,  swelling  and  oedema  of  the 
muscles.  At  first  the  muscle  is  swollen,  doughy  and  feels  solid.  After  a 
variable  period  it  undergoes  ossification  and  bony  plates,  nodules  or  masses 
may  be  felt,  sometimes  intra-muscular  or  connected  with  the  subjacent  bone. 
A  striking  feature  is  microdactyly  of  the  great  toes.  This  was  found  by 
de  Witt  in  70  per  cent,  of  recorded  cases  in  which  the  condition  of  the  toes 
was  noted.  The  phalanges  are  short,  broad  and  synostosed.  The  thumbs 
are  often  smaller  than  normal.  In  a  few  instances  there  are  numerous 
exostoses  or  bony  masses  involving  the  muscles  and  attached  to  the 
subjacent  bone. 

The  course  is  gradually  progressive,  sometimes  with  remissions  in 
warm  weather,  or  in  successive  attacks  at  variable  intervals.  It  leads  to 
progressive  crippling,  limitation  of  movement,  and  occasionally  scoliosis 
and  muscular  atrophy.  Sometimes  there  are  long  intervals  of  arrest.  It  is 
usually  fatal  in  10-12  years  from  pulmonary  complications,  if  the  respiratory 
muscles  are  affected,  or  from  involvement  of  the  muscles  of  mastication.- 

Its  causation  is  unknown.  Myositis,  fibrous  myositis  and  ossification 
occur  successively,  with  the  formation  of  disseminated  nodules  or  plates  of 
bone  in  the  muscles,  exostoses,  and  ossification  of  the  muscular  attachments. 
It  is  not  congenital  but  may  be  due  to  an  endogenous  defect  of  the  meso- 
blast,  a  constitutional  state  rendering  the  muscles  abnormally  sensitive 
to  irritation.  The  irritation  may  be  external,  for  many  cases  follow  injury. 
It  leads  to  subacute  inflammatory  processes,  embryonal  infiltration, 
fibrous  induration  and  ossification.  Carpenter  and  Edmunds  examined  a 
portion  of  muscle  removed  during  life  in  the  stage  of  brawny  swelling  and 
found  a  fibro-cellular  infiltration  suggestive  of  degeneration  rather  than 
inflammation.  De  Witt  has  described  a  phlebitis  with  an  exudation,  rich 
in  osteoblasts,  into  the  connective  tissue  of  the  muscle.  Nothing  can  be 
done  except  protect  the  patient  against  cold  and  injury.  Hot  baths, 
salicylates  and  iodides  can  be  tried.  The  disease  is  usually  mistaken  for 
rheumatism  at  the  onset. 


The  Muscles,   Bones  and  Joints.  801 

Torticollis. — Wry  neck  is  due  to  contraction  of  the  sterno-mastoid 
muscle  from  changes  in  the  muscle  or  from  tonic  or  clonic  spasm.  "  False  " 
wry  neck  may  arise  from  the  cicatrisation  of  burns,  wounds  or  other  neck 
injuries.    In  rare  instances  cervical  caiies  produces  a  similar  appearance. 

An  acute  or  simple  stiff-neck  follows  exposure  to  cold,  or  rheumatic 
myositis.  It  is  of  little  importance  and  quickly  gets  well  when  treated  by 
local  heat,  massage,  salicylates  and  alkalies.  Reflex  wry  neck  is  due  to 
reflex  irritation  of  the  spinal  accessory  nerve,  to  enlarged  glands  and 
perhaps  spinal  caries.  The  spasmodic  type  is  practically  unknown  in 
infants,  being  most  common  in  adult  females  and  rarely  a  sequel  of  acute 
stiff  neck.  It  is  not  limited  to  one  muscle  and  is  probably  cortical  in  origin. 
In  the  paralytic  variety  the  deformity  is  due  to  the  contraction  of  the 
opposite  muscle,  when  one  is  paralysed  from  poliomyelitis.  Subsequent 
atrophy  of  the  affected  muscle  may  lead  to  fibrosis  and  contracture. 

The  infantile  or  congenital  type  is  probably  never  congenital.  Cases 
occur  as  a  result  of  injury  to  the  muscle  at  birth  or  of  congenital  syphilis. 
They  are  sometimes  called  fixed  or  permanent,  to  distinguish  them  from 
temporary,  reflex,  and  spasmodic  forms.  The  etiology  is  the  same  as  that 
of  sterno-mastoid  tumour.  Yet  few  cases  are  secondary  to  sterno-mastoid 
tumour  and  even  gummatous  deposits  in  the  muscle  do  not  produce  it. 
Both  factors  may  be  absent.  It  is  due  to  injury  of  the  muscle,  rupture  of 
muscle  fibres,  perhaps  effusion  of  blood,  and  a  certain  amount  of  myositis. 
This  condition  is  rarely  permanent  but  occasionally  the  muscle  is 
replaced  wholly  or  in  part  by  dense  cicatricial  tissue.  The  sternal  portion 
is  the  most  often  affected  and  may  even  be  tendinous  throughout,  up  to 
its  attachment  to  the"  mastoid  process.  The  trapezius,  splenius  and  deep 
neck  muscles  may  be  also  involved.  In  prolonged  cases  the  deep  fascia 
of  the  neck  is  shortened  and  the  vertebral  bodies  are  unequally  compressed, 
becoming  wedge-shaped  and  causing  scoliosis. 

The  primary  change  is  shortening  of  the  sterno-mastoid,  drawing 
down  the  head  to  the  affected  side  and  rotating  the  face  and  chin  to  the 
opposite  side.  The  other  changes  are  secondary.  The  face  on  the  affected 
side  develops  imperfectly,  so  that  there  is  marked  asymmetry,  for  the  carotid 
artery  is  partly  compressed.  If  there  is  atrophy  of  the  muscles  and  bones, 
the  case  is  probably  of  nerve  origin. 

Treatment. — Rely  on  mercury,  massage  and  manipulation,  if  there 
is  congenital  syphilis.  In  other  infantile  cases  operation  is  necessary. 
Subcutaneous  tenotomy  is  justifiable,  if  the  sternal  attachment  alone 
requires  division  and  if  it  stands  out  well  above  the  subjacent  tissues. 
Otherwise  it  is  unsafe  and  generally  ineffective,  for  the  danger  and  fear  of 
injuring  underlying  veins  and  arteries  usually  lead  to  incomplete  division, 
and  fascial  bands  cannot  be  dealt  with.  In  the  open  operation  an  incision 
1-2  ins.  long  is  made  obliquely  along  the  anterior  border  of  the  muscle  or 
vertically  between  its  two  attachments.  The  skin  is  retracted  and  a 
director  inserted  under  the  muscle  which  is  divided  from  above.     The 

3  F 


802  Chapter  LIX. 

anterior  fibres  of  the  trapezius  and  fascial  bands  are  divided  if  necessary. 
The  head  is  put  up  straight  or  in  an  over-corrected  position,  and  fixed  by 
sandbags  or  a  suitable  apparatus.  The  muscle  soon  unites  ;  the  child  may 
sit  up  in  bed  in  7-10  days,  or  2-3  weeks  in  bad  cases,  and  get  up  a 
few  days  later.  Recovery  is  complete  in  3  weeks.  Massage  and  exercises 
must  be  adopted  in  old  standing  cases  or  if  there  is  any  tendency  to 
recurrence. 

Lateral  Curvature  or  Scoliosis  is  congenital  or  acquired.  Congenital 
cases  are  rare,  and  due  to  the  presence  of  an  abnormal  wedge-shaped 
vertebra  between  the  eleventh  dorsal  and  the  third  lumbar.  This  is  either 
an  extra  ill-developed  dorsal  vertebra,  with  a  rib  attached  to  it  on  one  side, 
or  an  atavistic  survival. 

The  acquired  variety  is  a  primary  lateral  deviation  of  the  spinal 
column  and  a  secondary  rotation  of  the  vertebrae  round  the  vertical  axis. 
It  is  a  common  deformity,  especially  in  girls  of  7-14  years  of  age,  though  it 
may  occur  later  in  life  or  much  earlier,  even  at  6  months  of  age.  A  family 
tendency  is  sometimes  found.  In  a  few  instances  it  depends  on  a  congenital 
defect  of  muscles  and  ligaments.  Rickets  is  the  chief  cause  in  infancy  and 
the  convexity  is  to  the  left.  Poliomyelitis  is  a  potent  factor  in  many  severe 
cases  and  may  occur  at  any  age.  Paralytic  scoliosis  usually  presents  only 
one  curve,  in  the  dorsal  or  dorso-lumbar  region.  A  few  cases  depend  on 
muscular  dystrophies.  In  growing  girls  the  chief  cause  is  muscular  weakness, 
the  back  muscles  not  keeping  pace  with  the  muscular  development  else- 
where. This  may  be  associated  with  anaemia,  excessive  mammary  develop- 
ment and  vicious  positions  at  work,  carrying  a  baby  exclusively  on  one 
arm  or  unbalanced  employment  of  one  upper  limb.  Many  are  due  to 
faulty  positions  at  school  when  writing,  the  curve  being  to  the  right.  Others 
depend  on  inequality  of  the  length  of  the  legs  from  infantile  palsy,  talipes 
or  hip  disease  ;  persistent  and  severe  wry  neck  ;  or  contraction  of  the  side 
after  empyema  or  pleurisy. 

Examination. — Strip  the  child.  Mark  the  spines  of  the  vertebrae 
with  a  carbon  pencil.  Take  note  of  any  obliquity  of  the  pelvis,  and  the 
level  of  the  anterior  superior  spines  and  of  the  iliac  bones.  Suspend  the 
child  by  lifting  under  the  armpits,  to  see  if  the  curve  disappears.  The  curve 
may  be  slight,  unilateral  and  C-shaped.  Such  a  curve  is  situated  in  the 
dorsal  or  dorso-lumbar  region,  involves  many  vertebrae,  and  constantly 
increases  from  the  weight  of  the  head  and  upper  limbs  and  from  the  muscular 
weakness.  In  the  next  stage  the  curve  is  double,  or  S-shaped,  consisting 
of  2  equal  and  opposite  curves  in  the  dorsal  and  lumbar  region.  The 
vS-shaped  curve  is  rarely  cervico-dorsal,  due  to  torticollis  or  astigmatism. 
The  primary  curve  is  the  least  mobile  and  less  easily  straightened  by 
extension.  In  the  third  stage  there  are  2  secondary  curvatures,  with 
lateral  protuberances  and  flattening  of  the  trunk.  Occasionally  the  spinous 
processes  project  and  suggest  Pott's  disease.  In  very  severe  and  prolonged 
cases  the  rotation  of  the  bodies  of  the  vertebrae  may  cause  obliteration  or 


The  Muscles,   Bones  and  Joints.  803 

reversal  of  the  curves.  The  weakness  of  the  muscles  is  on  the  convex  side 
of  the  primary  curve. 

Symptoms. — The  back  becomes  tired  on  standing  or  sitting  for  long. 
•One  shoulder  is  higher  than  the  other,  the  flanks  arc  not  symmetrical  and 
one  hip  projects.  As  the  deformity  increases,  pain  is  felt  on  the  sides  of  the 
spinous  processes  and  is  diffused  in  the  hips,  flanks  or  chest.  Pain  is  due 
to  stretching,  of  muscles  and  ligaments  on  the  convex  side  of  the  curve. 
Later  still  the  deformity  becomes  extreme  and  the  child  dwarfed. 

In  the  common  variety  the  primary  curve  is  convex  to  the  right  in  the 
■dorsal  region  and  the  secondary  one  convex  to  the  left  in  the  lumbar.  The 
right  shoulder  is  prominent,  "  is  growing  out,"  the  scapula  being  raised 
and  more  horizontal.  The  right  shoulder  is  higher  than  the  left  and  the 
.arm  more  closely  approximated  to  the  side.  The  ribs  on  the  right  side  are 
flattened  in  front  and  pioj  ect  behind.  In  bad  cases  the  right  clavicle  becomes 
much  curved.  The  right  flank  is  depressed  and  the  hip  sticks  out.  The  ends 
of  the  spinous  processes  are  displaced  to  the  left  in  the  dorsal  region  and 
to  the  right  in  the  lumbar,  that  is  toward  the  concave  side.  The  transverse 
processes  become  more  prominent  on  the  convex  side.  The  xiphoid  car- 
tilage and  umbilicus  are  displaced  to  the  left,  and  the  right  mamma  is  much 
■less  prominent  than  the  left.  The  viscera  are  displaced.  The  right  lung  is 
smaller  than  the  left,  the  cardiac  apex  is  displaced  upward  and  outward, 
;and  the  liver  is  depressed. 

The  diagnosis  is  self-evident  on  examination  of  the  spine.  The  degree 
of  severity  depends  on  the  extent  of  the  curve,  its  duration,  and  the  amount 
of  straightening  in  recumbency  and  on  extension.  It  is  distinguished  from 
Pott's  disease  by  its  shape,  absence  of  rigidity  and  comparatively  slight 
pain.  These  two  varieties  of  curvature  may  co-exist.  A  paralytic  curve 
is  frequently  single  and  dorsal  or  dorso-lumbar. 

Prognosis. — Under  suitable  treatment  mild  curves  get  well.  Those  due 
to  infantile  paralysis  of  spinal  muscles  and  to  empyemata  are  the  most 
serious.  Rachitic  cases  are  bad,  for  the  curve  is  liable  to  be  accentuated 
•during  growth.  In  girls  it  is  more  serious  than  in  boys,  because  of  the 
weaker  muscular  development.  The  later  the  onset  the  better  is  the 
prognosis,  for  the  parts  are  more  fully  developed.  The  gravity  is  increased, 
if  the  spine  is  long  and  flabby.  The  S-shaped  dorso-lumbar  curve  is  the 
least  and  the  long  C-shaped  curve  the  most  serious.  The  latter  may  be 
extreme  in  a  couple  of  months.  Once  the  condition  is  severe  and  of  long 
standing,  it  is  incurable,  for  the  bodies  of  the  vertebrae  have  become 
permanently  deformed  as  a  result  of  rotation  and  unequal  pressure.  If  the 
•curve  does  not  disappear  on  suspension,  there  is  bony  deformity  and  it 
cannot  be  completely  cured. 

Treatment. — Prevention  consists  in  teaching  the  child  not  to  stand 
on  one  leg,  and  to  sleep  on  a  flat  hard  mattress  with  a  low  pillow  or  none 
at  all.  Excessive  use  of  one  arm  and  faulty  positions  at  work  must  be 
•avoided.    The  back  of  the  chair  should  be  high  and  sloping  backward,  the 


804  Chapter  L1X. 

feet  should  easily  reach  the  floor,  and  the  desk  should  be  of  suitable  height 
and  slope  at  an  angle  of  25-30°.  Upright  handwriting  should  be  taught 
with  the  elbow  on  the  arm  of  the  chair,  the  body  upright,  the  feet  on  a. 
stool  and  the  thighs  horizontal.  If  one  leg  is  shorter  than  the  other,  a 
suitable  boot  must  be  worn.  The  child  should  lie  down  in  the  prone  or 
supine  position  for  2  hours  daily,  and  the  back  muscles  be  massaged  for 
half  an  hour.  Every  case  of  lateral  curvature  requires  treatment,  which 
must  be  persisted  in  as  long  as  growth  continues,  in  order  to  prevent  the- 
curve  getting  worse.  Correction  and  maintenance  of  correction  are  both 
necessary. 

Attend  to  the  general  health  and  for  this  the  seaside  is  most  suitable.. 
Restore  spinal  mobility  which  has  become  impaired  by  contraction  of 
ligaments  and  atrophy  of  muscles  on  the  concave  side.  Teach  the  patient 
correct  attitudes,  and  exercises  planned  to  increase  the  strength  of  the 
weaker  side.  All  exercise  must  be  followed  by  a  period  of  recumbency  flat 
on  the  back.  A  cool  or  cold  bath  should  be  given  in  the  morning  and 
followed  by  rubbing  with  a  rough  towel  and  exercises,  which  bring  the- 
back  muscles  into  play  and  expand  the  chest. 

Exercises  may  be  given  at  9  a.m.  and  5  p.m.,  followed  by  recumbency 
for  1  hour.  The  following  exercises  are  suitable  : — (1)  Crawling  on  the 
hands  and  knees,  with  the  head  turned  at  each  step  toward  the  side  on 
which  the  hand  and  knee  are  approximated  ;  (2)  Swimming  movements 
while  lying  on  the  back  or  stomach  ;  (3)  Let  the  patient  lie  flat  on  the  back 
on  a  table  with  the  arms  by  the  side.  The  arm  is  then  flexed  at  the  elbow 
and  fully  extended  above  the  head  by  the  operator,  the  patient  resisting.. 
(4)  With  the  head  over  the  edge  of  the  table,  the  arms  are  first  flexed  and  then 
fully  extended  laterally  and  above  the  head.  (5)  With  the  arms  fully 
extended  above  the  head  the  legs  are  elevated  at  a  right  angle  to  the  body~ 

(6)  Both  arms  and  legs  are  simultaneously  moved  in  a  circular  manner. 

(7)  Wliile  lying  on  the  face,  the  trunk  is  elevated  on  the  hands  and  then  on 
the  arms  and  the  body  flexed  backward  and  forward.  (8)  With  the  legs, 
fixed  and  the  arms  fully  extended  above  the  head  the  body  is  bent  backward 
from  the  waist  over  the  edge  of  the  table.  (9)  With  the  patient  prone  the- 
spine  is  manipulated  by  pressure  on  the  prominent  ribs  to  force  the  verte- 
brae more  into  position.  At  first  the  exercises  should  be  easy  and  continued 
for  a  few  minutes.  They  are  gradually  increased  to  more  difficult  ones 
for  half  an  hour  daily,  carried  out  slowly  with  intervals  of  rest.  Dumb-bells,, 
not  more  than  1  lb.  in  weight,  can  be  used  in  addition.  Firm  corsets  should 
be  worn  while  at  lessons  and  after  exercises. 

School  life  is  unsuitable  unless  the  child  has  a  special  desk  and  long^ 
intervals  for  rest  and  games.  Sculling,  fencing,  drilling  and  the  use  of 
clubs  are  good  exercises.  Supports  may  be  necessary  to  relieve  pain  due  to 
displacement  of  the  viscera  and  to  prevent,  if  possible,  the  deformity 
getting  worse.  They  should  only  be  used  in  incurable  cases  which  are 
severe,  fixed  and  unchanged  by  alteration  in  position,  or  temporarily  in  less. 


The  Muscles,   Bones  and  Joints.  805 

severe  ones.    Spinal  braces  are  probably  the  best,  they  must  not  be  worn 
■continuously  and  must  not  prevent  movement  of  the  spine  and  muscles. 

Sprengel's  Deformity,  or  Congenital  Elevation  of  the  Scapula,  was 
•described  by  Eulenburg  (1860)  and  more  fully  by  Sprengel  (1891).  Up  to 
the  end  of  1908  about  130  cases  were  on  record.  The  scapula  is  in  develop- 
ment a  cervical  appendage.  Deformities  resemble  conditions  found  in 
lower  animals. 

The  most  common  variety  is  that  described  by  Sprengel,  and  is  due 
to  intra-uterine  fixation  of  the  arm  behind  the  back  or  more  probably  to 
■developmental  error,  possibly  of  the  scapular  mesoblast.  It  is  most  common 
in  females  and  on  the  left  side,  but  is  sometimes  bilateral.  The  scapula  is 
■elevated  2-2|  ins.  above  the  level  of  its  fellow  and  somewhat  rotated,  so 
that  it  is  placed  rather  obliquely  with  the  lower  angle  abnormally  near  the 
spine  and  fixed  to  it  by  short  bands  of  muscle  and  ligaments.  Elevation  of 
the  arm  above  a  right  angle  is  impossible  and  the  movements  of  the 
shoulder  are  limited.  The  bone  is  usually  smaller  than  its  fellow  and  its 
muscles  are  short  and  defective.  The  neck  is  fuller  and  the  neck  muscles 
short  and  tense,  so  much  so  that  the  chin  may  be  drawn  down  to  the  chest. 
There  is  sometimes  slight  curvature  of  the  dorsal  spine  towards  the  affected 
side  and  this  may  lead  to  secondary  scoliosis  in  the  lumbar  region. 

In  another  variety  the  scapula  is  united  to  the  spinous  process  of  the 
seventh  cervical  or  first  dorsal  vertebra  by  a  triangular  bony  or  carti- 
laginous ridge,  the  base  of  which  is  attached  to  some  part  of  the  vertebral 
border.  It  is  probably  an  abnormal  development  of  the  supra-scapular 
•epiphysis,  a  reversion  to  a  lower  type.  It  is  sometimes  regarded  as  an 
•outgrowth  from  the  vertebra  or  scapula,  or  an  ossified  rhomboid  muscle. 
The  movements  are  seriously  inconvenienced.  The  arm  cannot  be  raised 
above  a  right  angle  nor  the  hand  placed  to  the  back  of  the  head.  Congenital 
scoliosis  is  present  in  half  the  cases. 

Elevation  of  the  scapula  in  rare  instances  depends  on  absence  of  one 
•or  more  muscles  of  the  shoulder  girdle,  eversion  of  an  abnormally  long 
supraspinous  portion,  deformity  in  the  upper  ribs,  or  congenital  dislocation 
of  the  humerus.  Associated  defects  may  be  found  in  the  ribs,  vertebra?, 
humerus  or  clavicle  ;  or  in  the  adjacent  muscular  tissues,  especially  the 
trapezius,  pectoralis  major  and  sterno-mastoid.  Sometimes  there  is  talipes 
•cquinus,  spina  bifida,  absent  ribs  or  radius,  and  strabismus. 

Treatment. — In  simple  cases  exercises  and  massage  are  beneficial. 
The  division  of  shortened  muscles  or  ligaments  may  do  a  little  good.  The 
best  results  are  obtained  by  the  removal  of  abnormal  bony  or  cartilaginous 
masses,  when  present. 

Club-foot. — The  common  variety  is  equino-varus,  an  exaggeration  of 
the  normal  tendency  to  inversion  and  due  to  malpositions  in  utero,  spina 
bifida,  or  imperfect  osseous  development.  It  is  a  compound  of  extension  and 
inversion.  The  heel  is  drawn  up  and  often  imperfectly  developed.  The 
foot  is  extended  at  the  ankle  joint,  and  the  part  anterior  to  the  midtarsal 


806  Chapter  LIX. 

joint  is  drawn  inward  and  rotated  so  that  the  sole  is  inverted.  The  internal 
border  of  the  foot  is  shortened  and  concave,  the  external  border  convex,, 
and  there  is  some  plantar  flexion.  On  walking  callosities  develop  in  the 
skin  over  the  external  border.  The  upper  surface  of  the  astragalus  projects, 
on  the  dorsum  of  the  foot. 

The  deformity  can  be  rectified  by  manipulation.  Even  if  the  bones  are 
badly  shaped,  persistent  manual  treatment  is  likely  to  be  successful  for 
they  are  cartilaginous  and  can  be  moulded.  In  untreated  cases,  in  children 
who  have  begun  to  walk,  the  muscles,  ligaments  and  tendons  are  shortened 
and  contracted  and  tenotomy  is  needed.  Later  in  life  the  bones  ossify  in 
the  bad  position,  ankylosis  takes  place  in  some  joints  and  new  joints  form. 

The  prognosis  is  good  in  infants,  systematically  treated.  It  must  be 
guarded,  if  contraction  has  been  allowed  to  occur,  but  the  result  is  generally 
perfect  under  15  years  of  age.  Recurrence  after  treatment  means  that  the 
extensor  muscles  have  not  been  allowed  to  contract  sufficiently  to  resist  the 
action  of  gravity  and  cannot  keep  the  foot  at  a  right  angle. 

Treatment. — The  varus  must  receive  most  attention.  Begin  treatment 
at  birth  and  even  do  tenotomy  then,  if  manipulation  does  not  bring  the 
foot  into  position.  Manipulation  is  directed  to  overcome  the  extension  of 
the  foot  at  the  ankle  and  the  inversion  of  the  anterior  parts  of  the  foot  at  the 
midtarsal  joint.  Evert  and  flex  the  foot  at  the  ankle  joint  and  keep  it  in 
this  position  for  half  a  minute  ;  repeat  both  movements  for  5  minutes- 
gently,  without  causing  pain,  3  times  daily.  The  anterior  tibial  and 
peroneal  muscles  must  be  systematically  massaged  to  strengthen  them 
and  enable  them  to  keep  the  foot  in  the  right  position.  Continue  this 
treatment  for  2-3  months  and  then  less  often,  until  the  child  walks. 
Standing  and  walking  aie  essential  to  retain  the  correction.  If  these  measures- 
are  insufficient  use  a  padded,  malleable,  metal  splint  to  maintain  the  foot 
in  the  correct  position  between  the  manipulations.  Should  relapse  occur 
on  walking,  a  surgical  boot,  which  will  not  allow  inversion  of  the  foot  or 
extension  at  the  ankle,  is  sufficient.  Tenotomy  is  required,  if  the  foot  cannot 
be  got  into  its  normal  position  by  manipulation.  It  is  of  the  utmost  impor- 
tance to  cure  the  inversion  before  dealing  with  the  equinus  and  therefore 
to  cut  the  tendon  Achilles  last.  Operation,  if  necessary,  should  be  done 
before  the  child  commences  to  walk.  Cases  must  be  kept  undei  supervision 
for  years  for  relapse  is  common.  Recovery  is  shown  by  voluntary  power 
to  correct  the  deformity. 

Fiat-Foot. — The  ordinary  or  static  variety  of  flat-foot  depends  on 
weakness  of  the  tibialis  posticus,  flexor  longus  hallucis  and  peroneus 
longus,  and  secondary  stretching  of  the  ligaments  which  maintain  the  arch 
of  the  foot.  It  is  common  in  rickets,  debility,  and  as  a  sequel  of  infantile 
palsy.  Treatment  is  directed  to  strengthening  the  muscles  by  exercises, 
viz.,  (1)  Raising  the  body  up  and  down  on  tip-toe  with  the  toes  in-turned; 
(2)  Raising  the  inner  border  of  the  foot  from  the  ground  till  the  foot  rests- 
on  the  outer  edge,  while  standing  ;    (3)  Circumduction  of  the  foot  from 


The  Muscles,  Bones  and  Joints.  807 

without  inward  while  sitting  with  the  knees  crossed.  These  movements  should 
be  repeated  quickly  for  a  few  minutes,  and  the  time  gradually  lengthened, 
and  followed  by  a  period  of  rest.  In  bad  cases  a  metal  arch  may  be  used 
as  an  in-sole  for  the  support  of  the  arch  of  the  foot  while  walking.  The 
muscles  must  be  strengthened  by  massage.  Moderate  walking  exercise  is 
advisable.  Long  standing  must  be  forbidden.  Preventive  treatment  con- 
sists in  keeping  fat  and  rachitic  infants  off  their  feet,  until  they  are  stronger. 
Attend  to  the  general  health. 

Enchondromata  and  Exostoses  are  not  infrequent  in  growing  children. 
They  may  be  hereditary  or  familial.  Thus  4  children  out  of  7  were  affected 
at  the  ages  of  4,  1^  and  2  years,  and  at  9  months.  These  growths  are 
often  multiple,  markedly  symmetrical,  and  usually  arise  in  the  neighbour- 
hood of  the  epiphyses.  They  are  hard,  painless,  immobile,  and  variable  in 
size  and  shape.  Large  ones  may  be  more  or  less  columnar,  pedunculated, 
or  expanded  and  tuberculated  at  the  fiee  end.  Others  are  small,  flat  and 
sessile.  They  give  rise  to  no  symptoms,  except  such  as  are  due  to  their 
position.  They  generally  remain  stationary  and  may  disappear  after 
puberty.  Sometimes  removal  is  necessary.  Enchondroma  cutis  is  very  rare. 
Plates  of  cartilage  develop  in  the  true  skin  and  may  show  signs  of  ossifica- 
tion. It  has  been  reported  in  a  girl  15  months  old  (S.  Taylor  and  Mackenna, 
1907). 

Acute  Septic  Diaphysitis. — Syn.  :  Acute  Epiphysitis,  Osteomyelitis, 
Osteitis,  Necrosis  or  Periostitis — Subperiosteal  Abscess — Acute  Bone 
Disease. — This  is  due  to  a  trifling  or  severe  injury  and  secondary  infection. 
The  injury  may  be  a  mere  strain,  the  effect  of  over-exertion,  or  a  blow  or 
fall.  It  starts  in  or  near  the  epiphysis,  in  the  medulla  or  under  the  perios- 
teum. Ill-health  and  local  sources  of  infection  are  predisposing  causes. 
It  is  a  very  serious  disease,  ending  in  necrosis  of  bone  and  pysemia.  It  is 
most  frequent  before  the  epiphyses  have  united  with  the  diaphyses.  It 
may  occur  in  the  first  weeks  of  life,  is  most  common  in  the  tenth  and 
eleventh  years,  infrequent  except  at  4-12  years,  and  raie  after  the  eighteenth 
year.  The  sex-incidence  is  5  males  to  3  females.  The  bones  most  exposed 
to  injury  are  chiefly  affected,  especially  those  near  the  knee.  Out  of  165 
cases  the  disease  began  in  the  femur  83,  tibia  47,  and  humerus  20  (Edmund 
Owen). 

Symptoms. — After  a  slight  injury,  which  has  apparently  got  well  in  a 
few  days,  a  local  tender  swelling  forms  and  the  child  develops  constitutional 
symptoms,  usually  a  rigor,  and  looks  very  ill.  A  local  and  painful  swelling 
is  found  near  a  joint.  The  pain  is  best  elicited  on  deep  pressure.  It  involves 
the  shaft  of  the  bone,  sometimes  about  the  middle  but  more  often  near  its 
junction  with  an  epiphysis.  Tenderness  is  extreme.  The  whole  limb  is 
often  swollen  and  presents  a  white  marbled  appearance  and  dilated  veins. 
In  early  stages  there  may  be  a  slight  red  blush.  The  skin  may  be  unaltered, 
unless  there  is  suppuration  and  an  abscess  near  the  surface.  All  the  parts 
surrounding  the  bone  are  thickened  and  give  the  impression  that  the  bone 


808  Chapter  LIX. 

itself  is  enlarged.  Sometimes  the  local  signs  are  very  slight  and  limited  to 
pain,  increased  heat  and  impaired  mobility.  There  may  be  no  swelling,  if 
the  pus  is  small  in  amount  and  deeply  seated.  Yet  the  constitutional 
symptoms  may  be  marked,  and  diminish  as  the  local  signs  increase. 

The  symptoms  are  due  to  septic  intoxication  and  infection.  At  the 
onset  the  child  is  fretful  and  cries  on  movement ;  the  pulse  and  tempera- 
ture are  raised  ;  and  there  is  headache,  anorexia,  restlessness  and  an 
earthy  complexion.  In  severe  cases  there  are  shivering,  vomiting,  con- 
vulsions and  delirium.  The  child  is  flushed  or  pallid,  and  may  sweat  freely. 
Diarrhoea  is  common.  Gradually  the  usual  signs  of  pyaemia  develop  and 
death  results  from  exhaustion  or  coma  in  a  few  days.  In  the  most  virulent 
type  the  symptoms  are  severe  from  the  onset,  pulse  frequent  and  small, 
temperature  103-105°  F.,  delirium  early,  and  death  may  take  place  from 
toxaemia  before  there  is  much  local  swelling.  Less  severe  ones  end  fatally 
from  septic  pneumonia,  pleurisy,  pericarditis  or  asthenia. 

The  whole  segment  of  a  limb  may  become  tense,  red  and  shiny.  Remis- 
sion indicates  that  the  pus  has  made  its  way  into  the  cavity  of  the  shaft  and 
tension  is  relieved.  If  it  spreads  under  the  periosteum,  the  tension  is  still 
high  and  pain  and  tenderness  severe.  It  sometimes  spreads  to  a  joint  by 
penetration  through  an  unossified  epiphysis  ;  by  tracking  along  the  surface 
of  the  cartilage  ;  or  by  intra-articular  separation  of  the  head  of  the  bone,  in 
the  case  of  the  hip.  Hence  septic  arthritis  is  common  in  the  hip  and  rare 
in  the  knee. 

Pathology. — As  a  result  of  injury  a  clot  forms  and  becomes  infected  by 
circulating  germs.  The  most  virulent  and  most  acute  cases  are  due  to  the 
staphylococcus  aureus  and  the  mildest  ones  to  the  staphylococcus  albus. 
Streptococcal  and  pneumococcal  infections  vary  in  severity.  On  the 
diaphysis  side  of  the  epiphysis  there  is  a  layer  of  actively  growing  vascular 
tissue,  which  is  continuous  with  a  similar  subperiosteal  layer.  Here  a  small 
abscess  forms  and  gives  rise  to  general  infection.  The  effects  vary  according 
to  whether  it  is  superficial  or  deep.  The  periostitis  and  osteomyelitis  are 
secondary.  The  periosteum  is  stripped  up  to  a  variable  extent  and  the 
whole  shaft  may  necrose.  Sometimes  the  necrosis  is  localised  at  the 
epiphysis  (acute  epiphysitis)  or  is  central.  Occasionally  it  appears  to  start 
beneath  the  periosteum  and  ends  fatally  from  pyaemia  before  pus  has  formed. 
Two  such  cases,  affecting  the  humerus  and  femur,  proved  fatal  in  3  days, 
yet  nothing  was  found  except  partial  detachment  of  the  periosteum  by 
dirty  grumous  fluid  and  pyaemic  infarcts  in  the  lungs.  The  chief  com- 
plications are  arthritis  of  the  neighbouring  joint,  secondary  infection  of 
distant  epiphyses,  and  lung  complications  ;  occasionally  endocarditis  and 
pericarditis,  pleurisy,  empyema,  and  abscesses  in  the  cellular  tissue. 

Diagnosis. — In  the  first  year  of  life  the  symptoms  are  often  ascribed 
to  gastric  or  dentition  troubles.  Later  it  is  liable  to  be  mistaken  for  rheum- 
atism, because  of  the  pain  and  swelling  about  the  joint  and  perhaps  septic 
pericarditis.     Delirium  with  acute  arthritis  in  one  joint  is  not  rheumatic. 


The  Muscles,   Bones  and  Joints.  809 

The  local  symptoms  may  suggest  erysipelas,  but  in  this  theie  is  no  deep- 
seated  tenderness  and  the  maigin  of  the  inflammation  is  clearly  defined. 
The  swelling  of  scurvy  may  simulate  periostitis.  Prolonged  fever  and 
■diarrhoea,  due  to  pyaemia,  have  been  mistaken  for  typhoid  fever.  The  main 
features  are  the  unilateral  distribution,  the  pain  over  the  epiphysis,  the 
thickening  of  adjacent  parts,  and  the  fact  that  the  swelling  is  either  not  in 
•or  not  limited  to  the  synovial  membrane. 

The  prognosis  is  bad.  Death  may  result  from  septic  intoxication,  the 
•cause  of  which  is  not  even  suspected.  The  symptoms  of  this  subside  rapidly, 
if  the  abscess  is  evacuated,  but  death  may  ensue  from  pyaemia. 

Treatment. — Make  an  immediate  incision  down  to  the  bone  at  the 
•epiphysis.  If  no  pus  is  found,  explore  the  bone  over  the  site  of  the  epiphy- 
sial cartilage.  If  pus  is  found,  wash  it  out,  drain  and  disinfect.  In  the 
absence  of  pus  insert  a  drainage  tube,  dress  the  wound  and  apply  a  splint. 
Pus  may  appear  in  the  wound  in  a  short  time.  A  timely  incision  may 
prevent  pus  formation  and  necrosis  by  relieving  bone  tension,  therefore 
always  drill  the  bone.  The  general  treatment  consists  of  liberal  diet, 
quinine,  strychnia  and  stimulants,  and  the  use  of  suitable  serum  or  vaccine. 
Subsequently  necrosed  bone  must  be  removed  and  amputation  may  be 
necessary. 

Osteomyelitis  of  the  Spine. — Tubby  (1905)  divides  this  into  three 
varieties  :  (1)  A  mild  periostitic  type  affecting  several  vertebrae  and 
generally  ending  in  complete  recovery.  (2)  A  more  severe  type  in  which 
the  periosteum  and  superficial  layers  of  the  bone  are  affected,  causing 
softening  and  much  deformity,  and  perhaps  suppuration.  (3)  A  virulent 
form  in  which  numerous  purulent  foci  are  found  in  the  bodies  of  one  or 
more  vertebrae,  or  necrosis  of  the  neural  arches  and  processes.  This  usually 
goes  on  to  suppuration  and  spinal  meningitis. 

Etiology.— It  is  rare,  most  common  in  children  and  adolescents,  and 
twice  as  frequent  in  males  as  females.  It  affects  the  lumbar,  dorsal  and 
•cervical  regions  in  order  of  frequency.  It  starts  in  the  body  of  a  vertebra 
as  a  sequel  of  various  local  infections,  specific  fevers  or  local  injury.  The 
staphylococcus  aureus  is  the  most  common  organism. 

The  symptoms  are  malaise  and  slight  fever,  with  local  pain,  tenderness, 
stiffness  and  loss  of  mobility.  The  severe  forms  are  of  sudden  onset  with 
shivering  or  rigors,  early  delirium,  and  all  the  signs  of  severe  septic  intoxi- 
cation. Locally  there  is  intense  tenderness,  agonising  pain  on  movement, 
and  dilatation  of  superficial  veins.  The  patient  lies  in  a  supine  position. 
If  the  neural  arches  are  involved,  there  is  local  swelling,  cedema,  and 
subsequently  signs  of  an  abscess.  If  the  mischief  is  in  the  body  of 
the  vertebra,  there  is  no  localising  sign  save  pain.  Secondary  nervous 
■complications  are  pain  in  the  limbs,  hyperaesthesia,  paresis,  and 
■exaggerated  reflexes ;  paralysis  of  motion,  micturition  and  defaecation  ; 
and  convulsions. 


810  Chapter  L1X. 

Disease  in  the  cervical  region  causes  stiff  and  painful  neck,  inflam- 
matory oedema  of  the  nape,  severe  headache,  vertigo  and  fits.  In  the  dorsal 
region  the  signs  are  very  obscure,  if  it  is  limited  to  the  bodies,  but  if  it 
affects  the  arches  there  is  evidence  in  the  back.  In  the  lumbar  region  it 
causes  flatulent  distension  of  the  abdomen. 

The  diagnosis  depends  on  the  sudden  onset,  rigidity  of  the  spine,, 
early  signs  of  septic  intoxication,  and  nerve  symptoms.  Agonising  pain  in 
the  back  is  a  most  important  sign.  X-ray  examination  is  useful.  It  must  be 
distinguished  from  rheumatic  and  other  forms  of  torticollis,  and  from 
Pott's  disease. 

The  prognosis  is  favourable  in  the  mild  periosteal  type.  In  the  more- 
severe  ones  40  per  cent,  suppurate  and  two-thirds  are  fatal.  The  neural  arch 
cases  are  the  most  easily  recognised  and  are  of  better  prognosis  for  they 
come  under  treatment  earlier,  but  they  are  liable  to  cause  spinal  meningitis. 
The  outlook  depends  on  early  recognition  and  evacuation  of  pus,  prolonged 
recumbency,  and  subsequent  support  for  the  spine.  In  the  vertebral  type 
the  pus  makes  its  way  forward  or  laterally  as  a  retropharyngeal,  cervical, 
psoas,  iliac  or  pelvic  abscess.  Mild  cases  may  be  followed  by  deformity,, 
whereas  severe  ones  die  before  deformity  develops. 

Coxa  Valga  is  a  condition  liable  to  be  mistaken  for  hip  disease.  The 
normal  angle  of  the  neck  with  the  shaft  is  110-135°  ;  in  coxa  valga  it  is 
above  140°.  It  may  be  so  much  increased  that  when  everted  the  neck 
and  shaft  are  almost  in  a  straight  line.  The  physical  signs  are  abduction 
and  external  rotation  of  the  leg,  limitation  of  adduction  and  internal 
rotation,  and  perhaps  slightly  limited  flexion.  The  symptoms  are  pain,. 
fatigue,  spasm  of  the  abductois,  and  limping  gait  with  the  trunk  inclined 
to  the  affected  side.  The  leg  is  lengthened.  In  standing  on  the  affected 
limb  the  body  is  inclined  to  the  same  side,  instead  of  to  the  opposite  side  as 
in  congenital  dislocation.  Other  signs  are  lumbar  scoliosis,  and  flattening 
over  the  great  trochanter  which  is  below  Nelaton's  line.  X-ray  photo- 
graphs should  be  taken  with  the  feet  straight,  fully  inverted  and  fully  everted- 
Signs  vary  somewhat  with  the  cause.  In  cases  due  to  infantile  palsy,  from 
traction  of  the  pendent  limb,  adduction  may  be  free.  The  trochanter  is- 
raised,  if  it  is  associated  with  congenital  dislocation.  The  treatment  is 
purely  surgical. 

Coxa  Vara  and  acetabular  separation  of  the  epiphysis  have  been  described 
as  separate  affections,  but  there  is  strong  evidence  that  one  is  a  consequence- 
of  the  other.  Congenital  cases  have  been  reported  and  are  probably  the 
result  of  intra-uterine  fracture  or  epiphysitis.  Both  affections  occur 
chiefly  among  the  poor,  in  males  14-18  years  old,  sometimes  at  an  earlier 
age  and  in  females.  The  common  age  of  separation  of  the  acetabular 
epiphysis  is  1-2  years  earlier  than  that  of  coxa  vara.  The  physical  signs 
are  almost  identical,  varying  somewhat  with  the  duration  of  the  injury. 
Possibly  coxa  vara  is  sometimes  primary,  due  to  bony  softening.  The  angle- 
of  the  neck  with  the  shaft  is  under  110°,  and  usually  a  right  or  even  an 


The  Muscles,   Bones  and  Joints.  811 

acute    angle.     It    is     also     bent    antero-posteriorly,    becoming    convex 
forward. 

Coxa  vara  is  a  unilateral  affection,  occasionally  bilateral  and  giving 
rise  to  "  seissor-leg  "  deformity.  It  may  be  slight  or  so  severe  that  crutches 
are  needed.  The  physical  signs  are  external  rotation  of  the  hip  ;  adduction, 
which  may  be  so  great  that  the  leg  is  crossed  over  the  opposite  side  or 
progression  is  impeded  through  it  knocking  against  the  sound  leg;, 
limitation  of  abduction  and  internal  rotation  ;  shortening,  1  in.  or  more, 
the  upper  limit  of  the  great  trochanter  being  above  Nekton's  line. 

Similar  signs  are  produced  by  separation  of  the  acetabular  epiphysis,, 
which  occurs  in  children  at  any  age  from  slight  causes  and  gives  rise  to 
little  or  no  pain.  The  leg  is  internally  or  externally  rotated.  In  the- 
clinical  history  of  coxa  vara  we  generally  obtain  a  history  of  pain  in  the  hip 
for  a  few  days,  of  slight  limping  and  aching  due  to  the  separation  of  the 
epiphysis,  and  of  trauma.  An  X-ray  photograph  frequently  shows  irregu- 
larity in  the  line  of  the  neck.  The  affection  has  nothing  to  do  with  late- 
rickets.  In  view  of  the  connection  between  these  two  diseases,  it  is  impor- 
tant to  examine  the  hip  by  X-rays  after  slight  injury,  and  adopt  surgical 
measures  for  treatment  if  the  epiphysis  is  separated.  Untreated  cases  end 
in  coxa  vara.  The  bone  is  wrenched  under  anaesthesia  and  the  limb  put 
up  in  an  immobile  position  of  abduction  for  2-3  months.  Crutches  and  a 
patten  must  be  used  for  a  year.  In  mild  cases  the  outlook  is  good.  In  more- 
severe  ones  it  may  be  necessary  to  screw  the  epiphysis  to  the  neck  of  the 
bone,  and  the  prognosis  is  less  favourable.  . 

Congenital  Dislocation  of  the  Hip. — The  sex-incidence  is  6  females 
to  1  male,  possibly  because  the  capsule  of  the  joint  is  more  lax  in  the 
female  foetus.  From  one-third  to  one-half  of  the  cases  are  bilateral.  It  is- 
rather  more  frequent  on  the  left  side.  The  cause  is  unknown.  Possibly  it 
depends  on  nialdevelopment.  It  is  unduly  frequent  in  some  families. 
Traumatism  in  utero  or  at  birth  is  an  unlikely  though  possible  explanation 
of  some  cases.  Multiple  dislocations  have  been  recorded  in  the  newborn. 
It  is  often  associated  with  imperfect  development  of  the  pelvis  and  other 
bones  of  the  limb. 

The  character  of  the  joint  varies  with  the  age  of  the  child.  Alterations- 
become  progressively  more  marked.  The  upper  lip  of  the  acetabulum  is 
always  defective.  At  first  the  acetabulum  is  circular  and  shallow  ;  later- 
it  becomes  triangular.  The  capsule  is  thin  and  slightly  distended  ;  later 
it  becomes  thicker  and  somewhat  hour-glass  in  form.  The  ligamentum 
teres  is  thin  or  absent  in  older  children.  A  new  socket  eventually  forms  on 
the  dorsum  ilii,  adjacent  to  the  true  joint.  The  head  of  the  femur  is  too 
large  for  the  acetabulum  and  becomes  flattened.  The  angle  of  the  neck 
of  the  shaft  is  decreased. 

The  deformity  may  be  noticed  in  the  first  month  of  life.  Usually  nothing 
is  noted  until  walking  begins,  when  a  limp  is  observed  which  progressively 
increases.     The  gait  is  waddling,  and  the  body  inclines  abruptly  to  the 


•812  Chapter  LIX. 

■side  of  the  leg  placed  on  the  ground.  The  child  generally  places  the  heel 
•on  the  ground  and  sways  the  body  over  the  hip.  Sometimes  she  walks  on 
the  toes.    She  gets  easily  tired  and  has  pain  in  the  joint  when  older. 

Lordosis  is  marked  in  bilateral  cases  and  less  in  unilateral  ones.  The 
waist  is  short,  the  buttock  flattened,  the  leg  shortened  and  the  thigh 
thinner  than  normal.  The  pelvis  seems  enlarged,  for  the  trochanter  is 
very  prominent  and  displaced  backward  and  above  Nekton's  line.  The 
head  of  the  bone  is  commonly  displaced  upward  and  backward,  below 
and  to  the  outer  side  of  the  anterior  superior  iliac  spine,  in  front  of  the 
great  trochanter,  and  is  easily  felt  on  rotation  of  the  limb  outward.  Earely 
it  is  subspinous  or  pubic  in  position.  The  displacement  of  the  head  causes 
an  abnormal  hollow  in  Scarpa's  triangle,  a  concavity  on  the  inner  side  of  the 
thigh  below  the  pubes,  and  asymmetry  of  the  groove  between  the  labium  and 
thigh.  There  is  slight  fulness  and  resistance  below  and  to  the  outer  side 
•of  the  anterior  superior  spine.  In  bilateral  cases  there  is  a  distinct  gap 
between  the  thighs.  The  two  sides  are  rarely  symmetrical.  The  deformity 
is  more  severe,  the  difficulty  in  walking  greater,  and  the  changes  in  the 
bones  and  soft  parts  more  extensive.  Passive  movements  are  free,  smooth 
and  painless.  Sometimes  they  are  too  free,  on  account  of  laxity  of  the 
ligaments,  but  more  often  they  are  limited  in  abduction  and  inversion. 
Telescopic  movement,  i.e.  in  an  upward  and  downward  direction,  may  be 
obtained. 

The  diagnosis  depends  on  localisation  of  the  head  of  the  femur  by 
X-rays  or  manipulation.  It  must  be  distinguished  from  traumatic  dislo- 
cation, coxa  vara,  and  hip  disease. 

Operation  is  essential,  for  the  affection  is  a  serious  handicap  because 
•of  the  deformity,  ungainly  gait,  attacks  of  pain,  and  arthritic  changes  in  the 
new  joint.  Some  children  can  only  walk  with  crutches.  Lorenz's  bloodless 
method  of  reduction  is  suitable  for  most  children  under  12  years  of  age, 
•especially  so  under  6  years.  Some  surgeons  prefer  the  open  operation  or  a 
•combination  of  the  two  methods.  There  is  danger  of  excessive  damage  in 
the  bloodless  method,  and  of  sepsis  also  in  the  open  method.  The  dislo- 
cation must  be  reduced  and  the  limb  put  up  in  a  position  of  complete 
abduction  for  6-12  months,  to  allow  the  surrounding  tissues  to  consolidate 
and  prevent  re-dislocation.  Take  X-ray  photographs  to  ascertain  if  true 
anatomical  reduction  has  been  secured.  Operation  must  be  followed  by 
massage  and  exercises  for  1-2  years. 

The  Painful  Pronation  of  Childhood. — Syn.  :  Paralysie  doulourcuse. — 
This  was  described  by  Kennedy  in  1850  and  by  Chassaignac  in  1856.  It 
occurs  in  children  from  1-4  years  of  age,  occasionally  older.  It  is  most 
frequent  in  females  and  on  the  left  side,  for  children  are  generally  led  by 
their  left  hand.  The  common  cause  is  a  sudden  pull  on  the  hand  or  forearm. 
The  symptoms  are  acute  pain  especially  on  movement,  complete  loss  of 
voluntary  movement,  pain  and  resistance  on  passive  movement  chiefly 
•on  supination  and  pronation,  and  the  arm  hangs  by  the  side  in  a  prone 


The  Muscles,   Bones  and   Joints.  813 

position  as  if  paralysed.  The  elbow  is  slightly  flexed.  It  has  been  ascribed 
to  stretching  of  the  brachial  plexus,  partial  luxation  of  the  joint  or  epiphysis^ 
and  to  psychic  or  inhibition  palsy.  Movement  returns  in  1-2  days  and 
the  child  is  well  in  4-5  days. 

Pulled  elbow  or  Goyraud's  accident  occurs  about  the  same  age, 
generally  in  females  and  on  the  left  side.  It  is  due  to  strain  on  the  forearm, 
and  the  arm  at  once  hangs  flaccid  by  the  side  with  the  forearm  slightly 
flexed  and  pronated.  Extension  is  impaired  and  supination  lost.  On 
examination  there  is  often  nothing  found,  but  sometimes  there  is  tenderness 
on  pressure  over  the  head  of  the  radius  and  separation  between  the  head 
of  the  bone  and  the  humerus.  The  most  probable  explanation  is  that  it  is 
due  to  partial  dislocation  of  the  head  of  the  radius.  It  has  also  been 
ascribed  to  subluxation  of  the  interarticular  cartilage  of  the  inferior  radio- 
ulnar articulation  (Goyraud),  upward  displacement  of  the  orbital  ligament 
(J.Hutchinson,  junior),  compression  of  the  interosseous  membrane  between 
the  two  bones  of  the  forearm  during  sudden  pronation,  or  jamming  of  the 
joint  capsule  at  the  humero-radial  articulation. 

It  is  usually  regarded  as  a  simple  sprain  of  the  elbow,  wrist  or  shoulder,, 
and  is  consequently  wrongly  treated.  According  to  the  description  it  is 
evidently  identical  with  "  the  painful  pronation  of  childhood."  The 
results  of  treatment  show  that  it  is  due  to  slight  subluxation  forward  of  the 
head  of  the  radius. 

Treatment. — Fix  the  arm,  extend  the  elbow  and  sharply  supinate  the. 
forearm.  Then  flex  the  elbow  rapidly,  while  pressing  with  the  thumb  on  the 
head  of  the  radius.  A  "  click  "  is  heard  and  the  symptoms  disappear  almost 
at  once.  There  is  stiffness,  if  the  lesion  has  existed  for  some  days,  but  the- 
child  can  use  the  arm  normally  within  2  hours.    It  is  liable  to  recur. 

Diseases  of  Joints. — Primary  synovitis  is  the  result  of  injury  or  haemo- 
philia. Secondary  arthritis  is  due  to  infective  disorders,  from  the  action  of 
micro-organisms  or  their  toxins,  or  to  chemical  poisons  as  in  gout.  The 
chief  bacterial  joint  affections  are  pneumococcal,  gonococcal,  septic,  tuber- 
culous, and  syphilitic  arthritis.  Less  common  ones  are  due  to  influenza 
and  cerebrospinal  fever.  Eheumatoid  arthritis,  or  ostco-arthritis,  and 
pulmonary  osteo-arthropathy  are  probably  toxic.  In  scarlatina  and  other 
infective  fevers,  purpuric  conditions,  malaria  and  Maltese  fever,  it  is 
doubtful  whether  the  arthritis  is  bacteria]  or  toxic.  Nervous  arthropathies,, 
e.g.  Charcot's  joint,  are  rare  in  children. 

Pneumococcal  Arthritis. — Weichselbaum  (1888)  showed  that  the 
pneumococcus  caused  arthritis.  Nattan-Larrier  (1905)  reported  the  first 
case  in  a  newborn.  It  is  the  common  variety  of  arthritis  in  infants.  Injury 
to  a  joint  is  an  important  predisposing  factor.  It  is  a  rare  complication  in 
pneumonia  but  may  occur  at  any  stage.  Usually  it  is  secondary  to  pneumo- 
coccic  otitis  media,  to  pneumococcal  infection  of  the  lungs  or  pleura, 
or  part  of  a  general  pneumococcal  pyamiia.     Some  cases  are  apparently 


'814  Chapter  L I X. 

primary.     Possibly  in  these  the  infection  is  transmitted  from  the  con- 
junctiva, mouth  or  naso-phaiynx  by  the  blood  stream. 

Up  to  the  end  of  the  first  5  years  of  life  purulent  arthritis- is  commonly 
pneumococcal.  It  is  most  frequent  in  the  first  and  less  so  in  the  second 
year  of  life.  Out  of  100  collected  cases  31  were  under  14  years  of  age  and 
of  these  18  were  in  their  first  and  7  were  in  their  second  year  (Nitch,  1907). 
Out  of  91  cases  28  were  under  2  years  and  8  between  2  and  14  years  old 
>{Herzog,  1906).  It  is  usually  monarticular  and  affects  the  knee,  shoulder, 
lip,  elbow  and  ankle  in  order  of  frequency.  In  severity  it  varies  from  a 
mild  synovitis,  with  thickening  and  effusion  of  serum,  to  an  intense  purulent 
-arthritis  with  erosion  of  cartilage  and  exposure  of  the  ends  of  the  bones. 
About  one-sixth  of  the  cases  are  serous.  The  contents  of  the  joint  vary 
Irom  turbid  serum  to  thick,  creamy,  yellowish  or  greenish  yellow  pus,  and 
may  vary  in  different  joints,  if  several  are  attacked.  The  constitutional 
symptoms  are  slight  unless  there  is  severe  general  infection.  Fever  is 
irregular  and  anaemia  marked.  The  whole  limb  may  be  swollen  and 
cedematous.  The  diagnosis  is  based  on  the  age  of  the  patient,  and  the 
bacteriological  examination  of  fluid  obtained  by  aspiration.  About  two- 
thirds  of  the  cases  die.  The  meninges,  pleura,  pericardium  and  peritoneum 
may  be  affected.  It  is  treated  by  incision  and  drainage,  if  the  effusion  is 
purulent.  Kuster  cured  some  cases  by  aspiration  and  injection  of  iodoform 
and  glycerine. 

Gonococcal  Arthritis  is  rare  in  children.  It  may  follow  urethritis, 
vulvo-vaginitis  or  ophthalmia.  Clement  Lucas  (1899)  collected  23  cases  in 
infants,  secondary  to  purulent  ophthalmia.  The  organism  has  been  cul- 
tivated from  the  fluid'  in  the  joints  but  is  only  found  with  certainty  in 
early  stages.  The  arthritis  may  begin  at  any  stage  of  the  gonococcal  infec- 
tion, commonly  in  2-4  weeks,  or  after  apparent  cure-  Lucas  states  that  it 
may  occur  as  early  as  the  fourth  day  or  as  late  as  the  thirteenth  week  of 
infantile  ophthalmia. 

It  is  somewhat  acute  in  onset,  with  effusion  and  no  synovial  thickening. 
Acute  cases  show  much  swelling,  redness  and  tenderness.  In  less  severe  ones 
there  is  much  effusion,  with  little  or  no  redness,  and  less  pain  than  in  true 
rheumatism.  Fever  is  slight  and  does  not  yield  to  salicylates.  Cardiac 
complications  are  rare.  When  occurring  in  epidemic  form  in  institutions  it 
may  cause  multiple  arthritis  and  pyaemia  without  evidence  of  a  local 
infection.  Pyaemic  cases  may  show  stomatitis,  purulent  infiltration  of  the 
muscles  about  the  joint,  broncho-pneumonia,  empyema  and  high  fever.  The 
knees,  wrists  and  ankles  are  very  susceptible  joints.  The  usual  duration  in 
infants  is  3-5  weeks.  It  terminates  in  resolution  and  unimpaired 
mobility.  Suppuration  is  very  rare.  In  older  children  there  is  marked 
"tendency  to  ankylosis.  The  treatment  consists  in  curing  the  source 
of  infection,  protection  from  injury,  and  the  use  of  evaporating 
lotions.  In  gonococcal  pyaemia  aspiration  and  incision  may  be 
necessary. 


The  Muscles,  Bones  and  Joints.  815 

Septic  Arthritis  is  due  to  direct  injury  or  to  secondary  infection  fiom 
•epiphysitis,  a  suppurating  wound,  etc.  Multiple  arthritis  in  infants  is 
usually  pycemic.  The  joint  becomes  acutely  inflamed,  swollen,  hot,  red  and 
painful.  The  severity  and  fever  vary.  Different  organisms  have  been  found. 
The  staphylococcus  albus  appears  to  give  rise  to  the  mildest  type  of  inflam- 
mation. The  arthritis  of  cerebrospinal  fever  is  somewhat  similar,  but 
usually  a  mild  type  not  requiring  aspiration  or  incision.  A  few  cases  of 
■septic  arthritis  can  be  cured  by  aspiration.  As  a  rule  incision,  washing 
out  and  drainage  are  required. 

Tuberculous  Arthritis. — Poverty,  cold,  slight  injuries  and  specific  fevers 
are  the  chief  predisposing  causes.  The  knee,  elbow  and  hip  are  the  most 
often  affected.  The  disease  may  start  in  the  epiphysial  end  of  the  bone,  or 
in  the  synovial  membrane  which  becomes  greatly  thickened  from  chronic 
inflammation.  Secondary  fatty  degeneration  and  necrosis  lead  to  the 
formation  of  caseating  abscesses.  The  cartilage  is  eroded  by  extension  of 
the  disease,  and  the  bone  is  laid  bare  and  becomes  carious.  Spongy  bone  is 
especially  susceptible  to  tuberculosis. 

It  is  often  overlooked  on  account  of  the  frequent  absence  of  pain  in 
the  early  stages.  The  onset  is  very  insidious,  with  slight  inflammation, 
effusion,  pain,  and  lameness  or  inability  to  walk  if  the  lower  limb  is  attacked. 
The  synovial  membrane  is  thickened  and  produces  the  chronic  "  white 
swelling."  Bone  is  rarefied  but  not  enlarged.  Occasionally  the  joint  is 
distended  with  fluid  and  contains  melon-seed  bodies.  Starting  pains  at 
night  arise  from  inflamed  bony  surfaces  rubbing  together. 

The  course  is  very  chronic.  Adjoining  muscles  waste.  Abscesses  may 
form  and  burst,  leave  discharging  sinuses  which  heal  with  great  difficulty. 
It  may  end  in  complete  destruction  of  the  joint,  necessitate  amputation,  or 
terminate  in  lardaceous  disease.  In  early  stages  it  is  distinguished  from 
rheumatism  by  its  monarticular  character,  gradual  onset  and  development, 
and  the  absence  of  cardiac  complications.  It  is  treated  by  rest,  the  usual 
measures  adopted  for  tuberculosis,  and  fixation  of  the  joint.  The  use  of 
splints  may  be  followed  by  stiff  joint,  but  the  stiffness  is  due  to  the 
inflammation  and  not  to  the  splint. 

Tuberculosis  of  the  Hip  Joint. — This  is  insidious  and  liable  to  be  mis- 
interpreted at  the  onset.  It  generally  begins  in  the  bone  and  may  be  rather 
advanced  before  it  causes  symptoms.  The  early  signs  are  pain  in  the  joint, 
limping,  slight  fulness  in  Scarpa's  triangle,  pain  if  the  joint  is  fully  extended 
or  fully  flexed,  and  possibly  a  visible  focus  in  an  X-ray  photograph.  In  the 
next  stage  the  hip  is  flexed  and  slightly  abducted,  due  to  contraction  of  the 
ilio-psoas  muscle  from  muscular  spasm,  keeping  the  limb  rigid  in  the 
position  of  least  pain.  To  compensate  this,  there  is  lordosis  and  tilting 
down  of  the  pelvis  in  walking.  The  tilting  causes  apparent  lengthening  of 
the  limb.  Comparative  measurements  should  be  made  from  the  anterior 
iliac  spine  to  the  internal  malleolus,  with  the  limbs  in  the  same  position. 
The  gluteal  and  thigh  muscles  waste.     Starting  pains  at  night  tell  that 


816  Chapter  LIX. 

the  articular  surfaces  are  involved.  In  a  later  stage  there  is  internal 
rotation  and  adduction,  due  to  erosion  of  the  acetabulum  and  weakening 
of  the  peri-articular  ligaments.  The  pelvis  is  now  tilted  up  on  the  affected 
side  and  there  is  apparent  shortening.  If  an  abscess  forms  it  may  point  on 
either  side  of  the  tensor  fasciae  femoris,  in  Scarpa's  triangle,  in  the  gluteal 
region,  or  above  Poupart's  ligament,  having  made  its  way  through  the 
acetabulum  into  the  pelvis  and  perhaps  only  found  on  rectal  examination. 
Occasionally  it  invades  the  psoas  muscle  and  foims  a  fluctuating  swellings 
above  and  below  Poupart's  ligament. 

The  joint  mischief  is  almost  invariably  secondary  to  some  tuberculous 
focus  elsewhere,  commonly  the  mediastinal  or  mesenteric  glands.  One  or 
more  joints  may  be  affected,  most  frequently  the  other  hip.  In  about  5  per 
cent,  it  is  bilateral.  Pulmonary  tuberculosis  occurs  in  less  than  1  per  cent. 
Tuberculous  adenitis  is  sometimes  present. 

The  prognosis  is  good,  if  the  disease  is  recognised  early  and  properly 
treated.  The  prospect  of  recovery,  whether  complete  or  incomplete,  depends 
upon  the  extent  of  the  disease  and  efficient  treatment.  No  case  is  incurable. 
Among  the  better  classes  bad  results  are  uncommon.  Bowlby's  statistics 
of  900  cases  at  the  Alexandra  Hip  Hospital  from  1885-1908  showed  a 
mortality  of  under  5  per  cent.  Complete  recovery  is  possible  if  the  disease  is 
limited  to  the  head  of  the  bone,  a  caseous  focus  being  seen  in  the  X-ray 
photograph  and  the  symptoms  limited  to  slight  aching  and  a  limp. 
Shortening,  destruction  of  the  head  of  the  bone,  or  displacement  of  the  head  of 
the  femur  on  to  the  dorsum  ilii  renders  a  perfect  cure  impossible.  Many 
cases  end  in  severe  lameness  from  incomplete  ankylosis,  displacement  of  the 
upper  end  of  the  femur  on  to  the  ilium,  or  arrested  growth  of  the  bone. 
Others  end  in  recovery  with  flexion,  adduction,  and  complete  ankylosis. 
This  is  a  good  result,  for  osteotomy  of  the  femur  will  straighten  the  limb. 
Speaking  generally,  the  older  the  child  the  better  is  the  prognosis  as  regards, 
life  and  local  recovery.  Younger  children  are  more  liable  to  succumb  from 
general  infection,  or  to  develop  permanent  lameness,  for  the  head  of  the 
femur  is  small  and  easily  destroyed. 

Treatment. — Perseverence  in  local  treatment  is  essential.  The  general 
treatment  is  that  of  tuberculosis  and  equally  imperative.  In  the  early  stages 
the  child  should  rest  in  the  recumbent  posture  with  the  joint  immobile, 
at  the  seaside  if  possible  for  at  least  4-6  weeks.  A  firm  mattress,  fracture 
board,  small  pillow  under  the  head  only,  shoulder  straps  to  fix  the  shoulders 
to  the  bed,  and  a  double  long  Liston  or  Thomas's  splint  are  required. 
Extension  is  applied  to  the  limb  with  a  pulley  and  weight  of  ^  lb.  per  year  of 
age  up  to  2  lbs.,  and  rarely  to  4  lbs.  At  first  the  extension  is  applied  in  the 
axis  of  the  displaced  limb,  supported  on  an  inclined  plane,  until  the 
muscular  spasm  is  overcome.  In  early  stages  this  takes  a  few  days  to  2  weeks. 
The  limb  must  be  so  flexed  that  lordosis  is  abolished  and  put  up  at  this 
angle,  resting  uniformly  on  a  pillow.  Eventually  it  is  brought  down  into  the 
position  of  normal  extension,  so  that  the  utmost  value  may  be  obtained  for 


The  Muscles,   Bones  and  Joints.  817 

it  as  a  useful  member  if  a  stiff  joint  results.  Extension  keeps  the  joint 
surfaces  apart  and  relieves  pain.  If  the  deformity  is  due  to  adhesion  and 
does  not  yield  to  extension,  the  joint  may  be  moved  very  gently  under 
anaesthesia.  Daily  massage  and  movement  of  the  other  joints  of  the  leg 
prevent  stiffness. 

Excision  is  never  needed.  Amputation  is  only  required  in  cases  of 
prolonged  suppuration  with  hectic  fever  and  destruction  of  the  bone  and 
joint. 

The  child  should  not  be  allowed  to  walk  on  the  bad  leg  until  a  year 
after  being  well  enough  to  use  crutches.  During  this  period  a  high  boot  or 
patten  is  worn  on  the  sound  limb  to  prevent  the  diseased  one  being  brought 
to  the  ground.  A  Thomas's  splint  is  only  suitable  for  those  in  whom  it  is 
impossible  to  obtain  prolonged  treatment  by  recumbency.  It  is  applied 
to  immobilise  the  joint,  as  soon  as  the  extension  has  overcome  the  spasm 
and  the  limb  is  straight.  It  must  be  worn  for  6  months  and  the  patient  can 
get  about  on  crutches.  If  an  abscess  forms  it  must  be  opened,  cleared  out 
gently,  and  efficiently  drained.  The  utmost  precaution  must  be  used  to 
prevent  secondary  infection  with  pyogenic  organisms. 

Syphilitic  Arthritis. — A  very  rare  form  of  symmetrical  arthritis,  not 
affecting  many  joints,  is  occasionally  seen  in  congenital  syphilis.  It  is 
a  rarefying  osteitis  of  cartilage  and  bone,  withcaseating  deposit  in  cancellous 
bone.  It  comes  on  about  puberty  and  is  incurable.  Possibly  this  is  tuber- 
culous. Syphilis  usually  causes  sclerosis  of  compact  bone.  Occasionally  a 
true  osteo-arthritis  is  seen  at  5-12  years  of  age,  with  much  osteophytic 
outgrowth  at  the  epiphyses.  This  is  apparently  a  coincident  rather 
than  a  syphilitic  affection. 

The  common  type  begins  after  the  second  dentition,  at  6-15  years  of 
age.  It  is  insidious  in  development,  perhaps  unilateral,  but  more  frequently 
symmetrical.  It  almost  always  affects  the  knees  and  less  often  other 
large  joints,  especially  the  elbow.  They  are  enlarged,  but  not  tensely  so, 
by  fluid  effusion  and  some  synovial  thickening.  There  is  very  little  inter- 
ference with  function,  much  mobility,  little  or  no  pain,  and  no  heat,  redness, 
starting  pains  or  muscular  wasting.  Sometimes  the  pain  is  severe.  Its 
course  is  chronic  and  relapsing,  but  there  is  little  or  no  destructive  change. 
Subvarieties  of  this  are  (1)  Palpable  gummatous  masses  in  the  synovial 
membrane,  with  inflammation  of  the  periosteum  of  the  ends  of  the  bone. 

(2)  Osteitis  and  simple  effusion,  the  end  of  a  long  bone  being  much  enlarged. 

(3)  Suppurative,  due  to  secondary  infection  and  sometimes  beginning  as 
epiphysitis  in  infancy.  Apart  from  the  last  variety,  syphilitic  joint  disease 
is  associated  with  interstitial  keratitis  in  75  per  cent,  of  the  cases,  and  often 
with  choroiditis  or  retinitis,  and  deafness.    Both  sexes  are  equally  liable. 

The  diagnosis  is  difficult  if  the  joint  affection  begins  before  eye 
symptoms.  It  is  liable  to  be  regarded  as  tuberculous  or  rheumatic.  The 
child  should  be  put  to  bed  and  a  splint  and  Scott's  dressing  applied,  the 

3  G 


818  Chapter  LIX. 

latter  being  renewed  weekly.  Give  mercury  and  pot.  iod.  internally.  Some 
cases  get  well  in  6-8  weeks  ;  others  are  very  intractable.  If  there  is  no 
definite  improvement  in  2  months,  rely  upon  tonic  treatment. 

Syphilitic  Epiphysitis. — This  was  described  by  Wegner  in  1870  and  by 
Parrot  in  1872.  It  is  a  manifestation  of  congenital  syphilis,  and  is  present 
in  most  syphilitic  infants  which  are  stillborn  or  die  shortly  after  birth. 
In  others  it  occurs  a  few  weeks  after  birth,  rarely  after  3  months,  and  only 
exceptionally  after  6  months  of  life.  It  affects  the  epiphyses  of  one  or  all 
of  the  long  bones.  The  symptoms  are  swelling  of  the  limb  in  the  region  of 
the  epiphyses  and  apparent  paralysis,  often  complete  immobility,  of  the 
affected  limb  from  pain.  The  swelling  may  be  limited  to  the  epiphyses  and 
simulate  rickets.  When  limited  to  the  upper  end  of  the  humerus,  it  is  liable 
to  be  mistaken  for  Erb's  paralysis  of  the  upper  arm  type.  It  is  often 
symmetrical,  and  may  even  affect  all  four  limbs  and  the  sternal  ends  of  the 
clavicles.    The  epiphyses  may  be  affected  simultaneously  or  successively. 

Inflammation  commences  in  the  layer  of  cartilage  next  to  the  bone. 
The  cartilage  may  be  separated  from  the  bone  along  the  line  of  junction,  and 
the  rubbing  together  of  the  fragments  gives  rise  to  pain,  irritation  and 
suppuration.  Under  proper  treatment  purulent  arthritis  is  uncommon. 
The  cavity  of  the  joint  is  rarely  penetrated.  Secondary  periostitis  causes 
extension  of  thickening  along  the  shaft  and  sometimes  inflammation  of  the 
peri-articular  tissues.  Slight  bone  crepitation  may  be  present,  if  the  epiphy- 
sis is  separated  and  not  retained  in  apposition  to  the  bone  by  the  periosteum. 

Symptoms. — When  the  arm  is  affected,  the  limb  hangs  down  motionless 
with  the  hand  pronated  and  the  fingers  semiflexed.  Drop-wrist  may  be 
present  without  any  local  evidence  of  disease,  if  the  lower  radial  epiphysis 
is  alone  affected.  Should  the  lower  limb  be  attacked,  it  appears  to  be 
dislocated  when  the  child  is  raised  by  grasping  him  under  the  armpits. 
Voluntary  movements  persist  in  the  hands  and  feet.  The  affected  joint 
and  surrounding  parts  are  swollen,  moderately  hot,  boggy,  painful  and 
tender.  There  may  be  very  little  tenderness,  but  usually  the  child  cries 
when  the  affected  limb  is  touched  or  moved.  Pain  is  often  so  severe  as  to 
interfere  with  rest  and  sleep.  The  elbow,  knee  and  wrist  are  the  joints  most 
frequently  involved.  There  is  no  disturbance  in  sensibility  and  little  or  no 
fever.  .  Untreated  cases  may  eventually  recover  though  one  limb  after 
another  becomes  involved.  Recovery  is  rapid  under  proper  treatment,  and 
in  the  worst  cases  takes  place  in  1-2  months.  Suppuration  due  to  secondary 
infection  is  rare.  The  bone  may  be  permanently  shortened  from  destruction 
of  the  growing  zone  of  cartilage.  Death  is  sometimes  due  to  marasmus 
from  the  underlying  cause. 

The  diagnosis  depends  on  the  character  of  the  swelling,  pain,  apparent 
paralysis,  and  other  evidence  of  syphilis.  Skin  eruptions  may  appear 
subsequently.  Eickets,  scurvy  and  simple  or  rheumatic  arthritis  occur 
at  a  later  age.     Pneumococcal  arthritis  may  give  rise  to  difficulty.     The 


The  Muscles,   Bones  and   Joints.  819 

treatment  consists  in  the  vigorous  use  of  mercury,  breast  -  feeding, 
good  hygienic  surroundings  and  rest  for  the  affected  limbs.  Splints  are 
unnecessary  and  local  applications  are  of  little  value. 

Rheumatoid  Arthritis. — Syn. :  Osteo-arthritis —  Arthritis  deformans — 
Rheumatic  Gout. — Although  this  affection  has  little  or  nothing  to  do  with 
•either  rheumatism  or  arthritis  in  many  cases,  the  name  is  a  convenient  one 
and  established  by  long  usage.  Osteo-arthritis  is  a  misnomer  in  that  the 
bones  are  not  affected  in  the  early  stages.  This  name  should  be  kept  for  a 
later  stage  in  which  the  cartilages,  the  ends  of  the  bones,  and  the  nervous 
system  are  affected.  Possibly  there  are  two  distinct  diseases.  An  arthritic 
tendency  is  present  in  some  families,  and  may  show  itself  in  the  form 
of  rheumatic  fever,  rheumatoid  arthritis  or  gout.  In  the  disease  under 
discussion  rheumatic  nodules  are  sometimes  present,  and  pericardial 
adhesions  in  prolonged  cases.  An  endocardial  murmur  is  not  uncommonly 
■due  to  anaemia  and  dilatation,  but  endocarditis  is  rare.  Acute  attacks  aie 
•often  mistaken  for  rheumatic  fever.  The  term  rheumatoid  arthritis  is  also 
used  for  the  monarticular  form  of  the  disease  occurring  in  the  large  joints 
•of  old  people,  with  formation  of  osteophytes  and  the  destruction  of  cartilage. 
It  is  a  true  osteo-arthritis,  secondary  to  injury.  In  the  disease  that  occurs 
in  younger  people  the  mischief  is  a  peri-arthritis  and  the  joints  are  little, 
if  at  all,  affected.  Occasional  cases  are  seen  which  approximate  to  the  true 
arthritic  type,  affecting  many  small  joints,  with  the  formation  of  osteophytes 
:and  Heberden's  nodes.  Thus  there  are  two  varieties,  a  true  osteo-arthritis 
.and  a  peri-arthritis.  The  description  here  given  applies  to  the  latter  variety. 

It  may  be  defined  as  a  specific  constitutional  disease,  acute  or  chronic 
in  its  onset,  of  prolonged  duration,  liable  to  periods  of  quiescence  and 
•exacerbation,  producing  profound  wasting  in  the  muscles  and  changes 
round  the  joints,  leading  to  crippling  and  deformity,  but  eventually  coming 
to  an  end.  The  effects  are  worse  than  the  disease.  Fundamentally  it  is 
an  inflammation  of  the  synovial  membrane,  the  bone  and  cartilages  being 
usually  healthy. 

It  is  most  common  in  girls  from  15-25  years  of  age,  and  may  occur  in 
■quite  young  children,  even  in  the  third  year  of  life. 

Etiology. — Nothing  reliable  is  known  about  its  causation.  It  occurs 
independently  of  soil  and  climate,  in  all  classes,  and  in  the  well  nourished, 
Due  importance  must  be  attached  to  a  family  history  of  arthritis  and 
tuberculosis,  to  malnutrition  from  any  cause,  and  to  tight-lacing  and  to 
insufficient  clothing.  Some  cases  have  followed  infective  diseases  such  as 
measles  and  influenza ;  in  others  there  is  evidence  of  an  intestinal  source, 
possibly  intestinal  toxaemia,  for  digestive  disturbance  is  common.  In  a  few 
patients  it  may  be  due  to  septic  absorption  from  the  generative  tract 
■or  the  respiratory  passages. 

Symptoms. — It  may  commence  insidiously  with  stiffness  and  enlarge- 
•ment  of  the  joints,  or  acutely  and  simulate  rheumatic  fever.    Aching  pains 


820  Chapter  LIX. 

and  localised  neuralgias  are  occasional  premonitory  symptoms.  The  fever 
is  rarely  high,  100-103°  F.,  and  is  more  or  less  continuous.  It  occurs  in 
attacks  of  a  few  days  to  a  week's  duration,  with  intervals  of  apyrexia. 
The  pulse  is  unduly  accelerated,  out  of  proportion  to  the  fever,  and  may 
remain  abnormally  frequent  after  the  fever  has  subsided.  The  patient 
presents  all  the  signs  of  febrile  malaise  and  becomes  markedly  aneemic. 
Occasionally  there  is  albuminuria,  if  there  is  much  fever.  During  the 
febrile  stage  the  spleen  and  the  lymphatic  glands  are  often  a  little  enlarged. 
The  glands  are  discrete,  sometimes  tender,  movable,  rather  hard,  reaching; 
the  size  of  hazel  nuts,  and  do  not  suppurate.  Splenic  and  glandular  enlarge- 
ment occur  in  older  people,  but  to  a  less  marked  extent.  This  is  what  one- 
would  expect,  for  both  these  structures  enlarge  with  greater  readiness  in. 
early  life  and  are  felt  with  greater  ease. 

The  disease  affects  the  small  joints  of  the  hand  and  to  a  less  extent  the 
feet.  It  especially  attacks  the  metacarpo-phalangeal  joints  of  the  first 
and  second  fingers  and  the  proximal  inter-phalangeal  joints.  These  joints 
present  a  soft,  fusiform,  peri-articular  swelling.  The  joint  capsules  and 
synovial  membranes  are  thickened  ;  the  ligaments  softened  and  infiltrated  ; 
and  the  joints  have  a  spindle-shaped  appearance.  Often  a  certain  amount  of 
effusion  takes  place  into  them.  The  knees,  wrists  and  ankles  are  next- 
affected,  and  often  the  disease  starts  in  the  knees  or  wrists.  The  cervical 
spine  is  affected  early,  and  frequently  the  temporo-maxillary  joints  are 
attacked.  X-ray  examination  shows  that  there  are  no  osteophytes  and  nc* 
bony  enlargement,  but  the  bones  are  abnormally  translucent.  The  amount 
of  pain  is  variable  and  rarely  as  great  as  in  rheumatic  fever.  In  the  pro- 
longed cases  the  cartilages  may  be  pitted.  Adhesions  of  the  pericardium  and 
pleura  may  be  found  after  death.  Associated  with  the  joint  mischief  there 
is  pronounced  muscular  atrophy,  as  well  as  moderate  wasting  from  disuse,, 
making  the  deformity  much  more  evident  and  the  crippling  more  severe. 
The  interossei  and  extensors  are  especially  affected.  The  extremities  are 
cold,  sweating,  and  present  a  livid  mottling.  Freckly  pigmentation  appears- 
on  the  limbs  and  sometimes  brown  pigmentation  on  the  face.  It  may  pass- 
off  as  the  acute  symptoms  subside. 

Course.— The  disease  is  very  intractable  but  rarely  fatal.  Usually  the- 
acute  attack  subsides  in  2-6  weeks  ;  and  the  child  gradually  recovers  from, 
the  anaemia  and  debility,  with  a  certain  amount  of  joint  swelling  and 
crippling.  Recurrent,  acute  or  subacute  attacks  of  variable  severity  occur,, 
each  leaving  the  patient  a  little  more  deformed  and  a  little  more  crippled. 
Finally  it  ceases  and  there  remain  behind  the  effects,  viz.  wasting,  deformity,, 
pigmentation,  pain  and  frequent  pulse.  Occasionally  mild  cases  are  seen 
in  which  almost  complete  recovery  takes  place.  If  it  begins  in  early  life 
it  interferes  greatly  with  proper  development.  The  true  osteophytic  form- 
is  rare,  associated  with  profound  cachexia  and  usually  fatal. 


The  Muscles,  Bones  and  Joints.  821 

Diagnosis. — It  is  most  important  to  distinguish  the  disease  from  iheu- 
matic  fever  and  gonococcal  arthritis,  because  of  the  treatment  and  prog- 
nosis. It  differs  from  rheumatic  fever  in  the  following  points.  The  fever 
does  not  yield  to  salicylates  and  is  of  longer  duration  ;  anaemia  is  of  more 
gradual  development ;  and  the  acid  sweats  of  rheumatism  are  absent,  but 
this  is  not  of  much  assistance  for  they  are  uncommon  in  the  rheumatism  of 
■childhood.  Many  joints  are  affected  symmetrically,  notably  those  of  the 
hands,  whereas  arthritis  in  rheumatic  fever  is  rarely  marked  in  children  and 
•chiefly  affects  the  middle  sized  joints.  Pigmentation,  local  sweating  of  the 
hands  and  feet,  and  muscular  atrophy  are  present.  There  is  no  endocarditis, 
but  the  presence  of  a  hsemic  murmur  renders  it  difficult  to  exclude  its 
■existence,  and  in  one  case  under  my  care  endocarditis  was  undoubtedly 
present.  An  unduly  rapid  pulse,  apart  from  cardiac  disease,  is  uncommon  in 
rheumatic  fever.  The  possibility  of  the  arthritis  being  toxic  or  tuberculous 
in  origin  must  be  remembered. 

Treatment. — During  the  acute  stages  try  the  effect  of  salicylates  or 
.aspirin,  discontinuing  the  drug  if  it  does  not  afford  relief.  Colchicum  and 
pot.  iod.  are  sometimes  useful.  Wrap  the  joints  in  cotton  wool  and  paint 
them  twice  a  day  with  guaiacol  1  part,  tr.  iodi  8  parts.  As  soon  as  the  fever 
has  subsided,  the  patient  can  be  liberally  fed  on  a  nutritious  diet  con- 
taining plentiful  fat  and  protein.  The  intestinal  tract  must  be  kept  in  a 
healthy  state,  in  view  of  the  fact  that  it  may  be  the  source  of  the  toxaemia. 
Subsequently  reliance  must  be  placed  on  warm  clothing,  liberal  diet,  dry 
•climate,  giavel  soil,  sunshine,  open  air,  exercise  and  massage.  Port,  stout, 
ale  and  Burgundy  are  admissible.  Massage  may  be  used  in  the  acute 
stages  for  the  muscles,  but  not  for  the  joints.  It  is  beneficial  to  the  joints  as 
long  as  they  are  not  tender  or  inflamed.  The  more  the  joints  are  used  the 
less  is  the  subsequent  crippling.  Benefit  is  also  derived  from  hot  fomen- 
tations, hot  sand  baths,  mud,  peat  and  brine  baths,  radiant  heat,  douches, 
massage  and  Spa  treatment.  These  measures  produce  temporary  improve- 
ment in  the  joint  condition  but  do  not  affect  the  disease.  For  the  prevention 
•of  recurrent  attacks  rely  on  general  treatment,  the  prolonged  use  of  cod-liver 
•oil,  and  pot.  iod.  or  the  syrup  of  iodide  of  iron  given  alternately  with  arsenic 
for  periods  of  3  or  4  weeks.  Good  results  have  also  followed  the  use  of 
.guaiacol  and  pot.  iod.  for  at  least  12  months.  Counter-irritation  of  the 
spine  by  blisters,  leeches,  cupping  or  the  actual  cautery,  in  the  cervical  and 
lumbar  regions  of  the  spine,  have  also  been  recommended,  on  the  supposition 
that  the  disease  is  due  to  lesions  in  the  spinal  cord. 

Pulmonary  Osteo-arthropathy  is  a  rare  disease  in  children,  except  in 
the  mild  form  of  clubbing  of  the  fingers.  It  is  due  to  suppurative  diseases 
•e.g.  chronic  phthisis,  empyema  and  bronchiectasis  ;  congenital  heart  disease, 
some  liver  affections  and  syphilis.  The  onset  is  insidious.  The  ends  of  the 
fingers  and  toes  are  clubbed  and  the  nails  become  large,  broad,  brittle  and 


822  Chapter  LIX. 

incurved.  The  hands,  wrists,  feet  and  ankles  are  enlarged.  Stiffness  is- 
followed  by  discomfort,  pain  and  swelling.  In  some  the  joint  signs  are 
most  marked  ;  in  others  the  bones  are  chiefly  affected,  becoming  enlarged 
at  the  ends,  painful  and  even  elongated.  Effusions  take  place  into  the 
joints,  the  cartilages  are  enlarged  and  eroded,  the  articular  ends  of  the 
bones  are  enlarged,  and  the  soft  tissues  hypertrophied.  X-rays  show  that 
increase  in  the  size  of  the  bone  is  due  to  symmetrical  deposit  of  subperiosteal 
bone,  usually  on  the  lower  ends  of  the  tibia  and  fibula  and  the  radius  and 
ulna.  It  especially  affects  the  metacarpo-phalangeal  joints  and  metatarsals 
and  the  ends  of  the  bones  of  the  forearms  and  legs.  The  joint  swellings  may 
appear  and  disappear.  The  neighbouring  muscles  waste.  It  is  either  toxic 
or  tuberculous  in  origin.  In  congenital  heart  disease  it  is  partly  mechanical,, 
though  possibly  toxic  substances  are  developed  locally.  Death  is  due 
to  the  primary  or  intercurrent  disease. 


CHAPTER    LX. 

EHEUMATIC    FEVER. 

Rheumatic  fever  is  pre-eminently  a  disease  of  childhood.  It  is  both 
frequent  and  serious.  Arthritis  is  a  symptom  of  minor  importance,  for  it 
is  neither  severe  nor  extensive  and  may  be  entirely  absent.  In  adults  the 
disease  especially  affects  the  joints,  whereas  in  children  it  is  the  heart 
which  alone  is  affected  or  on  which  the  main  stress  of  the  disease  falls.  As 
age  advances  the  arthritis  increases  in  prominence  while  the  liability  to 
cardiac  complications,  chorea,  erythematous  rashes,  and  rheumatic  nodules 
decreases.  Growing  pains,  epistaxis,  tonsillitis,  chorea  and  pleurisy  are 
undoubted  rheumatic  signs  in  children. 

Etiology. — The  disease  is  ubiquitous,  most  common  in  temperate 
zones,  and  rare  at  high  altitudes.  It  is  more  prevalent  in  some  years  than 
in  others,  and  may  assume  an  epidemic  character  for  a  year  or  so  at  a  time. 
It  is  more  urban  than  rural ;  and  in  London  most  prevalent  from  September 
to  November.  It  is  most  common  among  the  poor,  the  ill-fed  and  the 
badly  housed.  There  is  no  reliable  evidence  that  it  is  in  any  way  connected 
with  dampness  in  the  air  or  soil,  or  low  level  of  the  ground  water,  or  that 
it  depends  upon  getting  wet  or  cold. 

A  rheumatic  family  history  can  be  obtained  in  about  two-thirds  of  the 
cases.  In  childhood  both  sexes  are  equally  liable.  The  disease  is  almost 
unknown  in  infancy.  Only  about  20  cases  during  the  first  year  of  life  are  on 
record,  and  several  of  these  arc  open  to  criticism.  Heart  complications 
have  not  been  noted  at  this  early  age.  It  is  rare  before  the  third  year,  infre- 
quent till  the  commencement  of  the  second  dentition,  and  most  common 
from  that  time  onward  to  puberty.  About  10  per  cent,  of  all  cases  occur 
in  the  first  and  30  per  cent,  in  the  next  decade.  It  approximates  to  the 
adult  type  after  the  age  of  ten. 

Bacteriology. — Klebs  (1875)  found  micrococci  in  the  cardiac  valves. 
Popoff  (1887)  cultivated  micrococci  from  the  blood,  and  by  intravenous 
injection  into  rabbits  produced  endocarditis,  pericarditis  and  polyarthritis. 
Dana  (1894)  isolated  a  diplococcus  from  the  meninges  of  the  biain  and  spinal 
cord  in  a  case  of  chorea  following  rheumatic  fever.  Many  other  observers 
have  found  similar  micrococci.  Wassermann  (1899)  obtained  a  diplococcus 
from  chorea  and  produced  what  he  regarded  as  typical  rheumatic  fever 
in  80  rabbits.  Poynton  and  Payne  (1900)  isolated  an  identical  organism 
from  cases  of  rheumatic  fever,  and  by  intravenous  injection  into  rabbits  and 


824  Chapter  LX. 

monkeys  produced  polyarthritis,  endocarditis,  and  other  signs  of  acute 
rheumatism,  recovering  the  organism  from  these  lesions.  They  found  it  in  the 
blood,  urine,  and  secretion  of  the  tonsils  from  the  living  ;  in  the  pericardial 
exudate,  cardiac  valves,  tonsils,  and  nodules  after  death.  According  to 
these  observers  it  grows  most  favourably  in  the  connective  tissues,  and  for 
this  reason  pericarditis  is  severe.  The  most  virulent  cultures  were  obtained 
from  the  pericardial  exudate.  This  organism  is  known  as  the  diplococcus 
or  micrococcus  rheumaticus.  Many  competent  observers  have  failed  to 
find  the  organism  during  life  or  after  death.  Some  regard  it  as  a  secondary 
infection  and  as  a  variety  of  salivary  or  faecal  streptococcus.  Its  morpho- 
logical and  staining  characters  are  indistinguishable  from  those  of  some 
varieties  of  streptococcus  pyogenes,  but  it  does  not  lead  to  pus  formation. 
In  highly  alkaline  media  it  produces  a  considerable  amount  of  acid.  Byffel 
and  Walker  found  formic  and  acetic  acids  in  such  media,  whereas  5  varieties 
of  streptococci  produced  very  little  formic  acid.  They  also  found  considerable 
quantities  of  formic  acid  in  the  urine  in  cases  of  rheumatic  fever,  rapidly 
decreasing  in  amount  if  salicylates  were  given.  At  present  we  cannot  admit 
that  this  organism  has  been  definitely  proved  the  specific  cause  of  rheumatic 
fever.  Nor  can  the  disease  be  justly  regarded  as  an  attenuated  form  of 
pysemia.    Even  in  acute  and  severe  cases  there  is  no  pus  foimation. 

Pathology. — There  is  no  reliable  evidence  in  favour  of  the  old  views 
that  the  disease  is  due  to  the  direct  influence  of  cold  on  joints  ;  to  nervous 
lesions  in  the  spinal  cord  ;  or  to  lactic  acid  or  uric  acid  in  the  blood.  It 
may  be  mentioned  that  B.  W.  Eichardson  (1853)  and  Eauch  produced 
endocarditis,  pericarditis,  and  polyarthritis  in  dogs  by  injecting  a  10  per 
cent,  solution  of  lactic  acid  into  the  peritoneal  cavity.  The  theory  that  it  is 
due  to  an  infective  organism,  whether  of  one  or  many  different  varieties, 
is  the  most  satisfactory  explanation.  Direct  infection  has  not  been  proved, 
but  cases  have  occurred  which  support  the  view  that  the  disease  has  been 
acquired  in  this  manner  or  by  exposure  to  the  same  infecting  agent.  Many 
arguments  can  be  advanced  in  favour  of  this  hypothesis.  Just  as  in  typhoid 
fever  seasonal  waves  occur.  Its  clinical  features,  viz.  mode  of  onset, 
preliminary  sore-throat,  course  of  the  fever  and  tendency  to  relapses,  are 
all  in  favour  of  it  being  a  specific  febrile  disease.  A  family  predisposition 
exists,  just  as  in  diphtheria,  scarlet  fever,  and  enteric  fever.  Two  children 
may  be  attacked  simultaneously.  Like  influenza,  erysipelas  and  diphtheria 
it  may  recur  in  the  same  patient.  As  in  cholera  and  enteric  fever  direct 
infection  is  rare.  Like  malaria  and  syphilis  there  is  a  drug  to  which  it  is 
especially  sensitive.  Possibly  infection  is  conveyed  by  dust.  Both  rheu- 
matic fever  and  all  forms  of  sore-throat  are  more  common  in  a  dusty 
autumn.  The  tonsils  and  naso-pharynx  are  probably  the  portals  of  entry 
for  the  infecting  agent,  although  there  is  not  necessarily  a  local  reaction. 
Different  observe! s  have  stated  that  rheumatism  is  preceded  by  tonsillitis 
in  percentages  varying  from  5-80.    It  is  certainly  true  that  some  affection  of 


Rheumatic  Fever.  825 

the  fauces  is  common,  e.g.  simple  erythema,  tonsillitis,  follicular  tonsillitis, 
and  quinsy.  On  the  other  hand  tonsillitis  is  so  common  that  not  much 
importance  can  be  attached  to  it.  It  may  even  occur  during  an  attack  of 
rheumatic  fever  while  the  patient  is  taking  salicylates. 

To  sum  up  : — All  the  clinical  evidence  is  suggestive  of  an  infectious 
disease  ;  namely,  epidemic  prevalence,  seasonal  variation,  rapid  onset, 
fairly  definite  course,  incidence  in  the  young,  variability  in  type,  liability  to 
relapses,  rapid  anaemia,  tonsillitis,  heart  lesions,  multiple  implication  of 
joints,  pleurisy,  pneumonia,  hyperpyrexia,  nervous  disturbance,  liability 
to  capillary  haemorrhages  and  albuminuria,  erythemata  and  the  effect  of 
salicylates. 

Morbid  Anatomy. — The  endocardium  shows  cell  degeneration  and 
necrosis,  with  secondary  fibrino-cellular  exudation  and  fibrosis.  The 
auriculo-ventricular  valves  are  more  often  and  more  severely  affected  than 
the  semilunar,  because  of  their  blood  supply  and  greater  amount  of  con- 
nective tissue.  The  semilunar  valves  can  only  be  infected  through  the 
lymphatics  or  by  the  poison  in  the  circulating  blood  directly  impinging  on 
them.  The  myocardium  shows  inflammation.  It  is  pale.  The  muscle 
fibres  are  large  and  swollen  and  their  transverse  striation  almost  lost.  The 
interstitial  tissue  contains  leucocytes  and  proliferating  cells.  Later  on  the 
muscle  fibres  become  finely  granular  or  fatty.  Some  escape  and  show  dis- 
tinct striation.  The  nuclei  appear  unaffected.  The  total  effects  are  much 
iess  than  in  diphtheria.  The  pericardium  may  show  pericarditis,  patches 
■of  thickening,  or  adhesions,  more  or  less  universal.  The  synovial  membiane 
of  the  joints  is  injected  and  the  effusion  contains  some  blood  cells  and 
leucocytes.  Minute  haemorrhages  in  the  heart,  liver  and  kidneys,  etc.,  may  be 
present. 

Subcutaneous  nodules  are  round  or  oval.  In  size  they  vary  from  a  pin's 
head  to  a  pea,  and  occasionally  that  of  a  marble.  They  are  single  or  multiple, 
neither  painful  nor  tender,  and  better  felt  than  seen.  They  are  composed  of 
•collections  of  inflammatory  lymph  among  fibrous  tissues.  They  are  attached 
to  the  fascia,  tendon  sheaths  or  underlying  fibrous  tissue  about  the  bony 
prominences  and  joints,  especially  the  margins  of  the  patella,  olecranon, 
malleolus  and  finger  joints  ;  on  the  extensor  tendons  of  the  hands,  fingers 
and  toes  ;  and  over  the  spinous  processes  of  the  vertebrae  and  scapula?. 
Sometimes  on  the  scalp  they  are  extraordinarily  large  and  numerous.  They 
are  not  adherent  to  the  skin,  never  suppurate,  and  eventually  disappear  and 
leave  no  ill  effects.  They  are  usually  transitory,  coming  and  going  quickly  ; 
but  they  may  come  out  in  crops  of  a  few  weeks'  duration,  or  in  successive 
•crops  in  the  same  situation  for  several  months. 

Symptoms. — Rheumatic  children  are  usually  of  a  decidedly  nervous 
temperament,  emotional  and  excitable,  and  more  liable  than  ordinary 
•children  to  habit  spasm,  insomnia,  night  terrors  and  somnambulism.  So 
much  is  this  the  case  that  the  neurotic  disposition  is  regarded  as  a  minor  sign 


826  Chapter  LX. 

of  rheumatism.  Important  minor  manifestations  are  vague  pains  (growing 
pains)  in  any  of  the  trunk  or  limb  muscles,  most  frequently  in  the  muscles 
of  the  calf  or  thigh.  Such  pain  may  occur  at  the  back  of  the  knee  ;  may 
affect  one  hip  joint  and  be  mistaken  for  tuberculous  hip-disease  ;  may 
affect  the  intercostal  muscles  and  simulate  pleurisy  ;  or  may  cause  rheumatic 
torticollis.  These  pains  may  be  due  to  a  rheumatic  toxaemia,  for  toxaemia 
is  a  common  cause  of  myalgia. 

Other  signs  of  rheumatism  are  anaemia,  mal-assimilation,  gastralgia,. 
epistaxis,  tonsillitis,  pharyngitis,  pleurisy,  headache,  migraine,  and  ery- 
thematous and  exudative  skin  eruptions.  Epistaxis  may  precede  or  come 
on  with  an  attack  of  rheumatism.  Occasionally  it  alternates  with  j  oint  pains- 
or  occurs  in  chorea.  Rheumatic  wry-neck  comes  on  suddenly  and  lasts  for 
a  few  days  with  much  muscular  soreness,  continuous  spasm,  and  moderate 
pain.  It  is  often  associated  with  sore-throat,  and  possibly  the  cervical  joints 
are  affected.  Another  feature  of  the  disease  is  the  frequent  attacks  of  gastric 
catarrh  with  pain  in  the  stomach  and  often  severe  headache.  Sometimes 
this  simulates  peritonitis. 

The  sore-throat  is  a  simple  or  follicular  tonsillitis,  occasionally  pharyn- 
gitis or  quinsy.  It  may  disappear  before  the  other  symptoms  develop.  The 
sore-throat  and  flying  pains  may  be  regarded  as  signs  of  the  incubation 
period.  The  disease  never  begins  with  vomiting,  though  frequently  ushered 
in  with  digestive  trouble,  abdominal  pain  and  furred  tongue.  The  face  is 
pale,  the  skin  moist,  but  the  profuse  sweating,  seen  in  adults,  does  not 
occur.  The  pulse  is  full  and  soft.  The  temperature  generally  rises  to 
about  102°  F.,  and  comes  down  gradually  in  a  few  days  unless  the  mischief 
extends.  In  articular  rheumatism  the  temperature  rarely  goes  up  above- 
102°  F.,  and  is  generally  100-101°  F.  Often  pain  alone  is  present,  but 
sometimes  there  is  well  marked  swelling.  The  joint  affection  may  be  slight 
or  absent,  monarticular,  and  occasionally  painless.  The  ankles,  knees,, 
wrists,  elbows,  hips,  and  cervical  vertebrae  are  affected  in  the  order  named- 
Redness  is  slight  and  often  absent.  There  may  be  fugitive  pains  and 
stiffness  of  the  joints  without  swelling  ;  or  the  swelling  only  apparent 
on  careful  examination.  Tenderness  is  limited  to  the  joint,  or  involves- 
ligaments,  tendons  and  muscles.  There  is  often  marked  muscular  spasm 
about  the  affected  joint.  The  articular  affection  lasts  for  a  few  hours  to^ 
about  3  days. 

The  general  condition  is  one  of  malaise  with  anorexia,  thirst  and 
constipation.  The  tongue  is  white  and  coated,  but  rarely  presents  the 
thick  white,  creamy  fur  seen  in  adults.  The  facial  aspect  is  anxious,  with 
pallor  and  hectic  flush.  Sweating  is  often  absent,  and  even  in  children  over 
10  the  synovitis  and  sweating  are  generally  less  than  in  later  life. 

The  heart  affection  is  the  first  and  only  sign  in  about  25  per  cent,  of 
the  cases.  It  usually  comes  on  in  the  first  week,  and  infrequently  later- 
It  bears  no  relation  to  the  severity  of  the  attack,  and  is  increasingly 


Rheumatic  Fever.  827 

prevalent  with  decrease  in  the  age  of  the  patients.  It  is  present  in  about  three- 
fourths  of  hospital  cases  under  10  years  of  age.  Any  portion  of  the  heart 
may  be  affected.  Endocarditis,  myocarditis,  and  pericarditis  are  often 
insidious  and  unsuspected  and  may  make  rapid  progress  before  the  child 
is  taken  for  medical  advice  or  the  heart  affection  is  suspected.  Some  of  the 
worst  cases  of  heart  disease  are  of  this  nature  ;  in  hospital  practice  a  child 
being  brought  on  account  of  marked  wasting,  shortness  of  breath,  or  loss 
of  appetite.  Symptoms  of  carditis  may  be  absent  or  unnoticed  for  some  time,, 
or  limited  to  mere  fretfulness,  anorexia  and  malnutrition.  The  pulse  is 
always  increased  in  frequency,  though  there  is  no  positive  evidence  of 
carditis.    In  half  the  cases  the  heart  is  permanently  damaged. 

It  is  generally  stated  that  endocarditis  is  the  most  common  lesion.  It  is 
almost  certain,  however,  that  the  myocardium  rarely,  if  ever,  entirely 
escapes.  The  signs  of  myocarditis  may  be  limited  to  dilatation  and  increased 
frequency  of  the  pulse,  perhaps  a  murmur.  Endocarditis  is  often  unnoticed 
in  the  absence  of  articular  pains,  until  serious  valvular  disease  has  developed. 
It  may  be  associated  with  considerable  pyrexia  and  no  definite  rheumatic 
manifestations.  The  early"  signs  are  irregularity  and  increased  frequency  of 
the  pulse,  slight  rise  in  temperatuie,  restlessness,  cardiac  uneasiness  and  a 
murmur.  It  comes  on  about  the  end  of  the  first  week  and  may  precede 
joint  symptoms.  The  murmur  is  almost  always  mitral.  Its  frequency  is 
exaggerated,  for  in  many  instances  it  is  due  to  dilatation  and  not  to 
endocarditis. 

Pericarditis  is  rare  before  the  commencement  of  the  second  dentition. 
It  is  usually  of  the  dry  variety  and  results  in  extensive  pericardial  adhesions. 
It  is  occasionally  sero-fibrinous  and  rarely  purulent.  Its  onset  is  indicated 
by  acceleration  and  perhaps  irregularity  of  the  pulse,  rise  in  temperature,, 
dyspnoea  and  restlessness.  Localised  friction,  audible  at  the  base  and 
over  the  left  auricle,  may  be  the  only  evidence.  It  is  usually  associated  with 
myocarditis  (p.  482).  An  insidious  form  is  not  uncommon  in  cases  of  tedious 
and  prolonged  course  with  slight  symptoms  and  little  joint  mischief  ;  some- 
times with  much  anaemia  and  headache. 

Pleurisy  is  less  frequent  than  in  adults  ;  multiple  serositis  may  occur. 
Nephritis  is  rare  but  in  one  case,  a  girl  of  7,  albuminuria  and  casts  were 
present;  for  a  few  days.  Hyperpyrexia  is  almost  unknown.  It  is  usually 
associated  with  pericarditis.  Meyler  (1908)  reported  a  case  in  a  boyr 
aged  9  years,  in  whom  the  temperature  rose  to  110°  F.,  with  coma, 
stertorous  breathing  and  contracted  pupils,  hot  and  dry  skin,  violent 
purging  and  uncountable  pulse.  It  occurred  during  a  mild  attack  of  the 
disease  and  ended  fatally. 

Anaemia  is  marked  during  and  between  the  attacks.  It  may  be  so- 
profound  as  to  give  rise  to  hsemic  murmurs,  impossible  of  diagnosis  from 
those  due  to  endocarditis  or  dilatation.  The  percentage  of  haemoglobin 
falls  to  60-75.    Theie  is  erythropenia  and  a  leucocytosis  of  15,000-20,000. 


328  Chapter  LX. 

Chorea  may  occur  during,  before,  or  subsequent  to  an  attack  of 
rheumatic  fever.  Its  relationship  to  rheumatism  is  considered  in  the 
section  on  chorea.  Subcutaneous  fibrous  nodules  were  first  described  by 
Barlow  and  Warner  in  1881  as  a  sign  of  rheumatism.  They  may  occur 
without  any  other  evidence  of  the  disease  and  persist  for  even  2  years;  as  in 
an  infant,  aged  17  months,  whose  hands  were  covered  with  nodules  of  this 
type  (Carpenter,  1901).  They  are  also  noted  sometimes  in  osteo-arthritis 
and  I  have  seen  them  in  large  numbers  in  a  girl  with  general  tuberculosis. 
They  are  common  in  childhood,  infrequent  when  youth  is  reached,  and 
very  rare  after  the  age  of  21  years  ;  yet  rheumatism  increases  in  frequency 
and  is  most  common  from  10-20  years  of  age,  and  nearly  50  per  cent,  of  the 
eases  are  between  20  and  40  years  old.  Poynter  and  Paine  found  the 
diplococcus  rheumaticus  in  these  nodules.  If  this  is  the  true  infective 
organism,  it  is  strange  that  multiple  nodules  can  occur  without  other 
evidence  of  rheumatism.  Either  the  organism  is  not  the  causative  agent, 
or  these  nodules  can  arise  from  other  causes. 

There  is  no  constant  or  characteristic  rash.  Erythematous  rashes  are 
less  frequent  than  nodules,  usually  accompanied  with  a  rise  of  temperature, 
and  indicate  severity.  The  common  types  are  an  exudative  erythema 
multiforme,  gyrate  or  papular,  E.  scarlatiniforme,  or  E.  marginatum.  The 
patches  are  sharply  denned,  spread  irregularly  at  the  edge,  fade  gradually 
in  a  few  days,  and  may  cause  brownish  discoloration.  Urticaria  and 
various  form  of  purpura  are  occasionally  seen. 

Diagnosis. — There  is  no  distinction  between  acute  and  subacute  cases, 
except  in  the  degree  of  fever,  and  no  indication  of  the  ultimate  result  on  the 
heart.  The  use  of  the  term  subacute  is  likely  to  lessen  the  care  needed  in 
the  mildest  attack.  Early  diagnosis  is  of  importance  because  of  the  liability 
to  heart  mischief.  Very  few  cases  correspond  to  the  adult  type.  The 
diagnosis  depends  on  the  association  of  several  symptoms  which  apparently 
a,re  independent  or  unrelated.  The  presence  of  arthritic  symptoms  is 
unnecessary.  Make  careful  inquiry  into  the  family  history  and  a  past 
history  of  growing  pains,  recurrent  sore-throats,  stiff  neck,  joint  pain  and 
swelling,  chorea,  etc.  Always  examine  doubtful  cases  of  fever  for  heart 
lesions  and  nodules.  Kheumatic  fever  is  rarely  confounded  with  other 
diseases  but  is  often  overlooked.  Its  rarity  in  infancy  prevents  it  being 
mistaken  for  scurvy,  syphilitic  epiphysitis  and  acute  periostitis.  Later  it 
has  to  be  distinguished  from  pneumococcal,  gonococcal,  septic  and  other 
forms  of  arthritis.  The  myocarditis  and  fever  may  be  mistaken  for  early 
phthisis.  Unilateral  affection  of  the  hip  or  lameness  from  injury  may  be 
ascribed  to  rheumatism  or  tuberculosis.  Other  conditions  to  be  remembered 
■are  muscle  soreness  from  fatigue,  influenza,  neuritis,  and  stiff  neck  from  other 
causes.  The  most  characteristic  features  are  the  migratory  character  of  the 
pain,  the  anaemia,  cardiac  troubles,  and  the  effect  of  salicylates. 


Rheumatic  Fever.  829~ 

Course  and  Prognosis. — Under  efficient  treatment  the  fever  rarely 
lasts  more  than  7-10  days,  and  the  total  illness  from  1-3  weeks.  Even 
without  treatment  the  symptoms  soon  subside  but  the  heart  lesions  persist 
and  progress,  and  on  these  the  ultimate  prognosis  depends.  The  outlook  is. 
good  as  regards  life,  but  the  disease  is  dangerous  in  both  its  immediate  and 
remote  effects.  It  depends  largely  on  the  degree  of  myocarditis,  which  may 
sooner  or  later  terminate  in  gradual  cardiac  failure.  Pericarditis  may 
subside  in  a  few  days  or  persist  for  1-3  months.  Although  the  patient  may 
recover  completely,  there  is  a  liability  to  progressive  cardiac  failure  on 
account  of  universal  adhesions.  Even  the  worst  attack  of  pericarditis  may 
be  recovered  from,  and  present  no  evidence  of  adhesion  some  years  later. 
The  prognosis  must  be  guarded  in  all  cases  of  rheumatism  because  of  the 
liability  to  recurrence  and  the  extension  of  cardiac  mischief  with  each  attack. 
The  mildest  cases  require  treatment  for  3  weeks. 

Treatment. — Rest  is  of  the  utmost  importance  and  must  be  complete,, 
in  the  horizontal  position,  with  no  needless  washing  or  movement.  More 
especially  is  it  necessary  if  the  heart  is  affected.  The  ordinary  methods  of 
treatment  in  fever  must  be  adopted.  The  child  should  wear  a  woollen  night- 
dress, frequently  changed  if  there  is  much  sweating,  and  be  covered  with 
blankets  but  no  sheets.    A  hair  mattress  and  firm  level  bed  are  required. 

The  diet  should  consist  of  milk,  diluted  if  necessary,  and  a  liberal 
amount  of  water,  barley  water,  lemonade  and  imperial  drink.  Farinaceous 
foods  are  added  when  the  fever  subsides.  Meat  extracts  should  be  avoided, 
and  no  meat  given  until  the  child  has  been  free  from  fever  for  a  week  or 
3  weeks  have  elapsed  from  the  onset.  Alcohol  is  only  necessary  in  severe 
heart  complications. 

The  old  systems  of  treatment  by  bleeding,  purgation,  alkalies,  calomel 
and  opium,  blistering,  and  rest,  have  left  behind  some  useful  hints.  The 
bowels  must  be  kept  open  daily  by  calomel  and  salines.  Blistering  has  been 
advocated  as  preventive  of  cardiac  complications  and  for  the  treatment  of 
prolonged  joint  swelling.  It  is  unsuitable  for  young  children,  must  be  used 
very  cautiously  in  older  ones,  and  is  of  doubtful  value  for  heart  mischief. 
Depressant  drugs,  such  as  aconite  and  coal  tar  preparations,  must  be 
avoided.  Practically  no  drug  is  used  now  except  salicin,  or  some  of  its 
compounds,  with  or  without  citrate  or  bicarbonate  of  soda  or  potash. 
Stockman  (1908)  has  shown  that  benzoic  acid,  cresotinic  acid  and  drugs 
which  are  converted  to  salicylic  acid  in  the  body,  namely  salicin,  saligenin, 
acetyl-salicylic  acid  (aspirin),  methyl-salicylate,  etc.,  have  similar  effects. 
Some  drugs,  practically  of  the  same  chemical  composition  as  salicylic  acid, 
are  inert  apparently  because  they  differ  in  the  position  occupied  by  the 
hydroxyl  group  in  the  molecule.  Other  drugs  are  inert  because  salicylic 
acid  is  not  formed  from  them  in  the  tissues.  Salicin,  salicylic  acid  and 
salicylate  of  soda,  preferably  made  from  the  oil  of  winter  green  and  not 


•830  Chapter  LX. 

the  artificial  compound,  and  aspirin  are  the  drugs  chiefly  used.  Aspirin 
has  the  most  prolonged  effect  for  it  is  most  slowly  excreted,  but  it  cannot 
be  combined  with  an  alkali.  On  the  whole  the  salicylate  of  soda  is  the 
most  satisfactory,  for  it  can  be  given  with  an  alkali  and  is  a  powerful 
hepatic  stimulant.  It  should  be  given  in  full  doses,  with  the  same  or  double 
the  amount  of  alkali,  every  2-4  hours,  according  to  the  severity  of  the  case, 
until  the  system  is  well  under  the  influence  of  the  drug  and  salicyluric  acid 
is  found  in  the  urine.  The  dose  is  then  reduced  to  4  times  a  day  and 
gradually  to  once  a  day,  and  continued  until  the  patient  is  taking  full  diet. 
Children  bear  salicylates  well  and  for  long  periods.  The  drug  does  not 
seem  as  efficacious  as  in  adults,  because  of  the  small  amount  of  joint  swel- 
ling and  pain.  It  has  little  influence  on  the  other  symptoms  and  com- 
plications, for  these  may  develop  while  the  child  is  fully  under  its  influence. 
It  has  no  marked  depressant  effect,  but  in  excessive  doses  may  give  rise  to 
giddiness,  tinnitus,  vomiting,  air-hunger  and  acidosis.  Poisonous  effects 
;are  more  apt  to  arise  if  the  synthetic  drug  is  used,  if  the  child  is  constipated, 
and  if  alkalies  are  not  given.  Rheumatic  fever  must  be  regarded  as  a  fever 
of  3  weeks'  duration  from  the  onset,  and  further  treatment  is  essential  to 
prevent  iecrudescences.  If  the  heart  is  at  all  involved,  the  child  should 
he  kept  in  bed  5  or  6  weeks,  and  perhaps  as  many  months  in  severe  cases. 
Not  nearly  sufficient  importance  is  attached  to  prolonged  rest  in  the 
treatment  of  myocardial  affections.  Complete  recovery  from  all  forms  of 
Theumatic  heart  disease  is  possible,  but  becomes  less  probable  in  proportion 
to  the  reduction  of  complete  rest.  The  child  is  growing  and  with  growth 
-the  work  for  the  heart  is  increased.  Therefore,  it  has  to  bear  a  greater  strain 
than  in  adults  and  fresh  endocarditis  is  easily  lighted  up.  Complete  rest 
from  the  onset  takes  the  first  place  in  the  prevention  and  treatment  of 
•cardiac  mischief.  It  should  be  combined  with  fluid  diet,  salicylates, 
•diuresis  and  mild  purgation.  Counter-irritation  by  mustard  leaf  or  tincture 
•of  iodine  may  do  good  in  pericarditis,  and  does  no  harm  in  valvular  disease. 
It  is  not  advisable  to  cause  actual  blistering,  or  to  apply  the  irritant  over 
the  cardiac  area,  and  thus  interfere  with  examination.  Such  applications 
•can  be  applied  just  outside  the  limits  of  cardiac  dulness.  The  treatment  of 
pericarditis  has  been  described  (p.  498). 

For  severe  joint  pains  and  for  the  cardiac  mischief,  when  the  patient 
is  excitable  or  suffers  from  much  pain,  distress  and  dyspnoea,  a  small  dose 
of  Dover's  powder  affords  relief.  The  joints  should  be  wrapped  in  cotton 
wool.  Methyl  salicylate  and  mesotan  are  readily  absorbed  by  the  skin. 
From  ^-1  dr.  is  sprinkled  on  cotton  wool  or  lint,  wrapped  round  the 
joint  and  covered  with  gutta  percha  tissue.  Ichthyol  is  also  useful. 
For  severe  pain  the  joints  can  be  painted  with  tr.  iodi.,  lin.  chlorof.  or  lin. 
helladon. 

As  the  patient  recovers,  iron  is  given  in  small  doses.  In  conjunction 
with  cod-liver  oil  and  malt  it  affords  an  excellent  tonic.    It  can  be  given  as 


Chorea.  831 

iron-containing  foods,  in  haemoglobin  compounds,  or  as  glycero-phosphate 
of  iron. 

The  preventive  treatment  consists  of  liberal  diet  in  which  there  is 
plenty  of  milk  and  no  great  excess  of  carbohydrates.  Protein  food  must  not 
be  diminished.  Moderate  hydrotherapy  is  good  but  the  hardening  process 
must  be  carried  out  with  great  discretion.  The  child  should  wear  flannel 
underclothing  and  not  be  allowed  to  sit  in  damp  boots  or  clothes.  Trivial 
ailments  should  be  carefully  attended  to  for  they  may  be  rheumatic  in 
•origin  and  associated  with  endocarditis. 


CHOREA. 

Eyn. :    Sydenham' 's    Chorea  (1686) — Chorea  Minor — Rheumatic    Chorea — 
Cerebral  Rheumatism — St.   Vitus'' 's  Dance. 

Chorea  was  the  name  originally  given  to  the  dancing  mania  or  saltatory 
■spasm  of  hysteria,  the  true  St.Vitus's  Dance  (Chorea  Sancti  Viti),  which 
•occurred  in  Germany  at  the  beginning  of  the  fifteenth  century.  Other 
■affections  of  a  somewhat  similar  name  must  not  be  confused  with  the  disease 
Tinder  consideration.  Among  these  may  be  mentioned  electrical  chorea, 
hysterical  chorea,  habit  chorea,  the  choreic  and  athetoid  choreiform 
movements  which  follow  gross  cerebral  disease,  and  Huntingdon's 
■chorea,  a  form  of  hereditary  tremor  occurring  later  in  life. 

Chorea  is  a  bad  name  for  this  particular  disease  for  there  is  no  dancing 
■or  rhythmic  movement,  and  there  is  much  more  than  irregular  muscular 
action.  It  is  an  exaggerated  form  of  fidgets,  an  exaltation  of  the  continual 
unrest  characteristic  of  childhood.  The  movements  become  irregular, 
involuntary,  disorderly,  with  lack  of  co-ordination  and  imperfect  control. 

Ziemssen  defined  it  as  "  A  neurosis  of  which  the  seat  (as  it  seems) 
may  sometimes  be  the  brain  alone,  sometimes  the  entire  nervous  system, 
•characterised  by  incessant  twitchings  or  jerks  of  groups  of  muscles,  which 
are  sometimes  spontaneous  and  sometimes  excited  by  voluntary  impulse, 
which  occur  almost  exclusively  in  the  waking  state,  and  are  accompanied 
by  more  or  less  developed  psychical  disturbance." 

Etiology. — There  is  no  definite  heredity.  A  family  history  of  organic 
nervous  disease  or  epilepsy  is  of  little  importance.  A  neurotic  temperament 
in  one  or  both  parents  occurs  in  10-20  per  cent,  of  the  cases.  The  most 
important  inherited  factor  is  rheumatism,  but  the  figures  given  by  different 
observers  are  so  variable  that  it  is  evident  that  what  is  accepted  as  significant 
of  rheumatism  by  one  man  is  disregarded  by  others.  Dana  obtained  a 
family  history  of  rheumatism  in  only  8  per  cent.  ;  Sturges  found  rheumatic 
iever  in  7  per  cent,  of  the  parents,  but  a  family  history  of  rheumatism  in 


832  Chapter  LX. 

25  out  of  100  cases.  Goodall's  figures  yielded  a  family  history  of  rheumatism 
in  17,  chorea  in  11,  and  of  both  in  3  per  cent  of  250  cases.  Guthrie  found  it 
present  in  47-3,  doubtful  in  9  and  absent  in  42*1  per  cent,  of  114  cases. 
H.  M.  Fletcher  found  it  in  an  immediate  relative  in  25-6  per  cent,  of  273 
out-patients. 

Sex. — The  disease  is  more  common  in  females,  but  the  younger  the 
children  the  less  marked  is  the  inequality  of  sex.  Guthrie  found  it  a  little 
more  common  in  males  up  to  the  ninth  year,  but  out  of  114  cases  under 
14  years  two-thirds  were  females.  Out  of  over  2,000  collected  cases  the 
proportion  of  males  to  females  was  closely  1-3. 

Age. — It  has  occurred  in  the  third  year  of  life,  but  cases  are  exceptional 
in  the  first  5  years.  The  most  common  age  is  5-10,  or  a  wider  limit  of  5-15, 
or  a  narrower  one  of  8-11.  Of  children  under  15  more  than  half  are  in  the- 
second  5  years  of  life.  In  boys  it  is  most  common  in  the  tenth  year  and 
decidedly  rare  after  puberty.    In  girls  it  is  rare  after  the  nineteenth  year. 

Except  for  the  fact  that  it  is  rare  among  negroes  and  Indians  and 
common  among  Jews,  there  is  no  special  race  incidence.  Nowhere  in  Europe- 
is  it  very  uncommon.  It  is  prevalent  in  England,  France,  Germany,  Austria,. 
Italy,  Russia  and  the  United  States.  It  is  very  rare  in  Northern  India,. 
Bombay  and  Abyssinia.  It  is  more  common  in  towns  than  in  country 
districts.  It  is  more  frequent  among  the  poor  than  the  rich,  and  especially 
affects  the  weak  and  nervous  childi  en.  It  is  most  prevalent  in  winter,  with 
a  maximal  incidence  in  December.  H.  M.  Fletcher  found  it  least  frequent, 
in  May  to  September  in  London.  A  rise  in  the  number  of  severe  cases  may 
be  noticed  in  March. 

Cases  have  followed  severe  fright  or  mental  shock,  generally  within  a. 
week.  Such  an  exciting  cause  has  been  found  in  15-7  per  cent.  (Fletcher), 
17  per  cent.  (Goodall),  22  per  cent.  (Koch),  25  per  cent.  (Gowers).  Sturges. 
found  a  close  connection  with  mental  shock  and  strain  in  65  per  cent. 
Overstudy,  teasing,  bullying,  punishment  and  barometric  disturbances,, 
such  as  thunderstorms,  appear  to  be  exciting  causes.  Not  much  impor- 
tance can  be  attributed  to  fright  as  a  cause.  The  early  emotional  state 
predisposes  the  child  to  fright  on  slight  provocation.  In  many  instances 
careful  inquhies  will  elicit  evidence  of  the  existence  of  the  disease  before, 
the  fright.  Other  cases  have  followed  a  fall  on  the  head,  injury  to  spinal, 
nerves,  or  have  been  associated  with  dental  irritation,  roundworms,  tape- 
worms and  other  local  sources  of  intestinal  irritation,  with  the  onset  of 
puberty,  menstrual  disorders,  or  have  followed  infectious  fevers.  Many 
of  these  affections  are  merely  coincident. 

Rheumatism  and  Chorea. — There  is  strong  evidence  that  chorea  is  an 
indication  or  symptom  of  rheumatism.  A  family  or  personal  history  of 
rheumatism  is  often  obtained.  The  chorea  may  be  the  first  symptom, 
and  the  rheumatism  may  not  appear  for  some  years  later.  In  235  non-fatal 
cases  Goodall  found  rheumatism  antecedent  by  days  or  weeks  in  59,  by 


Chorea.  833 

months  or  years  in  25.  In  16  the  chorea  preceded  the  rheumatism  by  months 
or  years,  and  in  none  by  days  or  weeks.  I  have  seen  it  develop  in  the  course 
of  acute  rheumatism,  and  subside  on  the  appearance  of  articular  inflam- 
mation. A  history  of  antecedent  rheumatism  has  been  found  by  various 
observers  in  percentages  varying  from  18-65.  In  130  out  of  270  collected 
cases,  examined  2-3  years  after  the  chorea,  organic  heart  disease  was  present. 
Valvular  disease  is  usually  of  rheumatic  origin,  so  this  is  a  strong  argument 
in  favour  of  a  connection  between  the  two  diseases.  In  almost  all  fatal 
cases  there  is  evidence  of  recent  endocarditis. 

Against  the  rheumatic  theory  of  origin  it  must  be  noted  that  there  are 
instances  in  which  no  rheumatic  element  can  be  traced  during  the  attack, 
or  in  the  family  or  past  history.  The  heart  is  usually  unaffected  or,  if 
affected,  merely  shows  dilatation  and  irregularity  without  any  evidence  of 
inflammation.  In  GoodalPs  statistics  of  250  non-fatal  cases  the  heart  was 
normal  in  135,  and  21  of  these  had  had  rheumatic  fever.  In  115  a  bruit  was 
present,  and  of  these  56  had  rheumatism  at  the  time  or  previously.  In  65 
out  of  the  115  a  systolic  apical  murmur  was  present,  but  no  mitral  regur- 
gitation was  thought  to  exist ;  of  these,  20  had  rheumatism  at  the  time  or 
previously.  Rheumatic  fever  had  occurred  in  22  out  of  33  with  mitral 
regurgitation  ;  and  in  2  out  of  13  with  mitral  stenosis.  Nine  had  peri- 
carditis and  in  5  of  these  were  valvular  lesions.  There  is,  therefore,  con- 
siderable evidence  of  rheumatism,  if  cardiac  mischief  occurs.  Taking  into 
consideration  the  fact  that  a  bruit  is  by  no  means  proof  of  endocarditis, 
it  appears  that  chorea,  per  se,  is  not  a  common  cause  of  endocarditis,  but 
that  both  may  be  symptoms  of  rheumatism.  When  chorea  and  rheumatism 
are  coincident,  there  is  no  obvious  relation  between  the  gravity  of  the 
chorea  and  the  rheumatism.  Many  mild  cases  occur  though  the  rheumatic 
infection  is  severe. 

It  is  a  remarkable  fact  that  nodules  are  not  present  unless  there  is 
associated  rheumatism.  This  is  very  curious,  if  nodules  are  accepted  as  a 
sign  of  rheumatism  in  early  life,  and  if  chorea  is  regarded  as  a  manifestation 
of  rheumatism.  Both  nodules  and  chorea  are  common  in  childhood  and 
rare  when  youth  is  reached.  If  they  are  both  rheumatic  manifestations, 
they  ought  to  be  frequently  associated.  Again,  the  maximal  seasonal 
incidence  of  rheumatic  fever  is  in  October,  showing  a  steady  rise  from  July 
onwards,  while  that  of  chorea  is  much  later  in  the  year.  In  Philadelphia, 
however,  it  has  been  noted  that  the  maximal  seasonal  incidence  of 
rheumatism  is  only  1  month  later  than  that  of  chorea. 

Pathology. — In  1850  Germain  See  stated  that  "  Chorea  is  due  to  the 
rheumatic  diathesis  acting  on  the  brain  and  spinal  cord."  Many  facts 
suggest  that  it  is  of  an  infective  nature,  and  not  a  neurosis.  The  general 
distribution  from  the  onset  in  some  cases  is  in  favour  of  a  primary  blood 
infection,  microbial  or  toxic,  and  secondary  involvement  of  the  nervous 
system.    The  virus  attacks  the  motor  cells  of  the  cortex  and  the  pyramidal 

3  h 


834  Chapter  LX. 

tracts,  the  cerebral  rather  than  the  spinal  parts  of  the  nervous  system.  The 
indications  of  a  blood  affection  are  anaemia,  diminution  in  the  number  of 
red  cells,  a  pulse  which  is  weaker  and  more  rapid  than  that  of  health, 
hseinic  murmurs  and  malnutrition.  Muscular  weakness  may  be  due  to  the 
anaemia,  rather  than  to  mere  lack  of  co-ordination. 

That  the  poison  is  a  microbe  rather  than  a  toxin  is  suggested  by  the 
frequent  unilateral  character  of  the  disease.  It  is  almost  invariably  more 
marked  on  one  side  than  the  other.  This  indicates  a  local  cerebral  lesion 
rather  than  a  general  cerebral  toxaemia.  Micro-organisms  have  been 
cultivated  from  the  brain  and  pia  mater,  the  cerebrospinal  fluid,  and  the 
cardiac  valves.  It  is  probable  that  more  than  one  organism  can  give 
rise  to  chorea,  for  attacks  have  followed  many  infectious  diseases. 

Functional  instability  of  the  nervous  centres  is  a  potent  cause  and  may 
depend  upon  malnutrition.  The  disease  is  particularly  apt  to  occur  among 
the  poor  and  the  ill-nourished.  It  is  not  unreasonable  to  suppose  that  the 
nutrition  of  the  cerebral  tissues  suffers  and  that  an  iiregular,  or  unequal, 
development  of  the  different  regions  ensues.  On  this  supposition  the 
choreic  movements  can  be  ascribed  to  irregulai  origin  and  conduction  of 
impulses  from  the  motor  cells.  In  favour  of  this  view  it  may  be  pointed  out 
that  many  cases  are  cured  by  rest  and  liberal  diet.  The  distribution  and 
character  of  the  movements  indicate  a  disorder  of  the  Rolandic  area  of  the 
cortex  of  the  brain,  causing  undue  irritability  and  weakness  or  paresis  of 
muscles.  The  psychical  changes  show  that  the  whole  brain  is  more  or  less 
affected.  The  spinal  involvement  is  perhaps  indicated  by  absent  knee  jerks, 
hyperaesthesia,  pains,  rigidity,  weakness,  muscular  wasting  and  some  kinds 
of  ataxia.  Joff  roy,  supported  by  Comby,  takes  a  similar  view  and  holds  that, 
"  It  is  a  cerebrospinal  neurosis  of  development,  a  disease  of  growth  ; 
•chorea  is  to  the  nervous  system  what  chlorosis  is  to  the  circulatory 
system." 

At  present  it  is  advisable  to  regard  the  disease  as  a  functional  disorder 
due  in  some  cases  to  imperfect  nutrition,  and  in  others  to  microbial  infec- 
tion which  may  or  may  not  be  the  same  as  that  of  acute  rheumatism.  In 
many  instances  it  is  a  manifestation  of  rheumatism. 

Morbid  Anatomy. — Extreme  emaciation  and  excoriations  of  bony 
prominences  are  almost  invariably  present.  Endocarditis  is  practically 
constant  and  was  noted  in  105  out  of  115  autopsies  collected  by  Osier. 
Sturges  found  oiganic  heart  disease  in  75  out  of  80  fatal  cases.  The  mitral 
valve  is  almost  always  affected,  and  sometimes  the  aortic  as  well.  Occasion- 
ally all  the  valves  are  covered  by  minute  bead-like  vegetations.  They  may 
be  present  in  supposed  non-rheumatic  cases.  Statistics  of  murmurs  during 
life  are  valueless  for  the  endocardium  has  been  found  normal,  although  a 
murmur  was  present.  The  myocardium  may  show  patches  of  early  fatty 
degeneration  and  foci  of  inflammatory  exudation  between  the  muscle 
fibres. 


Chorea.  835 

Reichardt  (1902)  found  changes  in  the  nervous  system  which  he 
regarded  as  due  to  general  toxaemia,  viz.  (1)  Degeneration  of  the  anterior 
and  posterioi  root  fibres  in  the  cord  ;  (2)  Small-celled  infiltration  throughout 
the  brain,  especially  in  the  perivascular  spaces  ;  (3)  Small  haemorrhages, 
■chiefly  in  the  neighbourhood  of  the  basal  ganglia  and  beneath  the  ependymal 
•  cells  of  the  ventricles.  Neuwerck  has  noticed  these  areas  of  infiltration  and 
haemorrhage.  They  are  not  constant,  and  may  occur  in  any  infective  disease. 
Poynton  and  Paine  (1906)  have  found  hypeiaemia,  thrombosis  and  peri- 
vascular round-celled  infiltration  in  the  brain  and  meninges,  and  chromato- 
lysis  of  nerve  cells.  Pianese  has  described  an  ependymyelitis.  Most  recent 
-observers  have  found  no  abnormality  in  the  cerebral  cortex  or  thalamus 
and  no  lesions  in  the  spinal  ganglia. 

Varieties. — Different  names  are  sometimes  used  according  to  the 
.severity  of  the  attack,  its  distribution,  special  characters,  or  the  age  of  the 
patient.  Maniacal  chorea,  or  chorea  insaniens,  is  very  fatal  and  unknown  in 
•children.  The  chorea  of  pregnancy  is  associated  with  violent  movements 
.and  fatal  in  about  one-third  of  the  cases.  In  hemiplegic  chorea  the  move- 
ments begin  on  one  side  and  are  worst  on,  but  rarely  entirely  limited  to, 
that  side.  Sometimes  there  is  a  transference  to  the  opposite  side.  Asthenic, 
pseudo-paralytic  or  paralytic  chorea  is  a  variety  in  which  the  paresis  is 
marked  and  the  movements  slight.  It  may  be  a  sequel  of  the  sthenic  or 
•explosive  variety,  either  mild  or  severe.  The  common  form  in  young 
•children  is  a  mild  chorea  of  long  duration  and  moderate  severity.  Some- 
times after  chorea,  clumsiness  in  the  use  of  the  limbs  persists  and  the 
gait  is  blundering  and  ataxic.  It  is  due  to  persistence  of  the  symptoms 
though  the  disease  is  cured  and  is  known  as  "  Residual  chorea." 

Symptoms. — The  most  obvious,  but  the  least  important,  are  the  motor 
symptoms.  The  onset  is  insidious,  except  perhaps  in  those  cases  which 
follow  severe  fright.  During  a  stage  of  subacute  development,  which  lasts 
1-6  weeks,  the  child  is  nervous  and  impressionable,  laughs  and  cries  for 
(little  or  no  cause,  is  unable  to  fix  her  attention,  has  a  pathetic  aspect,  and 
•exhibits  languor,  irritability  of  temper,  trembling  and  awkwardness,  perhaps 
headache  and  sleeplessness.  She  becomes  anaemic,  constipated,  and  may 
have  variable  pains.  The  muscles  used  to  express  emotion,  and  those 
requiring  the  most  careful  co-ordination,  suffer  first  and  most.  The  child  is 
noticed  to  "  make  faces,"  "  drop  things,"  wriggle,  shuffle,  stumble  or  fall, 
•and  to  be  more  emotional  than  normal.  As  the  movements  increase,  a 
variety  of  emotions  are  expressed  in  the  face  in  rapid  succession 
•and  exaggerated  manner,  independently  of  feeling.  Eventually  the 
•child  is  unable  to  stand,  walk  or  sit,  and  even  flings  herself  violently 
about  the  bed. 

The  psychical  and  mental  state  varies  in  character  and  extent.  Often 
there  is  a  peculiarly  stupid  or  fatuous  appearance,  and  the  child  is  unduly 
•dull,    slow    in    understanding  and    answering    questions,    or    profoundly 


836  Chapter  LX. 

apathetic.  This  is  partly  the  result  of  weakness  and  loss  of  tone  in  the- 
muscles  of  expression,  and  partly  from  mental  dulness.  Frequently  the 
child  cries,  smiles  or  laughs  for  little  or  no  cause  ;  is  excitable  and  easily 
frightened  ;  fretful  and  tearful,  and  bursts  into  fits  of  weeping.  She  is 
irritable,  fearful,  obstinate,  with  defective  power  of  attention  and  impaired 
memory.  The  more  severe  the  attack  the  more  marked  is  the  emotional 
disturbance.  It  may  be  accompanied  by  great  excitement,  pavor,  hallu- 
cinations of  vision,  delirium  and  delusions.  Both  emotions  and  movements- 
are  most  marked,  when  the  child  is  under  observation. 

Motor  Disturbances. — The  muscles  show  involuntary  movements,, 
inco-ordination  and  paresis.  The  movements  are  more  or  less  ataxic,  and 
affect  many  different  groups  of  muscles  simultaneously  or  successively  r 
shifting  from  limb  to  limb.  They  are  not  repeated  constantly  in  the  same 
groups  of  muscles,  like  the  movements  of  habit  spasm  or  habit  chorea.  They 
vary  in  severity  from  severe  general  spasms  to  slight  twitches.  In  mildi 
cases  the  twitches  or  jerks  are  of  a  fibrillary  character,  beginning  and 
ending  quickly,  sometimes  only  in  the  trunk  muscles  and  invisible,  but  felt- 
when  the  hand  is  laid  on  them.  Commonly  clonic  movements  are  present 
during  rest  and  increased  on  voluntary  effort.  Sometimes  they  are  con- 
tinuous while  at  rest  and  disappear  or  are  little  altered  on  movement.  In 
rare  instances  they  only  appear  on  voluntary  effort.  As  a  rule  purposive 
movements  with  the  extremities  cannot  be  performed  efficiently,  for  the 
motor  impulse  gets  off  the  rails  and  stimulates  unintended  muscles.  Spasms 
are  first  seen  in  the  face,  tongue,  muscles  about  the  mouth,  zygomatics,, 
and  in  the  hands,  especially  the  left  hand.  A  good  test  of  their  presence  in 
the  hand  is  to  make  the  child  put  the  tip  of  the  extended  forefinger  of  each 
hand  in  turn  on  the  end  of  the  nose  while  the  eyes  are  shut.  The  lack  of 
co-ordination  will  be  at  once  apparent.  Even  if  co-ordination  is  brought 
about  it  is  only  momentarily  sustained.  Writing  affords  a  fair  means  of 
dividing  cases.  It  may  be  done  by  snatches  in  detached  motor  acts  ;  be 
quite  steady,  there  being  more  or  less  control  over  the  movements  ;  show 
much  inco-ordination,  although  movements  are  absent  or  slight ;  or  be 
quite  unintelligible,  even  if  severe  movements  are  inhibited  during  the  act.. 

The  lower  limbs  are  never  affected  alone  and  always  least  severely, 
though  they  may  be  the  first  involved.  The  movements  of  the  legs  may  be  so 
ataxic  and  violent  that  the  child  is  unable  to  walk  or  stand.  Facial  spasms 
are  never  limited  to  one  side,  and  the  trunk  is  always  involved  bilaterally. 
The  thoracic  muscles  seldom  escape  entirely.  Usually  the  fidgets  are  more 
marked  on  one  side  than  the  other,  practically  hemiplegic.  True  monoplegia 
does  not  occur,  though  the  spasms  may  be  most  marked  in  one  limb.  The 
whole  muscular  system  may  be  severely  involved.  Except  in  the  worst 
cases  the  movements  cease  during  sleep  and  recur  on  waking. 

The  decubitus  partly  indicates  the  severity.  If  the  spasms  are  continual 
the  child  slips  down  in  the  bed  and  lies  on  the  back  to  allow  full  play  of  the 
limbs,  which  stay  where  they  fall. 


Chorea.  837 

The  tongue  is  protruded  with  a  jerk,  held  out  by  closing  the  teeth,  and 
withdrawn  with  a  still  more  characteristic  jerk,  but  it  is  rarely  bitten. 
Often  it  is  large  and  somewhat  flabby.  Mastication  and  deglutition  are 
spasmodic  and  difficult.  The  food  reaches  the  mouth  with  difficulty,  because 
of  the  inco-ordination  of  the  hands  and  arms,  and  is  bolted  because  the 
muscles  concerned  in  swallowing  and  mastication  are  involved.  Food  must 
be  soft  or  semi-solid.  It  may  be  necessary  to  feed  the  child  by  nose  or 
rectum. 

Speech  defects  are  common  in  severe  cases  and  may  be  the  first 
symptom  noted.  •  They  are  purely  muscular,  due  to  imperfect  command  of 
respiration,  to  weakness  of  laryngeal  muscles  and  difficulty  in  starting  the 
vocal  apparatus,  and  to  weakness  and  imperfect  co-ordination  of  the 
tongue  and  lips.  The  voice  may  suddenly  cease  or  drop  to  a  whisper  in  spite 
•of  violent  effort,  then  a  few  more  words  may  be  jerked  out,  and  the  process 
is  repeated  till  the  child  collapses  in  a  flood  of  tears.  In  sthenic  chorea 
mutism  is  due  to  spasm  and  inco-ordination.  Dumb  chorea  occurs 
from  paresis  in  the  asthenic  or  paralytic  type  ;  speech  returns  as  the 
•child  improves.  It  may  be  lost  for  weeks  or  months.  True  aphasia  is  said 
never  to  occur,  but  I  cannot  help  thinking  that  in  some  cases  the  sudden  and 
■complete  loss  of  speech  is  due  to  an  effect  on  the  speech  centre. 

Paresis,  or  paralysis,  and  marked  loss  of  muscular  tone  aie  present 
in  every  case  to  a  certain  extent.  It  is  usually  monoplegic  but  may  be 
hemi-,  para-,  or  di-plegic.  It  may  precede,  coincide  with,  or  follow  the 
attack.  The  loss  of  power  is  most  marked  in  the  muscles  most  affected. 
It  may  be  more  apparent  than  real,  being  due  to  loss  of  co-ordinating 
power  and  partly  to  anaemia. 

Paralytic  chorea,  limp  chorea  or  chorea  mollis,  is  most  common  in  girls 
aged  7-14.  The  loss  of  power  is  so  marked  as  to  cause  wrist-drop  or  an 
apparently  complete  paralysis.  The  whole  body  is  affected  with  extreme 
flaccidity  in  24-48  hours,  or  as  a  sequel  of  sthenic  chorea.  The  choreic 
movements  are  slight  and  only  obvious  on  very  careful  examination. 
Paresis  has  been  known  to  be  the  fhst  sign,  disappearing  as  the  spasms 
develop.  Usually  it  is  monoplegic  or  hcmiplegic.  A  well  marked  case 
exhibits  almost  complete  loss  of  voluntary  movement,  emaciation,  pros- 
tration and  imbecile  expression.  The  lips  are  pursed  and  the  upper  eyelids 
retracted.  The  tongue  cannot  be  protruded,  and  both  speech  and  sphincter 
■control  are  lost.    Occasionally  there  is  mania  or  dementia. 

Reflexes. — The  knee  jerks  are  often  normal  at  the  onset,  but  later  on  are 
increased,  diminished  or  abolished.  They  may  disappear  quite  suddenly 
in  the  course  of  the  disease,  even  when  no  drugs  are  given.  Such  loss  of 
reflex  might  be  attributed  to  arsenic  in  cases  treated  by  that  drug.  One 
striking  peculiarity  of  the  reflex  is  the  "  hung-up  "  response  to  stimulation 
of  the  patella  tendon.  Instead  of  dropping  immediately  after  the  con- 
traction the  leg  lemains  momentarily  suspended,  from  a  prolonged  or 
■choreic  contraction  of  the  rectus  femoris.    Or  the  limb  gradually  rises  to  a 


838  Chapter  LX. 

position  of  extreme  extension  and  rigidity  and  remains  there  for  some- 
seconds.  Both  the  superficial  and  deep  reflexes  may  be  exaggerated,  or  one- 
set  may  be  exaggerated  while  the  other  is  absent.  The  sphincters  are 
unaffected,  but  the  calls  of  nature  may  be  neglected  in  severe  eases.. 
Involuntary  micturition  and  defaecation  are  extremely  rare. 

The  electrical  reactions  and  tactile  sensibility  are  generally  unaltered- 
There  may  be  some  general  blunting  of  sensation  or  mild  anaesthesia,, 
numbness,  pins  and  needles,  and  occasionally  hyperaesthesia.  Pain  in  the 
back,  joints  and  limbs  may  be  due  to  rheumatism  or  to  fatigue. 

The  external  ocular  muscles  are  rarely  choreic,  giving  rise  to  momentary 
squint  and  diplopia.  The  pupils  are  generally  dilated  and  frequently 
unequal,  reacting  unequally  to  accommodation  on  the  two  sides.  True- 
rhythmical  oscillations,  or  hippus,  are  sometimes  seen  when  the  patient  is 
quiet.  At  other  times  the  variations  are  wide  and  rapid  in  response  to  light 
and  accommodation. 

The  general  health  is  impaired  but  there  is  no  failure  of  nutrition, 
unless  there  is  difficulty  in  taking  food  and  marked  insomnia.  In  cases  of 
medium  severity  the  appetite  is  capricious,  the  bowels  constipated  and  the 
child  anaemic.  The  number  of  red  cells  may  be  reduced  to  2,000,000  per 
c.mm.,  and  the  haemoglobin  in  proportion.  Eosinophilia  is  often  present,, 
whereas  it  is  absent  in  rheumatism.  The  temperature  is  raised,  if  there- 
are  rheumatic  complications.  Fatal  hyperpyrexia  has  been  reported  by 
Carpenter  (1907)  in  a  child  aged  3  years  with  post-rheumatic  chorea.  Ees- 
piration  is  often  irregular,  sighing,  and  interrupted,  in  consequence  of 
deranged  innervation  of  the  diaphragm. 

Heart. — The  pulse  is  increased  in  frequency,  uneven,  irregular  and 
intermittent ;  mainly  because  of  the  irregularity  of  respiration.  Tachy- 
cardia is  rare.  Irregularity  of  the  heart  is  commonly  due  to  irregularity  of 
breathing.  It  is  sometimes  called  "chorea  cordis"  and  is  characterised  by 
arrhythmia,  a  murmur,  and  variability  in  the  area  of  dulness.  If  due  to 
chorea  of  the  cardiac  muscles  it  persists  during  sleep.  It  is  probable  that 
there  is  no  such  thing  as  true  chorea  of  the  heart. 

Haemic  murmurs  may  be  present  and  may  be  ascribed  to  endocarditis. 
A  pulmonary  systolic  murmur  is  often  due  to  dilatation  of  the  right  ven- 
tricle and  an  apical  one  to  dilatation  of  the  left  ventricle,  or  both  may 
depend  on  anaemia .  Dilatation  of  the  heart  is  often  present  without 
causing  a  murmur,  so  the  area  of  cardiac  dulness  must  be  carefully  mapped 
out.  It  is  due  to  anaemia,  myocarditis  or  fatty  degeneration.  Pericarditis 
probably  only  occurs  in  those  cases  in  which  there  is  definite  rheumatism. 
A  slight  rub  is  liable  to  be  overlooked.  Endocarditis  gives  no  sign  of  its 
existence,  or  is  indicated  by  rise  of  temperature,  a  systolic  mitral  murmur 
and  an  accentuated  pulmonary  second  sound.  The  rise  of  temperature 
may  be  irregular  and  exist  for  some  days  or  weeks  before  the  murmur  is 
heard.    Rarely  the  endocarditis  is  limited  to  the  aortic  valves.    It  may  occur 


Chorea.  839 

at  any  time  in  the  course  of  chorea.  A  reduplicated  second  sound,  or  a 
definite  mid-diastolic  murmur  at  the  apex,  may  be  due  to  early  endocarditis 
or  commencing  mitral  stenosis.  Reduplication  at  the  base,  frequent  in 
children,  is  due  to  asynchronism  of  the  semilunar  valves.  Nodules  have 
been  found  in  cases  in  which  the  heart  is  involved  and  may  be  present 
without  any  evidence  of  arthritic  change. 

The  urine  contains  an  excess  of  urea,  uric  acid  and  phosphates,  in 
proportion  to  the  movements.  Urohsematoporphyrin  occurs  in  rheumatic 
subjects  and  was  found  by  Garrod  in  14  out  of  20  cases.    Albumin  is  rare. 

Psychical  Effects. — The  temperament  and  disposition  are  generally 
altered.  General  intractability,  spitefulness,  and  violent  temper  are 
common.  After  the  age  of  10  years  these  children  are  fretful,  passionate 
and  capricious.  Dementia  may  occur  in  severe  paralytic  cases.  Visual 
hallucinations  may  be  present  after  12  years  of  age.  Attacks  at  puberty  are 
sometimes  associated  with  a  state  almost  of  terror.  Mania  is  very  rare  in 
the  sthenic  stage  and  in  children.  Delirium,  in  acute  grave  cases,  usually 
ends  in  convulsions,  coma  and  death.  Mental  deterioration  may  result  from 
relapses  and  moral  perversion  may  be  a  sequel  of  long  attacks. 

Complications. — Excoriations  and  bed-sores  will  cause  trouble  in 
neglected  cases  and  maybe  followed  by  secondary  infection.  Bruises,  cuts, 
broken  teeth  and  other  injuries  are  due  to  violent  movements.  The  most 
important  complications  are  those  of  the  heart  and  rheumatism.  Joint 
effusions  cause  little  pain  and  are  accompanied  by  subsidence  of  the 
movements.  Meningitis,  encephalitis,  and  acute  paralytic  distension  of  the 
stomach  are  exceptional. 

Diagnosis. — The  movements  must  be  discriminated  from  those  of  habit 
spasm,  a  constant  source  of  erroneous  diagnosis.  Unilateral  distribution 
suggests  post-hemiplegic  chorea  and  bilateral  spasms  may  be  mistaken  for 
those  of  cerebral  diplegia  and  other  gross  lesions.  A  prolonged  duration  is 
suspicious  of  organic  nerve  disease.  The  diagnosis  is  difficult,  if  there  is  loss 
of  power  and  very  little  twitching.  The  association  of  hemiplegia  with 
morbis  cordis  suggests  embolism.  In  chorea  the  face  is  not  paralysed,  the 
tongue  is  jerky,  and  slight  choreic  movements  are  present  in  the  palsied 
limbs.  The  paresis  is  flaccid,  incomplete  and  of  gradual  onset.  The  severe 
paralytic  form  may  be  mistaken  for  acute  anterior  poliomyelitis,  but  some 
choreic  movements  will  be  noted  on  careful  examination.  Hysterical  chorea 
and  palsy  are  more  common  at  a  later  age.  In  myoclonus  the  movements 
are  simple  and  shock-like. 

Course  and  Prognosis. — The  mortality  at  all  ages  varies  from  2-3  per 
cent.  Death  is  rare  in  children.  Mild  cases  tend  to  recover  quickly  and 
steadily  in  4-10  weeks  under  suitable  treatment  by  rest  and  food.  Conse- 
quently not  much  importance  can  be  attached  to  the  drugs  given.  Violent 
symptoms  rarely  last  more  than  3-4  weeks.  Bad  cases  may  last  6  months  or 
more.     The  duration  is  not  proportionate  to  the  initial  severity.     Often 


840  Chapter  LX. 

the  mild  cases  are  the  most  prolonged.  During  the  ordinary  course  of  the 
disease  there  is  a  gradual  increase  in  the  symptoms  followed  by  a  stationary 
period,  then  a  gradual  decrease,  and  finally  disappearance  of  the  spasms 
from  the  fingers  and  face.    Some  cases  exhibit  an  ingravescent  tendency. 

Severe  cases  terminate  fatally  from  exhaustion  and  cardiac  asthenia, 
even  in  the  absence  of  endocarditis,  although  it  is  nearly  always  found 
present  after  death.  Chorea  is  rarely  fatal  unless  there  is  associated  endo- 
carditis and  myocarditis.  Hyperpyrexia,  pyaemia  and  intercurrent  disease 
are  exceptional.  A  serous  meningitis,  such  as  may  occur  in  any  infection, 
may  prove  fatal.  It  causes  a  sudden  and  inexplicable  "rise  of  temperature, 
small  and  frequent  pulse,  pallor  and  cyanosis,  and  disturbed  breathing. 
Chorea  has  proved  fatal  within  6  days  of  the  onset.  Sudden  death  is  most 
liable  to  occur  if  the  psychic  phenomena  are  extreme.  Dyspnoea,  dysphagia, 
grave  mental  symptoms,  convulsions  and  coma  are  unfavourable  signs. 
Paralysis  and  loss  of  speech  are  not  of  serious  importance.  As  the  paralysis 
gets  less,  the  movements  may  increase  and  the  child  seem  worse,  though 
Teally  better.  The  worse  the  movements,  the  greater  the  inability  to  sleep 
and  the  more  the  evidence  of  cardiac  mischief,  the  worse  is  the  immediate 
and  ultimate  prognosis.  Cases  associated  with  recent  articular  rheumatism, 
a  marked  preponderance  of  heart  symptoms,  endocarditis  and  pericarditis, 
increasing  pulse  rate  and  respirations,  are  very  grave.  In  these  death  is  due 
to  the  heart  mischief.  Encephalitis  is  indicated  bydieadache,  hebetude,  a 
tendency  to  slight  unconsciousness  or  delirium,  increasing  spasms  and 
convulsions.  A  scarlatiniform  rash  has  been  seen  in  some  cases  before 
death. 

Cure  is  a  relative  term.  The  fibrillary  movements  may  continue  for 
months  or  years  after  the  cessation  of  treatment.  Relapses  or  recrudescences 
are  frequent  and  often  due  to  emotional  disturbance,  nightmare  or  thunder- 
storms. Relapses  are  more  frequent  in  girls  than  boys,  occurring  in  about 
a  third  of  the  cases,  and  may  be  numerous.  They  are  more  common  after 
mild  than  severe  attacks,  are  less  severe  than  the  first  attack,  and  more 
likely  to  cause  endocarditis.  Sometimes  they  are  slight  cases  with  incom- 
plete remissions,  or  really  due  to  neurotic  auto-suggestion.  True  second 
attacks  generally  occur  after  a  year's  interval,  and  the  heart  is  more  often 
affected  than  in  the  first  attack.  Muscular  and  mental  weakness  may  persist 
for  some  time.    Permanent  injury,  except  cardiac,  is  almost  unknown. 

Treatment. — Especial  attention  must  be  directed  to  the  heart,  for  here 
lies  the  great  source  of  danger.  Physical,  mental  and  emotional  rest  must 
be  insisted  on.  Put  the  child  to  bed  for  a  period  varying  with  the  severity 
of  the  attack,  and  until  free  from  movements  for  1  week.  In  mild  cases 
3-6  weeks  may  be  sufficient.  Forcible  detention  in  bed  may  be  injurious, 
and  does  harm  if  it  causes  mental  depression.  If  the  child  is  allowed  up, 
long  hours  of  sleep  and  a  rest  in  the  middle  of  the  day  must  be  insisted  on. 
The  constant  movements  indicate  an  irritant  lesion  of  the  motor  nervous 


Chorea.  841 

•system.  They  cause  tissue  waste  and  consequent  exhaustion,  increased  by 
lack  of  sleep.  Consequently  the  expenditure  of  energy  must  be  restricted 
and  complete  rest  in  bed  is  the  best  treatment.  The  child  should  see  no 
one  but  her  nurses,  and  do  nothing  all  day.  Toys,  books  and  simple  games 
may  be  allowed  in  mild  cases.  If  there  is  mental  weakness,  delusions  or 
hallucinations,  isolation  is  still  more  essential.  All  patients  recover  most 
quickly  when  removed  from  home  surroundings  and  the  care  of  relatives. 
A  gentle  moral  effect  can  be  exerted  beneficially  by  a  good  nurse. 
Mechanical  restraint  is  injurious.  Bandaging  the  arms  to  the  sides,  or  the 
legs  together,  occasionally  affords  relief.  The  patient  must  not  be  left  alone 
or  in  the  dark.  The  bony  prominences  must  be  protected  and  the  mattress 
put  on  the  floor,  with  raised  padded  sides,  if  the  movements  are  violent. 
Splints  are  rarely  beneficial.  The  child  should  be  amused,  but  not  excited, 
helped  when  necessary,  and  the  movements  disregarded.  Attend  to  all 
•causes  of  reflex  irritation  and  ill-health. 

Sunshine  and  fresh  air  are  advantageous.  Wet  packs  for  several  hours 
are  sedative.  A  hot  pack  for  1  hour  at  night  is  conducive  to  sleep.  In  mild 
and  chronic  cases  the  child  may  have  alternate  hot  and  cold  baths  each 
morning  ;  a  warm  bath  followed  by  a  cold  spinal  douche  ;  or  galvanism 
along  the  spinal  column. 

The  food  must  be  soft,  semi-solid  or  minced,  nutritious  and  easily 
digestible.  Three  pints  of  milk  may  be  given  daily,  and  a  liberal  supply  of 
iron-containing  foods.  Gavage  and  rectal  feeding  are  sometimes  necessary. 
Insufficient  food  is  a  cause  of  sleeplessness  ;  a  full  meal  with  a  little  alcohol, 
given  by  nasal  tube,  is  then  beneficial.  Use  an  enamel  feeding  cup,  as  china 
ones  are  apt  to  be  broken  and  cause  injury.    Keep  the  bowels  open. 

Iron  and  arsenic  are  given  to  combat  the  anaemia.  Arsenic  is  given  in 
large  doses  for  its  supposed  specific  effect.  Probably  the  apparent  benefit 
is  due  to  the  coincidence  of  the  passage  of  the  sthenic  into  the  asthenic  type 
■of  the  disease  or  to  toxasmia.  The  large  doses  sometimes  given  are  unlikely 
to  be  absorbed,  for  the  rapid  emaciation  shows  that  assimilation  is  at  a  low 
ebb.  Fowler's  solution  is  given  in  doses  of  m.  10-15  t.d.s.,  in  plenty  of 
water,  in  the  middle  of  or  immediately  after  a  meal,  and  given  for  a  week, 
unless  vomiting  after  the  medicine  comes  on  and  indicates  intolerance. 
The  patient  must  be  kept  in  bed  and  seen  daily.  A  less  satisfactory  method 
is  to  begin  with  doses  of  m.  3,  and  increase  by  the  addition  of  1  drop  daily 
until  15  or  even  more  are  taken  for  a  dose.  Arsenic  may  give  rise  to  gastric 
irritation,  foul  breath,  coated  tongue,  vomiting  and  diarrhoea,  and  dinginess, 
pigmentation  or  bronzing  of  the  skin.  It  may  also  set  up  herpes  zoster, 
■erythematous  and  vesicular  rashes,  desquamation,  oedema  of  the  eyelids, 
albuminuria,  peripheral  neuritis,  hyperkeratosis  of  the  palms  and  soles,  or 
•even  ascending  paralysis.  The  nervous  symptoms  may  follow  comparatively 
small  doses  and  come  on  after  the  omission  of  the  drug.  They  may  account 
for  the  loss  of  knee  jerks  and  cessation  of  movements. 


842  Chapter  LX. 

Chloral  is  a  most  valuable  drug  in  severe  cases  and  grave  insomnia- 
Give  syrup  of  chloral,  m.  10-20,  every  2-4  hours  according  to  circumstances, 
and  push  it  up  to  the  point  of  inducing  sleep.  Large  single  doses  are 
dangerous.  It  can  be  given  by  rectum.  Phenazone  is  useful  in  some  acute 
cases  without  cardiac  or  rheumatic  complications.  Chlorelone,  in  doses  of 
gr.  5  t.d.s.  for  children  7-12  years  of  age,  is  given  for  2  or  3  days  and  then  in 
half  doses  for  a  like  period.  It  acts  as  a  soporific  and  may  give  rise  to  skin 
eruptions,  exfoliation  of  the  skin  of  the  hands  and  feet,  loss  of  deep  reflexes- 
and  drowsiness. 

Among  other  drugs  may  be  mentioned  bromate  of  camphor  gr.  3-6 
t.d.s.  ;  bromide  of  zinc  ;  bromides  and  belladonna  ;  belladonna  in  large 
doses,  combined  with  potassium  acetate  if  there  is  any  puffiness  of  the 
eyelids  or  deficient  secretion  of  urine  ;  phenacetin  and  exalgin.  As  seda- 
tives trional  or  sulphonal  grs.  5  t.d.s.  ;  hyoscin.  hydrobrom.  sub  cutem  for 
mania  ;  morphine  for  severe  restlessness,  and  even  inhalations  of  chloro- 
form. Apomorphine  gr.  lio-srr  su^  cutem  may  be  tried  if  all  else 
fails.  Ext.  ergotse  liq.  m.  20-60  every  3  or  4  hours,  with  or  without 
liq.  strychn.  m.  1-2,  is  recommended  by  Eustace  Smith.  Trousseau  also 
gave  strychnia.  D.  B.  Lees  is  an  enthusiast  for  huge  doses  of  salicylate  of 
soda  combined  with  double  the  quantity  of  an  alkali.  The  beneficial  effects- 
may  be  fallacious  because  of  the  general  malaise  induced  by  the  drug. 
He  recommends  sod.  salicyl.  grs.  20  and  sod.  bicarb,  grs.  40  every  3  hours. 
To  children  6-10  years  old  he  gives  10  half-doses  at  intervals  of  2  hours,, 
increasing  it  in  2  or  3  days  to  three-fourths,  and  in  another  2  or  3  days- 
to  the  full  dose.  It  is  important  that  the  bowels  should  be  kept  open.  It  is- 
probable  that  these  large  doses  are  not  absorbed,  and  the  consequent 
danger  to  the  child  is  reduced.  The  signs  of  poisoning  are  acetone  in  the 
breath  and  urine,  air-hunger,  thirst,  vomiting,  delirium,  drowsiness,  coma 
and  death.  In  my  experience  anti-rheumatic  treatment,  even  on  this 
vigorous  scale,  is  not  particularly  beneficial,  but  salicylates  should  be 
given  if  there  is  any  evidence  of  rheumatism.  In  mild  cases  I  prefer  to  rely 
on  rest,  liberal  feeding,  good  hygiene  and  nursing,  moderate  doses  of 
arsenic  or  arsenic  and  iron,  and  cod-liver  oil  and  hypophosphites  during 
convalescence.  In  severe  ones  chloral  and  chloretone  are  perhaps  the  most 
efficacious  drugs. 

In  asthenic  and  paralytic  cases,  and  acute  cases  with  heart  complica- 
tions, similar  treatment  is  adopted  but  stimulants  and  tonics  are  required 
rather  than  sedatives.  Brandy,  digitalis,  caffeine,  and  strychnine  or  nux: 
vomica,  are  necessary  in  cardiac  failure. 

Massage  can  be  used  early  in  mild  cases,  with  passive  motions  as  soon 
as  the  child  is  sufficiently  calmed.  It  is  very  useful  in  convalescence.  At 
this  period  the  improvement  in  co-ordination  will  be  more  rapid,  if  the 
child  is  encouraged  in  moderate  use  of  the  hands.  At  first  she  should  be 
taught  by  suggestion  to  keep  the  limbs  still.     This  may  be  followed  by 


Chorea.  84$ 

passive  movements,  voluntary  movements  under  guidance,  and  voluntary- 
ones  without  such  guidance.  The  usual  simple  games  and  toys,  a  solitaire 
board  and  bricks,  etc.,  are  all  that  is  necessary  in  the  way  of  apparatus. 
Later,  threading  beads,  drawing  and  sewing  should  be  practised.  Super- 
vision is  necessary  or  the  child  gets  careless  and  a  state  of  residual  chorea, 
due  to  lack  of  attention,  remains  behind.  For  this,  drill  and  general* 
supervision  are  required. 


Chapter  LXL 

TUBEKCULOSIS. 

The  Bacillus — Mode  of  Infection — Age- Incidence — Varieties — Miliary  or 
General  Tuberculosis — Tuberculous  Broncho-pneumonia  and  Pneu- 
monia—  Chronic  Phthisis. 

Tuberculosis  is  dependent  on  the  activity  of  the  tubercle  bacillus  in  a 
soil  rendered  suitable  for  its  growth  by  virtue  of  an  inherited  debility  or 
peculiarity  of  structure  or  by  modification  of  the  tissues  as  the  result  of 
■environment  or  disease.  It  is  general  or  local.  Its  course  varies  from  extreme 
acuteness  and  a  fatal  issue  to  marked  chronicity  or  recovery.  It  is  a  truly 
•acquired  disease,  and  may  be  acquired  in  utero,  through  placental  infection 
{p.  22).  Germinal  infection  is  incredible,  in  spite  of  the  evidence  afforded 
by  Friedmann's  experiments.  He  injected  tubercle  bacilli  into  the  vaginae 
of  guinea  pigs  after  coitus.  At  the  end  of  1  week  the  bacilli  were  found  in  the 
foetuses  though  the  mothers  were  healthy.  Many  cases  of  Congenital  or 
Foetal  Tuberculosis  are  on  record  (40  human,  100  bovine  ;  Huss).  Trans- 
mission by  this  means  is  not  very  frequent.  The  calves  of  tuberculous  cows 
■do  not  react  to  tuberculin,  and  remain  well  if  they  are  separated  from  the 
mother  and  brought  up  under  healthy  conditions.  Many  children  of 
tuberculous  parents  remain  healthy  when  separated  from  them.  Inheri- 
tance of  tuberculosis  must  be  limited  to  the  transmission  of  a  suitable  soil, 
a  special  proclivity.  Of  this  there  is  no  reliable  proof,  and  indeed  there  is 
a  certain  amount  of  evidence  in  favour  of  inherited  immunity.  Probably 
the  special  proclivity  is  not  a  peculiarity  but  merely  dependent  on  general 
debility  from  tuberculous  as  well  as  other  causes. 

The  predisposing  factors  include  all  the  causes  of  lowered  vitality. 
€hief  among  these  are  lack  of  maternal  nursing,  insufficient  or  improper 
iood,  lack  of  fresh  air  and  sunlight,  unsatisfactory  clothing,  dirt,  dust  and 
bad  hygienic  conditions  generally,  and  digestive  and  pulmonary  troubles. 
Mouth  and  throat  affections,  enlarged  tonsils  and  adenoids,  and  neglected 
teeth  are  liable  to  induce  cervical  adenitis  and  render  the  glands  more 
prone  to  infection.  Measles,  pertussis,  influenza  and  bronchitis  have  a 
similar  effect  on  the  thoracic  glands.  In  babies  and  infants  there  is  great 
susceptibility,  just  as  there  is  to  other  infections.  The  excess  of  pharyngeal 
lymphoid  tissue  affords  a  suitable  soil  for  the  deposition  and  growth  of  the 
bacillus.    The  disease  is  often  of  slow  development.    The  infection  may  be 


Tuberculosis.  845- 

acquired  in  infancy  or  in  utero,  to  a  mild  extent,  and  may  remain  latent 
for  years. 

The  Bacillus. — Different  varieties  are  described  as  bovine,  human  and 
avian.  The  disease  can  occur  in  fishes.  Carp  in  a  pond  were  infected  by 
tuberculous  sputa  and  dejecta  (Dubar,  Bataillon  and  Terri,  1898).  The 
liver  and  spleen  were  found  full  of  tubercle  bacilli.  Apparently  they  were 
attenuated  by  cultivation  in  a  cold-blooded  creature,  for  inoculation  into 
fowls  and  rabbits  proved  negative.  The  avian  bacillus  is  a  modified 
descendant  from  a  common  ancestor.  It  affects  the  abdominal  organs  and 
lungs  of  all  kinds  of  birds,  caged  and  wild  ;  and  is  conveyed  by  infected 
food,  inhalation  and  inoculation.  Both  the  human  and  bovine  bacillus 
may  affect  caged  birds  to  a  limited  degree.  The  human  bacillus  cannot  be 
converted  into  the  avian  bacillus  by  passage  through  birds.  Of  more 
importance  is  the  question  of  identity  of  the  human  and  the  bovine  bacilli. 

Moller  states  that  there  are  9  acid-fast  bacilli  which  stain  like  the 
tubercle  bacillus.  Those  found  in  smegma,  butter  and  timothy  grass  are 
the  most  important.  The  smegma  bacillus  is  more  rapidly  decolorised  by 
alcohol  and  acids  than  the  tubercle  bacillus.  The  best  differential  test  is 
intra-peritoneal  inoculation  of  guinea  pigs.  Morphology,  cultural  characters 
and  virulence  depend  greatly  on  environment.  The  bovine  bacillus  may 
undergo  metamorphosis  into  the  human  type  in  the  human  body.  It  is 
usually  shorter,  thicker,  more  irregular,  and  stains  less  uniformly  than  the 
human  variety,  but  its  characters  vary  with  the  change  in  culture  media 
and  are  of  minor  importance.  Culturally  the  bovine  organism  is  more 
stabile  in  character,  grows  more  slowly  and  with  greater  difficulty.  Accord- 
ing to  Calmette  and  Guerin  it  grows  well  in  the  presence  of  glycerinated  ox 
bile,  whereas  the  human  bacillus  does  not  grow.  Bacilli  in  all  respects 
identical  with  the  bovine  bacillus  can  be  obtained  from  human  tuberculosis. 
Those  of  human  type  can  be  converted  into  the  bovine  type  by  "  passage  " 
experiments.  They  are  therefore  grades  of  the  same  species,  growing  less 
freely  on  human  soil.  The  bovine  bacillus  is  the  more  virulent  one  and 
produces  general  tuberculosis  in  guinea  pigs,  rabbits,  pigs,  goats,  bovines 
and  apes.  The  virulence  of  the  human  bacillus  can  be  increased  by  passage 
through  calves,  rabbits  and  cats.  Bovine  tuberculosis  can  be  produced  in 
various  animals  by  inoculation  with  the  human  organism,  and  there  is  no 
distinguishing  features  between  the  tuberculosis  produced  by  these 
organisms  (Report  of  the  Royal  Commission,  1904).  Many  of  the  con- 
tradictory results  of  animal  inoculation  with  the  human  bacillus  have  been 
due  to  insufficient  dosage,  for  undoubtedly  it  is  much  less  virulent  than  the 
bovine  organism.  It  is  merely  a  question  of  dosage  and  susceptibility  of  the 
particular  animals  used  for  experiment.  The  Royal  Commission  found  that 
the  human  bacillus  produced  general  tuberculosis  in  guinea  pigs,  monkeys 
and  anthropoid  apes  ;  and  limited  lesions  in  oxen,  rabbits,  pigs  and  goats. 
The    bovine    bacillus,    even    if    of    human    origin,     caused    generalised 


•846  Chapter  LXI. 

tuberculosis  in  bovines  and  monkeys.  The  bovine  organism  is  more  frequent 
in  children  than  in  adults,  and  is  said  by  some  observers  to  be  almost  limited 
to  children  under  10  years  of  age.  It  chiefly  affects  the  abdomen  and 
glands.  In  this  connection  it  is  interesting  that  animals  are  practically 
immune  from  the  adult  type  of  phthisis,  and  that  adults  rarely  have 
•caseous  mesenteric  glands  unless  there  is  intestinal  ulceration.  Children 
often  have  such  glands,  and  are  less  liable  to  the  adult  type  of  phthisis. 
It  is  curious,  if  true,  that  the  virulent  bovine  organism  is  apt  to  cause 
generalised  infection  or  a  localised  glandular  one,  and  that  the  milder 
human  bacillus  is  more  likely  to  set  up  pulmonary  tuberculosis  of  the 
chronic  excavating  type. 

Mode  of  Infection. — The  disease  may  be  introduced  by  the  placental 
circulation  ;  inoculation  of  the  skin,  mucous  membranes  or  subcutaneous 
tissues ;  the  alimentary  or  the  respiratory  tract.  Contagion  in  the  home 
is  common  in  infancy  and  early  childhood.  The  infection  is  conveyed  by 
kissing,  coughing,  infected  handkerchiefs,  etc.,  from  a  phthisical  parent  or 
nurse  ;  by  creeping  on  the  floor  and  absorbing  infected  dust ;  through  the 
food  supply,  or  even  from  a  midwife.  Reich  (1878)  reported  a  remarkable 
instance.  Two  midwives  divided  between  them  the  obstetric  practice  of  a 
town  of  1300  people.  Both  practised  mouth  to  mouth  aspiration  and 
blowing  into  the  nose  of  the  newborn.  One  was  tuberculous  and  within 
14  months  10  of  her  infants  died  from  tuberculous  meningitis.  Those  under 
the  other  midwife  were  unaffected.  Infected  dust  is  conveyed  by  the 
fingers  to  the  mouth  or  nose,  especially  in  the  second  year  of  life  during  the 
crawling  stage.  Dieudonne  of  Wurzburg  (1903)  examined  the  dirt  on  the 
hands  and  the  nasal  secretion  of  children,  aged  9  months  to  3i  years,  and 
found  tubercle  bacilli  almost  always  present.  The  results  were  confirmed 
by  inoculation  of  guinea  pigs.  Numerous  experiments  have  shown  that  in 
coughing  and  loud  speaking  droplets  of  spray  containing  tubercle  bacilli 
are  disseminated.  It  is  obvious  that  the  liability  to  infection  is  great,  if 
a  child  of  susceptible  age  is  brought  in  contact  with  a  case  of  open  tubercu- 
losis, and  that  the  utmost  precautions  must  be  adopted  to  prevent  this 
mode  of  infection. 

Accidental  infection  of  a  wound  by  sputa  and  tuberculous  inoculation 
of  a  circumcision  wound  are  rare  occurrences.  The  two  great  channels  of 
infection  are  the  alimentary  tract  from  the  lips  to  the  anus,  inclusive  of  the 
tonsils  and  pharynx,  and  the  respiratory  tract.  The  impossibility  of 
separating  these  two  systems  in  the  mouth  and  naso-pharynx  has  led  to 
great  difficulty  in  ascertaining  whether  infection  is  alimentary  or  respiratory 
in  origin.  Tubercle  bacilli  in  air  inspired  through  the  mouth  may  be 
deposited  on  the  mucous  membrane  and  cause  local  infection,  enter  the 
lymphatics  or  blood  stream  without  causing  a  local  lesion,  or  be  swallowed. 
Admission  of  the  occurrence  of  intestinal  infection  does  not  logically  lead 
to  the  assumption  that  the  infection  is  of  bovine  and  not  of  human  origin. 


Tuberculosis.  847 

The  frequent  introduction  of  the  bovine  organism  into  the  human  body 
may  have  an  immunising  effect  or  may  perpetuate  the  disease.  The  matter 
ns  of  great  importance  in  view  of  the  opinion  held  by  many  that  infected 
milk  is  the  chief  cause  of  tuberculosis  in  children. 

Sociological  Considerations. —  If  milk  infection  is  the  main  ca\1se,  the 
•disease  should  be  most  prevalent  among  children  brought  up  on  cow's  milk 
and  least  among  the  breast-fed.  Kitasato  states  that  the  cattle  in  Japan 
•do  not  suffer  from  tuberculosis.  The  infants  are  suckled  for  2-3  years  and 
•cow's  milk  is  little  used  for  infants.  Yet  tuberculosis,  including  the  intes- 
tinal type,  is  as  common  in  children  and  adults  as  in  other  countries.  In 
India  infants  are  suckled  2-3  years.  Tuberculosis  is  rare  in  cattle,  and  all 
milk  is  boiled  and  butter  converted  into  "  ghi "  before  use.  Glandular, 
peritoneal  and  pulmonary  tuberculosis  are  rare.  Infants  are  suckled  2-3 
years  in  Egypt,  and  both  glandular  and  peritoneal  tuberculosis  are  rare. 
In  China  artificial  feeding  of  infants  is  unknown,  yet  tuberculosis  is  very 
prevalent.  In  Bohemia  Biedert  found  that  the  incidence  of  phthisis  varied 
•directly  as  the  density  of  population,  although  the  urban  dairies  were 
under  better  control.  Heller  found  intestinal  tuberculosis  more  prevalent 
round  Kiel  than  in  Berlin  where  milk  is  boiled  or  pasteurised.  These 
observations,  except  as  regards  Japan  and  China,  are  not  of  great  assistance. 
They  suffice  to  show  that  milk  infection  is  not  always  the  cause  and  suggest 
that  it  is  not  the  chief  cause.  Tuberculosis  is  more  common  among  the  poor 
than  the  better  classes,  although  they  use  less  milk.  It  may  be  that  they 
•obtain  inferior  and  contaminated  milk  and  that  it  is  given  uncooked.  On 
the  other  hand  the  possibilities  of  direct  infection  are  much  greater  among 
the  poor  ;  and  there  are  many  cases  of  infantile  tuberculosis  in  all  classes 
in  which  the  child  has  never  taken  cow's  milk  in  any  form.  In  9  out  of  17 
•successive  hospital  patients  under  1  year  old  there  was  strong  reason  to 
suppose  that  infection  was  direct. 

MilJc  Infection. — Stress  has  been  laid  on  the  frequency  of  tuberculosis 
in  cattle  and  of  bacilli  in  the  milk.  It  is  stated  that  2  per  cent,  of  all  milk 
cows  in  England  have  tuberculous  udders  and  that  50  per  cent,  show  some 
tuberculous  lesion  in  the  carcase.  Klein  found  tubercle  bacilli  in  7  out  of 
86  samples  of  London  milk  examined  in  the  years  1901-1906.  There  is  no 
•doubt  that  cows  are  liable  to  disease  of  the  udder,  that  tubercle  bacilli 
are  not  infrequent  in  milk,  and  that  they  may  be  present  although  there 
is  no  udder  affection,  even  in  large  numbers.  The  bacilli  may  be  numerous 
in  the  fseces  of  affected  cows. 

According  to  the  Beport  of  the  Boyal  Commission  (1907)  tuberculosis, 
■especially  in  children,  is  in  certain  cases  the  direct  result  of  infection  by  the 
bovine,  bacillus  and  in  most  of  them  the  infection  is  carried  by  the  milk. 
Cow's  milk  containing  the  bovine  bacillus  is  clearly  a  cause  of  tuberculosis. 
A  very  large  proportion  of  tuberculosis  contracted  by  ingestion  is  due  to  the 
bovine  bacillus.     Tuberculous  cow's  milk  ought  never  to  be  used  as  food. 


848  Chapter   LXI. 

These  conclusions  were  based  on  feeding  experiments  which  showed  the 
bacillus  highly  pathogenic  to  animals  in  the  following  descending  order  : — 

(1)  Chimpanzee,  baboon,  rhesus  monkey,  lemur,  rabbit  and  guinea  pig  ; 

(2)  Pig,  goat,  calf,  cat  and  dog,  the  adults  being  less  susceptible  than  the 
young  ;  (3)  Rats  and  fowls  apparently  insusceptible.  A  remarkably  small 
dose  was  needed  for  anthropoid  apes.  The  infection  may  be  localised  in  the 
mucosa,  may  leave  no  local  trace  and  pass  into  the  glands,  or  may  quickly 
reach  the  lungs  although  there  is  no  trace  in  the  mucosa  or  glands.  The 
bronchial  glands  are  almost  invariably  affected  after  the  lungs,  sometimes 
alone. 

Von  Behring  maintains  that  the  disease  in  adults  is  due  to  the  recru- 
descence of  infection,  latent  since  infancy,  and  that  it  is  the  result  of  the 
ingestion  of  tuberculous  milk  in  infancy.  Caseous,  calcified  and  healed 
fibrous  foci  are  frequently  found  after  death  from  all  causes,  according  to 
Naegeli  in  97  per  cent.  If  the  resistance  is  lowered  from  any  cause,  a  latent 
tuberculous  process  may  become  active  and  disseminated.  But  there  are 
other  sources  of  infection  as  well  as  milk. 

Feeding  experiments  must  be  carried  out  with  great  care,  in  order  to 
exclude  the  possibility  of  infection  via  the  tonsils  and  pharynx.  Calmette 
and  Guerin  (1905)  inoculated  the  udders  of  goats  through  the  milk  ducts 
with  human,  bovine,  avian  and  timothy  grass  bacilli.  Those  inoculated 
with  the  last  two  organisms  did  not  react  subsequently  to  tuberculin, 
nor  did  their  kids  develop  tuberculosis.  The  bovine  bacillus  proved  fatal 
in  less  than  2  months,  though  there  was  little  extension  beyond  the  udder. 
Their  kids  showed  extensive  infiltration  of  the  mesenteric  glands.  Those 
inoculated  with  the  human  bacillus,  and  their  kids,  were  less  severely 
affected. 

Infective  material  was  introduced  by  tube  into  the  rumen  of  goats  and 
kids.  The  bovine  bacillus  set  up  acute  dissemination  in  kids  in  the 
mesenteric  glands,  lungs  and  mediastinal  glands ;  in  one,  the  lesions  were 
limited  to  the  mesenteric  glands.  In  the  adult  goats  extensive  pulmonary 
mischief  was  induced,  with  little  affection  of  the  mesenteric  glands.  This 
suggests  that  pulmonary  phthisis  in  the  adult  is  of  intestinal  origin  and  that 
the  glands  have  less  protective  power  than  in  earlier  life.  Similar  experi- 
ments by  Whitla  and  Symmers  of  Belfast  (1908)  on  anthracosis,  by  the 
introduction  of  carbon  particles  into  the  intestine,  showed  that  the  lungs 
were  more  readily  infected  in  adult  animals  and  that  in  the  young  the 
mesenteric  glands  acted  as  a  barrier.  These  glands  should  therefore  be 
often  infected  in  children. 

These  and  other  experiments  show  that  the  tracheo-bronchial  glands 
and  lungs  can  be  infected  by  ingested  tubercle  bacilli,  without  any  infection 
of  the  intestinal  tract.  It  must  be  noted  however  that  the  pulmonary  lesions 
are  miliary  in  type,  a  general  tuberculosis,  and  not  like  those  of  chronic 
phthisis. 


Tuberculosis.  849 

A  local  lesion  is  not  essential.  In  feeding  experiments  the  cervical 
glands  of  the  pig  become  tuberculous  although  there  is  no  lesion  of  the 
mucous  membrane.  The  mesenteric  glands  of  guinea  pigs  and  other 
animals  become  infected  apart  from  local  mischief.  Tubercle  bacilli  have 
been  found  in  tonsils  with  an  unimpaired  mucosa.  Sputum  rubbed  on  the 
nasal  mucosa  of  animals  produces  tuberculosis  but  no  local  lesion.  It  is  a 
curious  fact  that  intestinal  ulceration  shows  little  tendency  to  dissemination 
and  may  be  very  extensive  without  any  caseation  of  the  mesenteric  glands. 
The  ulcers  are  probably  due  to  infection  carried  by  the  blood  or  lymph. 
The  small  tuberculous  ulcers  found  in  the  stomach  are  almost  undoubtedly 
due  to  this  mode  of  infection  and  not  to  infection  by  ingested  bacilli.  These 
glands  frequently  contain  virulent  bacilli.  MacFadyen  and  MacConky 
(1903)  examined  the  glands  of  20  non-tuberculous  and  8  tuberculous 
children,  26  under  2  years  of  age.  The  mesenteric  glands  yielded  virulent 
bacilli  in  5  tuberculous  and  5  non-tuberculous  cases,  though  in  7  of  the  10 
microscopic  examination  of  the  glands  was  negative.  They  also  found  the 
organism  in  the  glands  of  a  still-born  child. 

We  must  conclude  that  the  bacillus  can  pass  through  the  stomach 
uninjured,  probably  more  readily  in  infants  because  of  the  deficiency  of 
HC1.  The  intestines  show  no  local  lesion.  The  mesenteric  glands  may 
appear  healthy  under  the  microscope  yet  may  contain  virulent  bacilli. 
The  organisms  reach  the  thoracic  duct,  the  vena  cava  superior,  the  right 
side  of  the  heart,  and  are  distributed  to  the  lungs.  Oberwarth  and 
Rabinowitch  (1908),  by  inserting  bovine  bacilli  through  a  gastric  fistula 
with  the  oesophagus  closed  in  sucking  pigs,  brought  forward  evidence  that 
the  bacilli  pass  into  the  blood,  lungs  and  other  viscera  in  22  hours.  Such  a 
result  may  be  possible  in  infants.  If  the  organisms  are  not  detained  in  the 
lungs,  they  will  pass  to  the  left  side  of  the  heart  and  may  reach  the  meninges, 
setting  up  meningitis,  and  thus  account  for  those  cases  in  which  no 
tuberculous  focus  is  found. 

The  bacilli  can  be  detected  in  the  chyle  of  dogs  within  3-4  hours  of 
ingestion.  Nicholas  and  Dercas  found  the  chyle,  collected  from  the 
thoracic  ducts  of  guinea  pigs  fed  on  an  emulsion  of  bacilli,  was  fatal  to 
dogs.  Ravenal  fed  dogs  on  the  bacilli  through  a  stomach  pump  and  found 
the  organisms  subsequently  in  the  chyle  and  glands.  Similarly  the  bacilli 
have  been  found  in  the  lung  capillaries  after  the  ingestion  of  tuberculous 
food.  From  the  evidence  it  may  be  justly  concluded  that  the  ingestion  of 
tubercle  bacilli  is  a  cause  of  tuberculosis  in  the  thorax. 

Tuberculosis  has  decreased  greatly  in  the  last  50  years,  except  in  the 
early  years  of  life.  This  is  somewhat  in  favour  of  milk  infection.  Although 
the  infectivity  of  such  milk  must  be  admitted,  it  may  not  be  so  great  as 
commonly  supposed,  for  there  are  numerous  other  modes  of  infection. 
Alimentary  infection  is  not  necessarily  from  milk.  It  is  quite  likely  that 
many  children  receive  a  mild  bovine  infection  and  are  thereby  protected  or 

3    i 


850  Chapter  LXI. 

rendered  immune.  Mild  infections  must  be  very  common,  for  the  specific 
organism  is  widely  distributed.  It  is  impossible  to  state  definite  distinctive 
features  between  a  tuberculosis  of  bovine  and  one  of  human  origin.  The 
bovine  bacillus  is  more  virulent  for  all  animals  and  perhaps  for  the  child. 
The  number  of  bacilli  which  get  into  the  system  must  be  taken  into  account. 
The  large  number,  due  to  contact  with  a  dirty  phthisical  patient  in  un- 
hygienic surroundings,  do  much  more  damage  than  a  few  scattered  through- 
out a  milk  supply.  The  milk  may  be  contaminated  by  human  tubercle 
bacilli. 

Air- Injection. — The  bacillus  is  conveyed  by  spray,  dust  or  direct 
contact.  One  c.c.  of  sputum  may  contain  a  million  bacilli  (Bollinger) 
and  a  single  patient  may  expectorate  4000  million  in  24  hours  (Nuttall). 
Fortunately  many  are  dead,  but  it  is  obvious  that  the  risk  of  infection  from 
contact  with  a  case  of  open  phthisis  is  considerable,  especially  among  the 
poor  and  unclean.  The  inspired  bacilli  are  deposited  on  the  mucosa  of  the 
naso-pharynx,  mouth,  tonsils,  larynx,  trachea  or  large  bronchi.  There  is 
no  certain  proof  of  direct  infection  of  the  lungs  by  inspired  air.  Inhalation 
of  the  bacilli  into  the  alveoli  is  most  improbable,  if  not  impossible.  Vallee 
found  calves  very  little  susceptible  to  direct  infection  of  the  trachea  or  naso- 
pharynx. The  inhalation  of  carbon  particles  does  not  apparently  cause 
antbracosis,  if  the  oesophagus  be  tied.  On  the  other  hand  inhalation 
experiments  on  animals  usually  cause  lesions  of  the  lungs  and  bronchial 
nodes  only  ;  possibly  through  ingested  bacilli.  Against  the  inhalation 
theory  it  maybe  pointed  out  that, although  infants  and  young  children  are 
extremely  susceptible,  primary  tuberculosis  of  the  larynx  or  bronchi  is 
almost  unknown.  Air-infection  probably  means  that  the  bacillus  enters 
through  the  mucous  membrane  of  the  throat  or  alimentary  tract.  Direct 
infection  of  the  lungs  is  negligible. 

Tonsillar  Infection. — The  tonsils,  adenoid  tissue  of  the  pharynx, 
and  cervical  glands  are  frequently  affected.  Possibly  in  chronic  phthisis 
they  are  coincident  and  not  the  primary  source  of  infection.  The  frequency 
of  tuberculosis  of  the  tonsils  has  been  considered  (p.  237.)  Cervical  adenitis 
does  not  prove  infection  through  the  mucous  membrane  of  the  mouth  or 
pharynx.  Calmette,  Guerin  and  Breton  infected  the  deep  cervical  glands  of 
guinea  pigs  by  the  introduction  of  bacilli  into  the  stomach.  The  whole 
lymphatic  system,  as  well  as  the  lungs,  can  be  thus  infected.  Grober  claims 
to  have  demonstrated  a  direct  route  from  the  tonsils,  through  the  cervical 
lymph  nodes,  to  the  lungs  and  pleura.  A.  Most  made  careful  injection 
experiments  with  coloured  liquids  and  seems  to  have  proved  that  there  is  no 
anastomosis  between  1he  cervical  and  subclavian  lymphatics  and  those 
of  the  pleura  and  mediastinum  ;  and  none  between  the  lymphatics  of  the 
mesentery,  liver  and  diaphragm  and  those  of  the  pleura  and  mediastinum. 
Tuberculous  infection  from  cervical  glands  takes  place  via  the  thoracic 
duct  and  blood  stream. 


Tuberculosis.  851 

Post  mortem  Evidence. — Only  a  limited  amount  of  importance  can  be 
.attached  to  the  apparent  age  of  a  tuberculous  focus,  as  indicative  of  the 
primary  source  of  infection.  It  may  have  completely  healed  and  the 
■disease  be  due  to  further  infection.  Localisation  of  the  lesion  affords 
little  evidence  of  the  portal  of  entry.  There  may  be  no  local  lesion  and  the 
iocus  situated  in  some  distant  region  from  the  point  of  entry  of  the  bacillus. 
Buhl  stated  100  years  ago  that  there  is  no  phthisis  without  an  antecedent 
•caseous  focus.  Certainly  it  is  extremely  rare  not  to  fmd  such  a  focus, 
if  the  autopsy  is  done  thoroughly.  In  children  there  is  a  remarkable 
tendency  to  infection  of  the  lymph  nodes.  After  the  third  year  cervical 
.adenitis  may  be  the  first  or  the  only  sign  of  infection.  The  thoracic  glands 
are  peculiarly  liable,  especially  those  on  the  right  side  and  the  pre-tracheal 
gland.  Although  these  glands  may  be  large  and  caseous,  it  is  possible 
that  general  tuberculosis  is  due  to  further  alimentary  infection.  For  the 
symptoms  of  tuberculosis  of  thoracic  and  mediastinal  glands,  vide  p.  520-523. 
Different  observers  have  found  the  thoracic  glands  tuberculous  in  73-100 
per  cent,  and  the  mesenteric  ones  affected  in  35-78  per  cent.  The  disease 
is  much  more  often  limited  to  the  thorax  than  the  abdomen. 

It  is  clearly  established  that  the  thoracic  glands  are  often  alone  involved 
.and  much  more  frequently  than  the  mesenteric.  Possibly  the  former  are 
more  susceptible  or  more  perfect  filters.  Bollinger  injected  tuberculous 
sputum  into  the  peritoneal  cavity  and  found  that  the  peritoneum  remained 
sound  in  two-thirds,  though  the  lungs  became  tuberculous.  And  much  experi- 
mental evidence  shows  that  these  glands  can  be  infected  by  organisms  carried 
from  the  intestines,  without  evidence  of  disease  in  the  intestinal  mucosa 
■or  the  mesenteric  glands.  In  most  cases  there  is  an  isolated  caseous  area 
in  the  lungs  and  the  corresponding  gland  is  the  one  affected.  The  disease 
is  primarily  pulmonary,  though  the  local  lesion  may  be  healed,  healing,  or 
■even  undiscoverable.  Possibly  in  a  few  instances  the  bacillus  has  been 
(Conveyed  to  the  glands  without  causing  local  mischief  in  the  lungs.  The 
■cervical  glands  are  affected  in  80-100  per  cent,  of  fatal  cases. 

The  lungs  are  constantly  affected  to  some  extent.  Froebelius  gives 
the  order  of  frequency  of  the  pathological  changes  in  infants,  aged  1-4 
.months,  as  : — lungs,  bronchial  glands,  liver,  spleen,  intestines,  meninges, 
kidneys,  mesenteric  glands,  heart  and  pericardium,  pleura  and  upper  air 
passages.  Occasionally  the  tonsils,  pharynx,  middle  ear,  skin,  bones 
and  joints  are  attacked.  The  lungs  were  infected  in  78  per  cent,  of  269  cases 
ainder  12  years  (Still)  ;  in  96  per  cent,  of  54  deaths  under  13  years  (Pendle- 
bury  Hospital)  ;  in  all  of  72  children  under  2  years  (Holt).  These  figures 
are  enough  to  show  the  extreme  frequency  of  lung  infection.  Cavities  may 
be  of  considerable  size,  even  under  6  months  of  age.  In  none  of  933  fatal 
-cases  did  Baginsky  find  the  lungs  alone  involved. 

Primary  Intestinal  Tuberculosis. — Accepting  as  primary  intestinal  tuber- 
culosis only  those  cases  in  which  the  lesion  was  limited  to  the  intestinal 


852  Chapter  LXI. 

mucosa  or  the  mesenteric  glands,  with  no  trace  in  the  lungs  or  bronchial! 
glands,  Albrecht  only  found  7  in  1060  autopsies  on  tuberculous  children 
under  12  years.  Other  observers  include  cases  in  which  the  lesions  are 
extensive  and  of  old  standing,  with  fresh  foci  elsewhere  ;  and  those  in  which 
the  disease  is  so  far  advanced,  in  comparison  with  that  in  other  foci  present,, 
as  to  be  probably  of  an  earlier  date.  But  the  site  of  the  oldest  lesion  is  not 
always  the  source  of  recent  infection.  Nor  is  a  more  advanced  focus- 
necessarily  an  earlier  one.  Consequently  statistics  based  on  these  data  are 
not  of  much  value  as  evidence  of  primary  intestinal  infection.  In  England 
they  are  given  as  18-25,  Berlin  1-5-25,  France  2-5,  and  America  3  per  cent. 
Councilman  of  Boston  regarded  37  per  cent,  of  tuberculous  cases  as 
abdominal.  Certainly  primary  intestinal  ulceration  is  rare.  Raw  found 
only  3  cases  in  600  autopsies  at  all  ages,  and  all  under  3  years  of  age- 
Intestinal  ulceration  is  not  necessarily  bovine.  It  may  be  absent  though 
the  lungs  are  diseased  and  much  sputum  is  swallowed.  Snow  reported  a 
case  in  a  3-months  old  baby,  the  infection  having  been  acquired  from  a  con- 
sumptive nurse.  Apparently  abdominal  tuberculosis  is  much  more  frequent- 
in  Glasgow  and  Edinburgh  than  it  is  in  English  or  Continental  cities. 

General  infection  is  usually  the  result  of  ulceration  of  pulmonary 
vessels  by  a  caseous  focus,  possibly  in  the  adventitia.  or  through  the 
thoracic  duct.  A  more  localised  infection  may  arise  from  the  breaking  down 
of  a  small  focus  and  ulceration  into  the  lumen  of  an  artery.  The  tuberculous, 
toxin  destroys  the  cellular  and  interstitial  tissue,  and  modifies  the  growth  of 
the  cells,  producing  spindle  and  giant  cells.  Finally  the  newly  formed  cells 
undergo  cheesy  degeneration. 

Age-Incidence. — The  disease  is  much  more  frequent  in  early  infancy 
than  commonly  supposed.  Out  of  a  series  of  127  autopsies  at  the  Belgrave 
Hospital  for  Children,  on  infants  under  1  year  old,  17  were  tuberculous, 
5  of  them  under  6  months.  Of  54  cases  of  tuberculous  meningitis  under 
5  years  old,  10  were  under  1  year.  Froebelius  found  that  4  per  cent,  of 
18.569  autopsies,  on  infants  dying  between  1  and  4  months  of  age  in  the 
St.  Petersburg  Infant  Asylum,  were  tuberculous  and  that  in  all  the  lungs- 
were  involved.  Post  mortem  evidence  shows  its  existence  in  2-6  per  cent. 
of  infants  under  3  months  ;  10-15  per  cent,  in  the  first  year  ;  and  25-40- 
per  cent,  under  15  years  of  age.  These  are  by  no  means  constant  figures, 
being  sometimes  considerably  lower,  e.g.  11  per  cent,  under  15  years- 
(Orth),  sometimes  higher,  e.g.  58  per  cent.  (Fibiger).  Ghon  found  no  healed 
lesion  under  3  years  of  age.  Of  110  cases  60  per  cent,  died  from  tuberculous 
meningitis,  and  in  64  out  of  67  it  was  secondary  to  tuberculosis  of  some 
other  organ  ;  23  died  from  miliary  tuberculosis  ;  27  showed  lesions  such  as 
are  seen  in  adults  ;  none  were  primarily  intestinal  and  in  only  4  were  the. 
mesenteric  glands  affected. 

The  mortality  statistics  of  the  presence  of  tuberculous  foci  show  that 
the  disease  increases  in  frequency  but  diminishes  in  severity  as  age  advances.. 


Tuberculosis.  853 

Both  autopsieo  and  tests  during  life  prove  that  it  is  less  frequent  during  the 
first  2  years  than  later.  The  mortality  is  greatest  during  the  first  2  years, 
being  highest  in  the  second  year,  because  of  the  danger  of  home  infection 
.and  the  liability  to  general  tuberculosis  and  meningitis.  In  conjunction 
with  the  fact  that  the  disease  is  common  in  countries  in  which  cow's  milk  is 
not  tasted,  this  is  an  argument  against  milk  infection.  But  in  those  places 
in  which  cow's  milk  is  used  the  frequency  of  fatal  tuberculosis  in  the  first 
4  years  of  life,  the  age  of  milk  feeding,  is  an  argument  in  favour  of  milk 
infection.  After  2  years  of  age  tuberculosis  accounts  for  about  half  the 
•deaths  in  children,  but  the  mortality  from  all  causes  is  small  at  this  period 
•of  life. 

Percentage  Age — Incidence  of  Tuberculosis  fatal  under  4  years. 


No.  of  cases. 

1st, 

2nd. 

3rd. 

4th. 

Brandenberg 

203 

18 

42 

21 

19 

Kinssford 

243 

29 

37 

22 

12 

Of  Kingsford's  324  cases  (Lancet,  1904)  under  10  years  old,  162  died 
in  the  first  2  years  and  270  in  the  first  5  years  of  life.  Freeman  of  New 
York  (1904)  stated  that  out  of  158  cases  61  died  in  the  first  year  and  34  in 
the  second.  These  figures  are  sufficient  to  show  the  general  incidence  of  the 
•disease.     The  mortality  is  lowest  from  5-20  years  of  age. 

Tuberculous  foci  are  found  with  increasing  frequency  as  age  advances. 
The  increase  is  rapid  up  to  the  end  of  the  first  year,  gradual  up  to  the  end 
■of  the  fifth  year,  and  slow  afterwards.  In  the  sixth  year  such  foci  are 
present  in  about  half  of  the  autopsies  ;  from  10-15  years  in  about  75  per 
-cent.  Statistics,  based  on  the  clinical  examination  of  school  children,  are 
unreliable  for  the  signs  are  often  indefinite  and  may  be  misinterpreted. 
Probably  from  1-2  per  cent,  are  affected  among  those  actually  attending 
school.    Those  seriously  ill  are  kept  at  home. 

Varieties  of  Tuberculosis.— The  tendency  to  generalisation  in  the 
form  of  miliary  tuberculosis  or  of  multiple  tuberculous  foci  is  a  characteristic 
•of  early  life.  The  other  main  peculiarity  is  the  liability  to  glandular  disease. 
Except  in  glands,  and  not  often  in  these,  it  is  rarely  localised  in  a  single 
■organ.  Usually  there  is  an  aggregation  of  yellow  tubercles  at  the  oldest 
focus,  and  miliary  or  yellow  tubercles  scattered  elsewhere.  The  disease 
may  preponderate  in  the  thorax,  abdomen,  cervical  lymph  nodes,  joints  or 
other  sites.  In  the  first  4  years  of  life  the  bronchial  glands  are  almost 
invariably  affected  and  the  lungs  little  or  not  at  all  involved.  As  already 
argued  it  is  probable  that  there  is,  or  has  been,  a  primary  focus  in  the  lungs 
and  the  glandular  infection  is  secondary.  At  the  time  of  death,  however, 
the  lungs  may  show  signs  of  secondary  dissemination  or  spreading  by 
^continuity  with  a  broken  down  gland.  Often  the  glands  are  much  affected, 
while  the  lungs  show  merely  a  few  miliary  tubercles.    General  tuberculosis 


854  Chapter  LXI. 

may  be  due  to  dissemination  from  foci  in  other  glands,  tonsils,  adenoids, 
etc.  In  rare  instances  no  such  focus  is  discoverable  and  it  is  possible  that 
the  disease  is  due  to  direct  infection  by  tuberculous  milk  or  dust.  At  this- 
early  period  of  life  there  is  marked  proclivity  to  bronchitic  and  pulmonary 
affections  which  render  the  tissues  more  prone  to  infection,  and  to  marasmus- 
from  numerous  causes  reducing  the  vitality  of  the  child  and  its  resistance 
to  infection. 

Chronic  bronchitis  is  often  due  to  tuberculous  disease.  Sub-acute 
caseous  broncho-pneumonia  is  not  infrequent.  The  middle  zone  of  the 
lung  is  the  most  often  affected,  and  the  lower  lobe  next  in  frequency. 
Occasionally  caseous  nodules,  some  of  which  have  broken  down  and  formed 
small  cavities,  are  profusely  distributed  throughout  the  lungs. 

The  chronic  phthisis  of  adults  is  rare  in  the  first  -1  years.  After  the 
seventh  year  pulmonary  tuberculosis  closely  conforms  to  this  type.  It  is 
more  diffused,  more  malignant,  showing  less  tendency  to  heal  and  greater 
tendency  to  dissemination,  and  rarely  follows  a  regular  chronic  course. 
All  these  features  decrease  in  prominence  as  age  advances.  According  to 
Louis's  Law,  after  puberty  the  lungs  are  almost  invariably  affected  when 
any  other  organ  suffers. 

Differences  from  Adult  Tuberculosis. — Tubercles  develop  rapidly  and 
coalesce,  caseation  is  almost  constant,  and  fibrosis  and  calcification  are 
rare,  especially  before  the  fifth  year.  The  disease  often  starts  from  the 
glands  at  the  root  of  the  lungs.  Such  a  gland  may  soften  and  ulcerate  into 
the  trachea  or  bronchus,  setting  up  diffuse  caseous  broncho-pneumonia. 
Often  it  spreads  by  the  lymphatics  along  the  bronchial  septa ;  and  small1 
cavities  at  the  root  of  the  lung,  or  in  1  lobe,  or  radiation  outward  toward 
the  periphery  may  be  present.  The  meninges,  brain,  glands,  bones  and 
joints  are  involved  more  frequently. 

No  matter  the  mode  of  infection  the  disease  is  disseminated  rapidly  and 
irregularly  through  the  lungs,  and  often  simulates  broncho-pneumonia. 
Typical  tubercles  and  giant  cells  are  numerous.  Cavities  are  quite  common, 
though  less  so  than  in  adults.  Death  usually  results  from  dissemination 
before  the  cavities  are  large  enough  to  give  rise  to  typical  physical  signs. 
On  account  of  the  course  of  the  disease  the  physical  signs  are  different. 
Thus  in  general  caseation,  without  cavitation  or  large  areas  of  consolidation* 
the  signs  may  be  merely  those  of  bronchitis.  The  phthisical  appearance  of 
adults  is  rarely  seen  in  children  under  10  years  of  age,  who  may  look  pretty 
and  healthy  until  removal  of  the  clothes  reveals  emaciation. 

Early  symptoms  are  debility,  loss  of  weight,  liability  to  colds,  morning 
anorexia,  headache,  sweating,  fever  and  variable  crepitations.  Night 
sweats  are  uncommon.  Such  sweating  comes  out  on  the  forehead  and 
round  the  neck.  It  is  inconstant  and  worse  in  cold  weather.  Heavy  bed 
clothes  and  rickets  must  be  excluded  as  causes.  Haemoptysis  and  laryngitis 
are  rare.    Sputum  is  swallowed  and  may  set  up  gastro-intestinal  troubles* 


Tuberculosis.  855 

so  it  is  advisable  to  give  calomel  and  intestinal  antiseptics.  The  skin  is  often 
dry,  discoloured  and  pigmented.  Fever  may  be  absent,  atypical,  or  due 
to  mixed  infections.  The  tuberculosis  of  glands  and  other  forms  of  localised 
disease  are  described  under  the  special  headings.  In  the  present  chapter 
general  dissemination  and  the  various  lung  affections  are  considered. 

The  Blood. — Leucocytosis  is  a  sign  of  secondary  infection.  An  increase 
in  eosinophiles  is  a  favourable,  and  decrease  is  an  unfavourable  indication. 

Miliary  or  General  Tuberculosis. — This  is  the  common  type  of  tuber- 
culosis of  the  lungs  in  infants.  From  2-5  years  it  is  much  less  frequent. 
After  that  it  is  uncommon  but  may  occur  at  any  age.  It  was  present  in 
48-3  per  cent,  of  238  children  (Still),  and  in  73  per  cent,  of  110  (Hamburger 
and  Sluka).  It  is  due  to  blood  infection.  The  irruption  of  the  bacilli  into 
the  blood  stream  is  the  first  scene  in  the  last  act  of  infantile  tuberculosis. 
Possibly  more  than  one  such  irruption  can  take  place.  Its  cause  is  the 
breaking  down  of  a  caseous  gland,  usually  a  thoracic  gland,  and  infection 
of  the  lymphatics;  or  the  breaking  down  of  a  nodule  in  the  wall  of  a  blood 
vessel.  In  the  latter  case  dissemination  may,  if  arterial,  be  limited  to  a 
definite  area  in  the  lung,  abdomen,  meninges,  etc. ;  if  venous,  the  bacilli  are 
carried  to  the  heart,  thence  to  the  lungs  where  they  are  mainly  detained, 
while  those  which  escape  may  be  distributed  by  the  arterial  system 
generally,  no  organ  being  exempt.  The  focus  may  not  be  discoverable.  In 
older  children  the  disease  may  be  secondary  to  tuberculosis  of  bones, 
joints,  glands,  testicles,  etc. 

Miliary  tuberculosis  is  almost  invariably  a  general  tuberculosis.  The 
tubercles  are  distributed  throughout  the  lung,  more  or  less  equally,  or  in 
patchy  areas.  They  are  often  in  enormous  numbers  and  of  the  small  grey 
type,  passing  into  yellow  tubercles  in  prolonged  cases.  The  lungs  may  be 
otherwise  healthy,  exhibit  general  catarrh,  or  show  patchy  broncho- 
pneumonia. The  visceral  and  parietal  pleura  are  often  studded  with  grey 
tubercles,  sometimes  the  under  surface  of  the  diaphragm,  and  less  often  the 
peritoneum.    A  variable  number  are  found  in  other  organs,  chiefly  the  spleen. 

The  onset  is  insidious  or  abrupt.  Wasting,  without  definite  cause,  may 
be  present  on  account  of  the  tuberculosis  in  the  glands.  Often  the  child 
appears  in  robust  health  and  the  onset  is  that  of  capillary  bronchitis  or 
broncho-pneumonia.  Anaemia,  anorexia,  malaise  and  fever  may  be  present, 
before  the  physical  signs  appear,  and  there  may  be  large  numbers  of 
tubercles  in  the  lungs  without  signs  of  pulmonary  mischief. 

General  Symptoms. — The  child  is  ill,  weak,  feverish,  and  frequently 
emaciated.  The  weakness  and  emaciation  are  progressive.  The  skin  is  dry 
and  in  marasmic  infants  may  develop  small  furuncles.  Blueness  or  lividity 
of  the  lips  and  face  may  be  noted  ;  increased  respiration  rate  ;  cough 
frequent,  dry,  sometimes  paroxysmal,  often  slight  or  absent  in  infants  ; 
frequent  pulse,  unless  there  is  meningitis  ;  and  often  a  diazo-reaction  in 
the  urine.     The  temperature  is  irregular,  rarely  above    102°  F.,   seldom 


856  Chapter  LXI. 

hectic.  It  should  be  taken  every  2  hours  in  doubtful  cases.  Fever  may  be 
trivial  or  absent. 

Localising  signs  are  secondary,  and  often  absent  or  late  in  development. 
The  chest  resonance  is  somewhat  diminished.  Fine  rales  and  occasionally 
friction  may  be  heard.  The  liver  and  spleen  are  generally  enlarged,  and 
the  latter  may  increase  in  size  because  of  the  fever.  The  liver  is  often 
fatty.  Further  evidence  of  dissemination  may  be  present,  e.g.  meningitic 
symptoms,  choroid  tubercles,  glandular  tuberculosis,  epididymitis,  etc. 

The  disease  assumes  various  types.  (1)  Marasmic  : — seen  in  infants  and 
characterised  by  wasting,  diarrhoea,  exhaustion,  little  or  no  fever,  and 
perhaps  no  pulmonary  signs  ;  (2)  Meningeal  : — the  common  type  in 
which  the  meningitic  symptoms  mask  the  lung  signs;  (3)  Pulmonary  : — 
insidious  or  acute  in  onset  and  simulating  general  broncho-pneumonia  ; 
(•i)  Acute  Febrile  : — suggestive  of  enteric  fever  and  characterised  by 
high  continuous  or  remittent  fever,  frequent  pulse,  wasting,  prostration  and 
enlarged  spleen.  The  dyspnoea  and  cyanosis  are  greater  than  the  pulmonary 
signs  warrant.  The  pulse  is  more  frequent,  fever  more  irregular  than  in 
enteric  fever,  and  there  is  no  leucopenia,  no  Widal  reaction  and  no  spots. 
Exceptionally  spots,  closely  resembling  rose  spots,  have  been  seen. 

Diagnosis. — The  marasmic  type  is  often  impossible  of  diagnosis.  If 
there  is  other  obvious  cause  for  fever  and  wasting,  do  not  be  in  a  hurry  to 
diagnose  tuberculosis.  In  infancy  debility,  marasmus  and  congenital 
syphilis  lead  to  wasting  which  may  be  associated  with  pulmonary  catarrh, 
a  condition  liable  to  be  mistaken  for  tuberculosis.  In  older  children  the 
wasting  of  intestinal  dyspepsia,  with  cough  and  some  fever,  may  lead  to 
similar  error.  Acute  cases  may  simulate  capillary  bronchitis  and  broncho- 
pneumonia in  infancy  and  enteric  fever  at  all  ages,  occasionally  sepsis, 
infective  endocarditis  and  malaria.  From  capillary  bronchitis  it  cannot  be 
clearly  differentiated.  Much  respiratory  distress,  in  the  absence  of  physical 
signs,  is  strongly  in  favour  of  general  tuberculosis.  Many  a  case  which  gets 
well  is  diagnosed  as  capillary  bronchitis  or  broncho-pneumonia  ;  and  many 
with  similar  symptoms  and  physical  signs  prove  to  be  miliary  tuberculosis. 
Choroid  tubercles,  bacilli  in  the  cerebrospinal  fluid,  and  the  various  tuber- 
culin tests  are  sometimes  of  assistance.  After  the  second  year  of  life  these 
cases  are  usually  diagnosed  as  meningitis,  because  of  the  predominance  of 
meningeal  symptoms.  Unhygienic  surroundings,  pre-tuberculous  con- 
ditions, and  association  with  phthisical  subjects  must  be  allowed  due 
weight. 

Prognosis. — The  disease  is  fatal  in  3-6  weeks  from  the  onset  of  acute 
symptoms,  occasionally  earlier.  Possibly  mild  outbreaks  of  miliary  tubercles 
into  the  lung  are  recovered  from,  just  as  similar  outbreaks  in  the  peritoneum 
get  well.  One  child  under  my  care  recovered  from  an  attack  which 
appeared  to  be  a  capillary  bronchitis.  About  6  months  later  a  like  attack 
ran  a  similar  course  and  ended  fatally,  and  miliary  tuberculosis  was  found. 


Tuberculosis.  857 

There  seems  no  inherent  reason  why  a  patient  should  not  recover  from  the 
irruption  of  a  crowd  of  bacilli  into  an  artery  and  distributed  locally. 

Tuberculous  Broncho-pneumonia.— This  variety  is  common  in  infancy, 
and  broncho-pneumonic  or  pneumonic  in  distribution.  It  is  more  prolonged 
in  its  course  than  general  tuberculosis.  It  is  stated  to  be  sometimes  a  sequel 
•of  simple  broncho-pneumonia,  especially  one  due  to  measles  or  pertussis. 
Localised  cases  can  depend  on  direct  spread  from  a  caseous  gland  to  the 
lung.  Generalised  ones  are  most  likely  a  sequence  of  rupture  of  a  caseous 
focus  into  the  trachea  or  bronchus  and  aspiration  of  the  debris.  This  may 
affect  a  large  portion  of  a  lobe,  a  whole  lobe  or  1  lung,  and  is  rarely  bilateral. 
It  is  usually  basal  and  causes  cheesy  consolidation,  tending  to  softening  and 
cavitation.  Section  of  the  lobe  may  show  miliary  tubercles  extending  from 
the  primary  focus  in  a  radiating  or  fan-shaped  manner  into  the  lung. 
Apart  from  this  variety  tuberculous  broncho-pneumonia  is  more  frequent 
.at  the  apex  than  the  base.    The  pleura  is  generally  thickened  and  adherent. 

Symptoms. — Acute  cases  are  like  simple  broncho-pneumonia  in  onset, 
•course  and  physical  signs.  Others  resemble  lobar  pneumonia  but  there 
is  no  crisis.  Bilateral  cases  are  analogous  to  acute  phthisis  or  galloping 
consumption,  with  yellow  tubercles  about  the  size  of  peas,  some  softened, 
throughout  the  lungs  and  partial  consolidation  round  each.  The  physical 
signs  of  this  type  are  those  of  catarrh,  and  impaired  resonance  if  there  is 
much  consolidation.  As  a  rule  the  disease  is  more  insidious  and  runs  a 
prolonged  course,  with  abatements  and  exacerbations,  and  even  intervals 
•of  comparative  good  health.  The  common  symptoms  are  pallor,  languor, 
.anorexia,  wasting,  dyspnoea,  cyanosis,  and  variable  cough  which  may 
be  absent  at  first.  The  physical  signs  are  dulness,  bronchial  breathing  and 
fine  crepitations  ;  and  subsequently  large  moist  rales  and  perhaps  signs  of 
a  cavity.  The  most  reliable  indications  of  a  cavity  are  loud  bronchial 
breathing,  altered  voice  resonance,  pectoriloquy,  splashing  and  bell  sound. 
•Cracked-pot  sound  is  of  little  value  in  infants  and  not  much  in  older 
•children.  On  account  of  the  yielding  chest  wall  it  can  be  produced  in 
health.  In  chronic  cases  the  signs  may  be  limited  to  1  lobe,  with  moderate 
fever,  malaise  and  cough.  Haemoptysis  seldom  occurs,  except  when  a 
broken  down  gland  extends  into  the  lung  and  invades  the  bronchus  or 
trachea.  Then  the  bleeding  may  come  from  the  lung  or  from  softening  and 
rupture  of  an  artery  in  the  gland.  Sometimes  the  disease  is  quiescent,  the 
signs  of  consolidation  alone  being  present. 

Diagnosis. — Simple  broncho-pneumonia  is  distinguished  by  its  acute 
•onset,  absence  of  factors  disposing  to  tuberculous  infection,  and  absence  of 
the  signs  suggestive  of  tuberculosis.  Both  varieties  may  last  for  months, 
but  the  longer  the  course  the  greater  is  the  probability  of  tuberculosis. 
Pleuritic  attacks  and  downy  hair  on  the  trunk,  common  in  chronic  tuber- 
culosis, are  in  its  favour.  It  may  be  possible  to  obtain  sputa  and  discover 
the  bacillus,  or  the  organism  may  be  found  in  the  little  masses  of  purulent 


858  Chapter  LXI. 

matter  in  the  stools  when  the  sputa  are  swallowed.  The  lobar  distribution! 
may  simulate  unresolved  pneumonia.  Basal  cavitation  is  also  found  in 
bronchiectasis.  The  temperature  chart  may  suggest  typhoid  fever  and  a. 
complication. 

Prognosis. — Acute  cases  end  fatally  in  6  days  to  6  weeks,  while 
chronic  ones  last  6  weeks  to  6  months.  Malignant  cases  are  often  fatal: 
in  2  weeks  ;  galloping  phthisis  in  10-12  weeks  ;  and  others  pass  into  chronic 
phthisis.  Those  occurring  in  the  course  of  measles  and  pertussis  are  very 
unfavourable  ;  to  a  less  extent  so,  if  the  primary  infection  has  subsided. 
The  most  favourable  cases  are  those  of  limited  area.  Though  quiescent 
there  is  always  a  liability  to  sudden  and  fatal  dissemination  from  trivial; 
illness.  Fibrosis  is  a  rare  termination  and  on  the  whole  acute  dissemination 
is  not  common.  Death  may  take  place  during  the  acute  stage  from  asthenia 
or  convulsions,  due  to  general  tuberculosis  or  meningitis. 

Tuberculous  Pneumonia. — At  all  periods  of  childhood  tuberculosis 
of  the  lung  may  be  of  an  acute  pneumonic  type.  The  whole  of  1  lobe  or 
1  lung  undergoes  massive  caseous  consolidation,  which  may  terminate  in 
extreme  caseous  disintegration. 

It  is  more  or  less  abrupt  in  onset,  with  chill,  high  fever  and  signs  of: 
consolidation,  and  may  resemble  simple  pneumonia.  In  a  few  days  the 
fever  becomes  hectic.  On  exploration  pus  may  be  obtained,  if  the  needle 
enters  breaking  down  lung,  a  caseous  pulmonary  abscess.  The  fever- 
continues,  dyspnoea  increases  and  cardiac  weakness  ensues,  ending  fatally 
in  a  few  days.  Or  it  passes  into  galloping  phthisis  with  hectic  temperature,, 
rapid  wasting,  asthenia,  caseation  and  death  in  a  few  weeks.  It  may  be 
mistaken  for  empyema. 

Chronic  Phthisis. — The  adult  type  occurs  at  all  ages,  but  is  rare  until 
the  fifth  year  and  more  frequent  after  the  seventh.  There  is  less  tendency 
for  it  to  begin  at  the  apex  and  extend  gradually  downward.  The  base  of 
the  lung  is  more  often  involved  than  in  adults  but  there  is  nevertheless  a 
prepondeiance  of  apical  cases,  increasing  as  age  advances.  Physical  signs- 
are  often  found  over  the  root  of  the  lung,  about  the  mammary  region, 
because  of  the  spread  of  the  disease  from  a  bronchial  gland.  These  glands 
are  usually  much  affected  and  cause  pressure  symptoms.  There  is  less 
tendency  to  fibrosis  and  to  extensive  cavitation.  Cavities  are  found  at  all- 
ages,  even  in  the  first  3  months  of  life.  They  are  frequently  situated  in  the 
apex  of  the  lower  lobe,  the  anterior  and  inferior  half  of  the  upper  lobe,  and 
the  root  of  the  lung.  The  liability  to  general  dissemination  and  meningitis 
is  much  greater  than  in  adults. 

In  infants  and  young  children  the  physical  signs  are  those  of  broncho- 
pneumonia, for  the  pathological  process  is  of  this  character.  Such  signs,, 
of  gradual  onset  and  limited  to  one  apex,  are  probably  tuberculous.  Older 
children  present  similar  signs  to  those  in  adults,  viz.—  deficient  movement,, 
unilateral  flattening,  impaired  note  ;   breath  sounds  weak  and  harsh,  jerkyr 


Tuberculosis.  859* 

tubular,  bronchial  or  cavernous  ;  expiration  prolonged  and  perhaps  louder 
than  inspiration  ;  rales,  sometimes  absent  in  early  stages,  and  later  of 
varying  size,  clicking,  bubbling,  etc.  Cavernous  breathing,  pectoriloquy 
and  cracked-pot  sound  may  be  present  over  consolidation  as  well  as  cavi- 
tation. Impaired  resonance  over  the  apices  of  the  lower  lobes  in  the 
intra-scapular  region  may  be  due  to  the  rhomboid  muscles.  Sometimes- 
there  is  extremely  little  found  on  examination,  and  the  physical  signs  are 
limited  to  a  unilateral  or  general  increased  resistance  on  percussion,  a  less 
resonant  percussion  note  than  expected,  weak  breath  sounds  and  a  few 
fine  crepitations  at  the  edges  of  the  lungs.  The  signs  of  enlarged  thoracic 
glands  may  be  present. 

The  symptoms  consist  of  fever,  cough,  dyspnoea,  haemoptysis,  wasting, 
and  increase  in  the  pulse  rate  and  respiration.  The  pulse  is  almost  invariably 
increased  in  frequency.  Dyspnoea  is  not  marked  but  breathing  is  usually 
somewhat  more  frequent  than  normal.  Cough  is  slight  or  absent,  dry  and 
irritating,  bronchitic  or  paroxysmal.  It  is  less  common  than  in  adults. 
Sputum  is  swallowed,  except  by  older  children  who  have  been  taught  to 
expectorate,  and  may  cause  vomiting  if  it  is  purulent  and  abundant. 
Haemoptysis  is  very  rare  under  3  years  of  age  and  uncommon  later,  occurring 
in  about  5  per  cent.  It  is  rarely  fatal  in  children  under  7  years.  It  is  due 
to  congestion,  rupture  of  a  blood  vessel,  or  perforation  of  the  trachea  or 
bronchus  by  a  necrotic  gland.  Fever  is  common,  without  special  features. 
It  may  be  continuous  in  an  acute  case,  perhaps  not  above  100°  F.,  or  may 
have  a  daily  range  of  3-4°  F,  Sometimes  it  keeps  quite  steadily  about  the 
normal  level.  Emaciation  is  almost  constant.  A.  few  of  the  older  children,, 
less  often  the  younger  ones,  remain  plump,  robust  and  of  a  good  colour,  and 
feel  Avell.  Night  sweats  are  uncommon  in  eaily  life.  The  older  the  child, 
the  more  likely  are  they  to  occur. 

Diagnosis. — Prolonged  broncho-pneumonia  is  liable  to  be  mistaken  for 
phthisis.  If  the  signs  and  symptoms  can  be  thus  explained,  it  is  rash  to 
diagnose  tuberculosis.  Stress  must  be  laid  on  exposure  to  infection, 
localisation  of  the  pulmonary  signs,  asymmetry  of  respiration  above  and 
below  the  clavicle,  loss  of  weight,  and  the  temperature  chart. 

Complications  are  common.  Infection  of  the  blood  stream  causes 
dissemination,  meningitis  and  even  endocarditis.  The  presence  of  endo- 
carditis in  a  girl  with  high  fever  and  pulmonary  catarrh  rendered  the 
diagnosis  between  general  tuberculosis  and  infective  endocarditis  a  matter 
of  difficulty  for  some  days.  In  chronic  types  there  may  be  secondary 
infection  of  the  tonsils,  larynx  or  intestines,  softening  of  caseous  glands  and 
its  effects,  and  abdominal  tuberculosis.  In  chronic  phthisis  every  variety  of 
tuberculous  lesion  may  be  found,  as  well  as  those  due  to  other  organisms  or 
dependent  on  malnutrition. 

The  prognosis  of  the  adult  type  is  better  than  that  of  other  varieties 
but  must  be  guarded  on  account  of  the  limited  tendency  to  fibrosis,  the 


860  Chapter  LXI. 

'liability  to  dissemination,  and  the  danger  of  further  outbreaks  in  apparently- 
cured  cases.  Such  an  outbreak  may  be  due  to  fresh  infection.  Quiet  and 
extinct  lesions  have  been  found  post  mortem  in  9  per  cent,  of  2,400  autopsies 
(Kingston  Fowler,  Middlesex  Hospital),  71  out  of  763  (Loomis  of  New 
York),  and  17  out  of  131  in  the  Paris  Morgue  (Vibert).  It  runs  a  prolonged 
course  and  recovery  is  not  infrequent,  even  in  infancy.  The  fact  that  it 
is  of  this  type  implies  resistance  to  general  infection  or  lack  of  virulence  of 
the  infective  agent.  As  a  standard  rule  it  must  be  remembered  that  the 
prospect  of  recovery  increases  with  the  increased  age  of  the  child  affected 
and  is  slight  in  the  very  young.  The  severity  seems  to  be  exaggerated  at 
puberty  in  girls,  especially  if  the  catamenia  have  begun.  Pressure  signs  are 
of  grave  significance.  Enlarged  bronchial  glands  without  pressure  signs  are 
less  serious  although  there  is  a  prospect  of  secondary  general  infection. 

Specific  Tests  for  Tuberculosis. — Seek  for  bacilli  by  staining  methods 
in  the  sputum,  faeces  and  cerebrospinal  fluid.  Sputum  is  obtained  by 
irritating  the  pharynx  with  a  gauze  swab  and  collecting  it  as  it  is  coughed  up, 
by  getting  the  child  to  cough  on  to  a  glass  slide,  by  Avashing  out  the  stomach 
in  the  morning  before  food,  or  by  aspiration  through  a  catheter  introduced 
into  the  larynx. 

The  withdrawal  of  1-2  c.c.  of  blood  and  inoculation  of  guinea  pigs 
is  rarely  available  and  takes  at  least  3  weeks  for  the  effect  to  be  ascertained. 
The  estimation  of  the  opsonic  index  (p.  91)  is  not  very  reliable.  X-ray 
■examination  may  afford  evidence  of  old  lesions  or  of  enlarged  thoracic 
glands.     Cyto-diagnosis  (p.  434)  is  of  value  in  effusions. 

The  cutaneous  reaction  of  von  Pirquet  is  simple  and  free  from  danger. 
Inoculation  of  25  per  cent,  old  tuberculin  into  the  scratched  skin  causes 
the  formation  of  a  flat  red  papule  within  24  hours.  A  simple  and  reliable 
method  is  to  make  parallel  and  crossed  double  scratches  on  the  forearm 
with  two  sewing  needles  held  together  and  dipped  in  undiluted  tuberculin. 
A  control  scratch  must  be  made  as  well.  Or  scrape  off  the  epidermis 
without  causing  oozing,  and  rub  in  the  tuberculin.  Comby  makes  3  pricks 
with  a  lancet  in  the  deltoid  region  and  rubs  in  1  per  cent,  tuberculin.  In 
24  hours  or  more  redness  appears  and  is  followed  by  simple  papules  which 
last  8-10  days.  The  papules  may  be  vesicular,  bullous,  and  rarely  show  a 
central  eschar.  The  skin  reaction  is  indicative  of  the  presence  of  a  tuber- 
culous focus  but  affords  no  information  as  to  its  latency  or  activity.  It 
is  valuable  as  a  negative  test  in  infants  and  young  children.  It  is  positive 
in  about  90  per  cent,  of  tuberculous  and  20  per  cent,  of  non-tuberculous 
children. 

The  ophthalmic  or  conjunctival  reaction  was  described  by  Wolff- 
Eisner  in  1907  and  by  Calmette  in  the  same  year.  Use  a  fresh  0-5  per  cent, 
solution  of  old  tuberculin  in  normal  saline  or  3  per  cent,  boric  acid.  If  there 
is  tuberculous  disease  it  sets  up  conjunctivitis  in  3-12  hours.  The  reaction 
is  supposed  to  depend  on  the  circulation  of  tuberculous  toxin  in  the  tissues. 


Tuberculosis.  861 

It  is  a  deceptive  and  unreliable  sign  and  may  do  great  damage.  It  has  set 
up  violent  conjunctivitis,  chronic  conjunctivitis,  a  local  tuberculous  process- 
and  ulceration  of  the  cornea,  and  even  total  destruction  of  the  eye.  The 
solution  recommended  here  is  unlikely  to  cause  a  violent  reaction .  Advanced 
cases  may  not  show  the  reaction.    The  test  is  negative  in  10-15  per  cent. 

The  tuberculin  test  consists  in  the  injection  of  old  tuberculin  m.gm.. 
xVJ  and  recording  the  temperature  at  short  intervals.  It  rises  slowly  in 
4-6  hours,  more  rapidly  in  another  2-4  hours,  and  falls  to  normal  within 
24  hours.  It  may  remain  up  more  than  the  24  hours  or  the  rise  may  be 
delayed.  If  there  is  no  reaction,  the  test  can  be  repeated  with  doses  of 
m.gm.  1-5  at  intervals  of  2  days.  It  must  not  be  employed  if  the  axillary 
temperature  is  above  normal,  or  in  the  presence  of  hgemoptysis,  bacilli  in  the 
sputum,  definite  physical  signs  of  tubercle,  grave  cardiac  or  renal  disease. 
The  sole  risk  is  recrudescence  of  activity  in  a  tuberculous  focus.  A  local 
lesion  shows  swelling,  redness  and  tenderness. 

Treatment. — The  prophylaxis  of  tuberculosis  is  so  well  known  that  it 
may  be  summed  up  briefly.  The  avoidance  of  exposure  to  infection  and 
increasing  the  resisting  power  of  the  body  are  the  two  chief  factors.  There- 
fore, keep  children  away  from  tuberculous  relatives  or  nurses.  Bring  babies 
up  on  the  breast  or  select  a  milk  supply  from  non-tuberculous  cows.  Take 
special  care  of  them  during  and  after  respiratory  catarrh,  lung  affections,, 
pertussis  and  measles.  Attend  to  hygiene.  Open  air  by  night  and  day, 
sea  air,  inland  air,  moderate  clothing  and  judicious  hardening;  liberal 
diet,  containing  plentiful  fat  and  protein  ;  breathing  exercises,  drill,  physical 
development,  games  and  sports  ;  and  the  conditions  of  school  life,  are  air 
of  great  importance.  Definite  cases  should  not  attend  school  and,  if  active,, 
should  be  segregated  in  the  home. 

For  active  cases  adopt  the  methods  of  prophylaxis  and  open  air  prin- 
ciples of  treatment,  viz. — a  sparsely  populated  locality  near  the  sea  or  a 
pine  forest  and  free  from  dust,  dry  soil,  equable  temperature  with  no  wide 
extremes,  bracing  and  not  relaxing  climate,  shelter  from  east  and  north 
winds,  and  a  large  airy  bedroom.  Seaside  air  is  best  for  pre-tuberculous 
stages  and  glandular  tuberculosis,  and  inland  air  for  pulmonary  disease. 
High  altitudes  are  unsuitable  for  children.  Over-fatigue  and  exposure  to 
any  infection,  even  that  of  the  common  "cold,"  must  be  guarded  against. 
Give  a  cold  or  tepid  morning  bath  and  dry  with  a  rough  towel. 

Tuberculin  Treatment. — Koch's  old  tuberculin  depends  for  its  activity 
on  the  extra-cellular  toxins  excreted  into  the  culture  fluid.  It  is  rarely  used 
for  treatment  and,  if  so,  is  given  in  doses  O001  m.gm.,  is  eventually  increased 
to  1  m.gm.  for  adults.  Begin  with  0-0001  m.gm.  for  an  infant,  and 
0-00025  m.gm.  for  a  4-year  old  child.  Malaise,  fever,  increased  pulse  rate 
and  loss  of  weight  indicate  too  large  a  dose.  Koch's  "  New  "  Tuberculin 
T.  R.  is  generally  given,  according  to  the  method  already  described  (p.  92). 
The  signs  of  improvement  are  better  appetite,  colour,  general  health  and 


862  Chapter   LXI. 

.gain  in  weight,  and  local  healing.  One  c.c.  of  ';  new  "  tuberculin  is 
standardised  to  represent  10  m.gm.  of  dried  comminuted  bacilli.  The  active 
agent  is  an  intra-cellular  toxin.  Tuberculin  can  be  given  by  mouth  in 
double  the  doses  recommended  for  subcutaneous  injection.  Apparently  it 
is  almost  as  efficacious  when  given  in  this  manner.  Its  value  is  difficult 
to  estimate,  for  the  cases  which  improve  are  those  that  usually  do  well  under 
ordinary  methods  of  treatment. 

The  injection  of  tuberculin,  hetero-inoculation,  is  unsafe  in  large  doses 
-and  if  the  patient  is  feverish.  Human  tuberculin  is  preferable  to  that  of 
bovine  origin,  but  the  latter  may  be  used  if  there  is  no  improvement. 
Auto-inoculation  causes  a  rise  of  temperature  and  a  high  temperature 
means  over-dosage.  This  is  reduced  by  rest.  If  the  temperature  falls 
Ihe  prospect  is  favourable.  The  course  of  auto-inoculation  is  shewn  best 
by  a  chart  in  which  a  series  of  evening  temperatures  are  joined  together 
(E.  C.  Hort).  A  rise  in  the  curve  is  unfavourable,  while  a  fall  is  a  good 
sign.  In  surgical  and  chronic  tuberculosis  in  which  auto-inoculation  does 
not  cause  rise  of  temperature,  supplementary  hetero-inoculation  may  prove 
of  decided  benefit. 

MarmoreTc 's  serum  is  given  per  rectum  in  doses  for  adults  of  5  c.c.  daily 
■or  10  c.c.  twice  a  week.  The  opsonic  index  rises  after  a  few  doses,  soon 
reaches  a  maximum  and  remains  there  for  3-4  weeks,  while  the  serum  is 
given,  and  does  not  fall  until  nearly  a  weak  after  its  omission.  Its  value, 
like  that  of  other  serums  and  vaccines,  is  uncertain. 

Apart  from  these  methods  the  treatment  is  symptomatic.  Education 
need  not  be  neglected,  if  the  child  is  over  6  years  old  and  the  disease  not 
acute,  and  can  be  given  in  the  open  air.  Massage  is  often  useful  and 
-stimulants,  preferably  malt  liquors,  may  be  needed.  The  diet  should  consist 
•of  small  frequent  meals,  much  milk,  protein  and  fat.  Baw  meat  is  taken 
well.  Usually  too  much  carbohydrate  is  given.  Children  do  not  stand 
much  over-feeding.     Prescribe  rest  before  meals. 

Drugs. — Be  careful  not  to  upset  the  digestion.  Give  ol.  morrhuse 
dr.  |-I,  t.d.s.,  after  meals,  except  on  Sundays.  Give  it  in  the  form  most 
agreeable  to  the  child,  e.g.  with  malt  and  hypophosphites.  Other  drugs  of 
value  are  ichthyol  in  capsules,  ichthalbin  in  chocolate  tablets,  creosote 
m.  |-1  (p.  80),  guaiacol  carbonate  gr.  1-5,  terebene,  arsenic,  arsenicated  waters, 
-and  preparations  of  iron  (p.  81). 

Cough  depends  on  irritation  of  the  fauces,  pharynx,  larynx  or  trachea. 
It  is  treated  by  local  demulcents  ;  a  simple  linctus  or  one  containing  tr. 
•camph.  co.;  liquorice,  glycerine,  cocaine  or  morphia  lozenges;  honey  and 
lemon  juice;  ammon.  chloride  spray  if  there  is  much  tenacious  mucus; 
bromides  at  night  and  heroin,  etc.  Inhalations  of  terebene,  eucalyptus, 
tr.  benzoin  co.,  creosote,  etc.,  are  also  beneficial.  D.  B.  Lees  is  a  warm 
advocate  for  the  continuous  inhalation  of  a  mixture  of  ac.  carbol.  drs.  2, 


Tuberculosis.  863 

■creosoti  drs.  2,  tr.  iodi.  dr.  1,  sp.  etheris  dr.  1,  sp.  vin.  rect.  drs.  2,  about 
-5  drops  being  put  on  a  respiratory  hourly  and  continuously  inhaled. 

Haemoptysis  is  treated  by  rest,  morphia  gr.  actf-sV  sub  cutem,  and 
light  diet ;  sometimes  by  inhalations  of  amyl  nitrite  or  subcutaneous 
injection  of  trinitrin  or  sodium  nitrite,  as  vaso-dilators  of  the  peripheral 
blood  vessels. 

For  dyspepsia  try  a  mixture  of  arsenic,  sod.  bicarb,  and  tr.  gent.  co. 
•or  infus.  gent.  co.  after  food  ;  for  vomiting,  bismuth  carb.  or  cerium 
■oxalate,  etc.  ;  for  diarrhoea,  salol  and  large  doses  of  bismuth.  During  fever 
the  child  must  be  kept  in  bed.  If  there  are  night  sweats  sponge  with  weak 
vinegar  and  water,  give  food  and  stimulants  shortly  before  the  sweating 
usually  begins,  and  possibly  atropin,  agaricin  gr.  ^-^,  or  other  drugs  such 
-as  are  used  in  adults. 

Attention  to  detail  is  of  the  utmost  importance  in  chronic  phthisis. 
In  generalised  tuberculosis  and  the  tuberculous  forms  of  pneumonia  and 
broncho-pneumonia  treatment  is  carried  out  on  general  principles,  such  as 
•are  adopted  in  capillary  bronchitis  and  simple  broncho-pneumonia. 


Chapter  LXII. 

SYPHILIS:    ACQUIRED    AND    CONGENITAL. 

Syphilis  is  due  to  the  trcponema  pallidum,  or  syirochata  pallida, 
a  spiral  motile  organism  discovered  by  Schaudinn  (1905).  It  is  best  seen 
in  fresh  preparations,  from  the  edge  of  a  sore  or  mucous  plaque,  by  means 
of  the  ultra-microscope.  Using  Giemsa's  method  of  staining,  avoiding 
nuclear  stains,  it  has  been  found  in  the  cut  sections  of  many  organs  in 
congenital  syphilis,  especially  the  liver.  Levaditi  (1906),  with  silver  nitrate 
staining,  found  it  most  often  and  most  numerous  in  the  liver,  lungs,  adrenals 
and  skin  in  descending  order,  and  absent  or  scanty  in  the  brain  and  kidneys. 
It  has  been  found  in  the  umbilical  cord,  spleen,  lymph  nodes,  blood,  and 
the  bullae  of  syphilitic  pemphigus.  It  is  mainly  present  in  the  organs  most 
often  affected  histologically.  In  acute,  rapidly  fatal  cases  it  is  widely 
distributed  ;  in  chronic  ones  it  is  chiefly  in  the  liver.  Although  it  is  spread 
by  the  blood  it  is  rarely  intra-vasculax.  It  quickly  makes  its  way  through 
the  walls  of  the  vessels,  becomes  perivascular,  and  multiplies  in  the  cellular 
tissue.  The  anatomical  changes  are  periarteritis,  endarteritis,  infiltration  of 
connective  tissue  with  mononuclear  cells  and  secondary  sclerosis,  and 
degeneration  of  parenchymatous  cells.  The  transmission  of  the  organism 
and  the  effects  of  its  toxin  produce  dystrophies  as  well  as  immediate 
pathological  changes. 

Acquired  Syphilis. — The  disease  may  be  acquired  in  early  life  by  infec- 
tion during  labour,  if  the  mother  has  secondary  or  primary  syphilis  of  the 
natal  passages  ;  and  after  birth  from  one  or  other  parent,  a  wet  nurse  or 
attendant,  or  by  accidental  contact.  Coincident  syphilis  in  mother  and 
child  is  due  to  infection  of  the  mother  about  the  time  of  parturition,  and 
secondary  infection  of  the  child.  Infection  is  conveyed  directly  by  kissing, 
sexual  contact,  infected  instruments,  or  in  the  Jewish  mode  of  circum- 
cision ;  indirectly  by  spoons,  teats,  feeding  utensils,  thermometers,  toilet 
apparatus,  etc. 

The  primary  sore  is  usually  extra-genital,  most  frequently  on  the  lips,, 
less  often  the  mouth,  tonsil,  eyelid,  cheek,  face,  neck,  etc.  It  may  be  a  mere 
papule,  with  no  characteristic  induration.  A  vulvar  chancre  is  most  likely 
to  be  of  criminal  origin.  The  disease  may  be  milder  than  the  congenital 
form  for  it  appears  later,  when  the  child  is  better  able  to  withstand  its. 
influence.  The  rash  is  usually  macular,  scanty  and  evanescent,  often 
absent.    Condylomata  are  frequent  and  sometimes  present  in  huge  numbers. 


Syphilis  :     Acquired  and  Congenital.  865 

on  the  mouth,  pharynx,  nose,  genitals,  anus  and  scrotum.  The  glands  are 
enlarged  generally.  It  runs  the  same  course  as  in  later  life  but  is  more  acute. 
It  is  much  more  contagious  than  the  congenital  type,  and  must  therefore  be 
diagnosed  early.  Probably  many  cases  of  late  syphilis,  ascribed  to  the 
congenital  disease,  are  really  due  to  the  acquired  form.  The  evidence  of 
acquired  syphilis  in  infancy  is  a  chancre  appearing  at  least  21  days  after 
birth  and  secondary  symptoms  after  about  45  days.  Secondary  symptoms 
in  the  first  2  months  of  life  and  lesions  such  as  snuffles,  pemphigus, 
epiphysitis  and  cranial  bossing,  are  signs  of  congenital  syphilis. 

Congenital  Syphilis.— There  is  no  true  heredity  of  syphilis.  The  disease 
is  acquired  during  intra-uterine  life,  or  the  separation  of  the  placenta,  by 
transmission  from  the  mother.  Yet  healthy  children  have  been  born 
though  both  parents  have  been  infected.  Probably  many  inherit  the 
taint  and  never  show  symptoms,  growing  up  healthy.  The  question 
constantly  arises  whether  a  woman  can  have  a  syphilitic  child  without  being 
infected  herself.  In  other  words,  can  the  infection  be  transmitted  directly 
by  the  sperm  cell  to  the  ovum,  the  mother  escaping  infection  or  acquiring 
immunity  from  the  foetus  in  utero?  Or  is  the  child  invariably  infected 
through  the  placental  circulation,  as  suggested  by  the  finding  of  syphilitic 
changes  in  the  placenta  ? 

Conceptional  Syphilis. — Many  women  have  borne  syphilitic  children 
and  have  remained  under  observation  for  years  without  developing  specific 
sequels.  They  have  either  been  rendered  immune  by  impregnation  or, 
much  more  probably,  have  been  very  mildly  infected.  The  absence  of 
signs  of  infection  is  not  proof  of  non-infection.  Lesions,  supposed  to  be 
typically  syphilitic,  may  be  found  in  children  whose  parents  give  no 
evidence  or  history  of  the  disease. 

Sperm  Transmission  is  most  improbable.  The  treponema  pallidum  is 
1-4  times  the  diameter  of  a  red  corpuscle  in  length,  and  it  is  difficult 
to  believe  it  could  become  entangled  with  the  impregnating  sperm  cell 
and  thus  infect  the  ovum.  Beneficial  results  on  the  offspring  are  produced 
by  anti-specific  treatment  of  the  father  only,  the  mother  being  apparently 
healthy.  Recurrence  of  the  disease  in  the  father  may  be  followed  by  the 
birth  of  a  syphilitic  infant,  healthy  ones  being  born  when  he  is  properly 
treated.  Possibly  this  means  that  the  nutrition  of  the  sperm  cell  is  impaired 
by  the  disease,  or  that  the  organism  is  conveyed  in  the  semen  to  the  vagina 
and  thence  to  the  uterus  or  blood  of  the  mother,  finally  reaching  the  foetus. 
The  organism  has  been  found  in  large  numbers  in  a  4-J  months  foetus  (Bar 
and  de  Kervilly,  1907).  Finger  (1903)  collected  16  cases  in  which  the 
mother  of  syphilitic  children  on  a  subsequent  marriage  to  a  healthy  male 
bore  healthy  children.  In  such  instances  it  is  probable  that  the  mother 
was  only  mildly  infected  and  the  effects  had  died  out.  Paternal  trans- 
mission is  improbable,  except  through  infection  of  the  mother. 

3    K 


866  Chapter  LXII. 

Maternal  Transmission. — The  mother  can  transmit  the  disease  when 
the  father  is  unaffected.  Inoculation  experiments  on  apparently  healthy 
women  who  have  borne  syphilitic  children  have  proved  negative.  Even 
though  a  woman  has  several  affected  infants,  she  may  remain  in  apparently 
good  health,  and  she  can  nurse  her  syphilitic  infant  without  contracting  the 
disease  though  the  child  is  potentially  capable  of  infecting  a  wet  nurse 
( Colles's  Laiv).  According  to  this  law  every  mother  of  a  syphilitic  child 
is  immune.  This  does  not  prove  that  she  has  been  infected  during  pregnancy 
nor  that  she  has  acquired  immunity  from  the  foetus  without  being  herself 
infected.  There  is  no  evidence  that  the  mother  can  be  infected  by  the 
foetus  in  utero.  Absorption  per  vaginam  of  an  immunising  substance  in  the 
sperm  is  a  remote  possibility.  Exceptions  to  Colles's  law,  chiefly  in  primi- 
parse,  have  been  recorded  but  are  of  doubtful  value.  A  man  had  syphilis 
6  years  before  marriage.  His  first  child  was  breast-fed,  had  syphilis  and 
died  in  the  third  year.  The  second  child,  born  19  months  after  the  first, 
had  a  papular  eruption  in  the  mouth  and  was  breast-fed.  The  mother 
acquired  a  hard  chancre  on  the  nipple  and  a  secondary  rash  (Novy,  1906). 
Such  a  case  is  strongly  in  favour  of  germinal  paternal  infection.  As  far 
as  I  know  it  is  unique.  Intra-uterine  infection  is  most  likely  to  occur 
in  the  early  months  of  pregnancy,  before  the  placenta  is  differentiated. 
Later  on  the  placenta  must  be  sufficiently  diseased  to  permit  the  trans- 
mission of  the  organism.  A  child  born  within  a  dangerously  short  time  of  the 
primary  disease  in  the  parent  may  escape.  As  a  rule  the  later  the  stage  of 
the  disease  in  the  parent,  the  less  severe  is  it  in  the  infant.  A  common 
sequence  is  one  of  miscarriages  at  later  and  later  stages  of  pregnancy,  the 
birth  of  still-born  infants,  then  of  others  with  the  disease,  and  finally  healthy 
babies.  The  sequence  may  be  irregular,  perhaps  on  account  of  recrudescence 
of  the  disease  in  a  parent  or  of  treatment.  One  child  may  suffer  very 
definitely  and  all  the  others  escape.  It  is  unusual  for  several  to  suffer  in 
succession,  probably  because  of  treatment.  In  a  few  instances  one  of  twins 
has  been  affected  and  the  other  healthy. 

It  is  not  infrequent  to  find  a  first  child  healthy  and  a  later  one  syphilitic. 
Although  this  may  depend  on  parental  recrudescence  of  the  disease,  it 
must  not  be  forgotten  that  it  may  be  due  to  syphilis  acquired  by  the  father 
during  the  wife's  first  pregnancy  or  confinement,  by  the  mother  subse- 
quently, or  by  the  child  through  transmission  from  another  male  progenitor. 
The  only  symptoms  may  be  malnutrition  and  arrest  of  growth.  The  absence 
of  early  signs  is  no  proof  that  the  child  will  be  exempt  from  those  of 
late  congenital  syphilis. 

Disease  in  the  mother  does  not  necessarily  imply  either  disease  or 
immunity  in  the  child.  According  to  Profcta's  Law  the  healthy  child  of  a 
recently  infected  mother  is  immune  ;  that  is,  it  is  syphilitic,  but  presents  no 
evidence  thereof,  or  there  is  a  germinal  transmission  of  immunity.  On  the 
other  hand  many  such  infants  have  become  infected.     Such  immunity  is 


Syphilis  :     Acquired  and   Congenital.  867 

only  temporary  and  docs  not  persist  beyond  puberty.  Re-infection 
increases  the  virulence  of  the  disease  and  its  effects  on  the  offspring.  The 
syphilitic  mother  of  a  non-syphilitic  child  can  nurse  her  baby  with  little 
risk  of  transmitting  the  disease. 

Contagiousness  of  Congenital  Syphilis. — The  discovery  of  the  treponema 
is  strongly  in  favour  of  the  infectivity  of  the  disease.  Clinical  evidence 
.affords  little  support.  Many  of  the  older  writers  regarded  the  congenital 
form  as  highly  contagious,  much  more  so  than  the  acquired  disease.  In 
1898  Bulkley  considered  it  a  constant  source  of  the  acquired  disease. 
Fournier  and  Sir  J.  Hutchinson,  probably  the  two  greatest  authorities  on 
the  subject,  hold  that  it  is  infective  and  may  cause  nipple  chancre  in  a 
healthy  wet  nurse.  Henoch  has  not  found  one  wet  nurse  become  infected. 
"Gunzburg,  Physician  to  the  Foundling  Hospital,  Moscow  (1872),  stated 
that  31  healthy  wet  nurses  suckled  120  syphilitic  children  for  a  total  period 
•of  395  months  and  remained  perfectly  healthy.  Each  nurse  was  in  the 
syphilitic  ward  for  6-10  months.  Most  recent  writers  regard  it  as  little,  if  at 
all,  contagious.  Coutts  has  only  seen  one  doubtful  case.  Still  has  not 
;seen  one,  nor  have  I. 

Colles's  Law  has  been  accepted  as  proof  of  infectivity.  But  the  fact 
i;hat  the  mother  does  not  acquire  the  disease  from  her  child  is  no  proof 
that  a  wet  nurse  will  do  so.  In  almost  all  cases  of  supposed  infection  it  is 
■difficult  to  exclude  the  possibility  of  the  infecting  case  being  one  of  the 
.acquired  disease.  The  following  instance  (W.  R.  Grove,  1906)  illustrates 
this.  On  second-hand  evidence  the  mother  was  said  to  have  had  syphilis 
2  years  before  the  birth  of  her  illegitimate  child.  She  returned  to  service 
.soon  after.  The  child  had  universal  pemphigus  shortly  after  birth  and 
recovered.  It  was  treated  for  4  months.  At  8  months  it  had  condylomata ; 
and  at  18  months  condylomata  and  stomatitis.  Then  the  grandmother  and 
:2  children,  aged  12  and  7  years,  developed  primary  sores  on  the  tonsils. 
Infection  was  supposed  to  have  been  cairied  by  feeding  utensils.  But  it 
is  possible  that  the  infant  had  acquired  syphilis,  or  that  the  family 
were  infected  from  another  source.  A  universal  pemphigus,  ending  in 
recovery,  cannot  be  accepted  as  proof  of  congenital  syphilis. 

There  is,  however,  proof  of  infectivity  in  the  discovery  of  the  treponema 
;and  in  the  transmission  by  vaccination.  Cory  had  to  make  use  of  4  children 
before  he  was  able  to  infect  himself  with  the  disease.  Hutchinson  collected 
a  number  of  cases  in  which  persons  acquired  syphilis  by  vaccination  with 
lymph  from  affected  infants.  It  must  be  admitted,  unless  we  assume  that 
in  all  these  instances  the  infant  was  suffering  with  acquired  syphilis,  that 
the  disease  can  be  transmitted,  though  its  contagiousness  is  slight  and  has 
been  much  over-estimated.  The  organism  is  not  always  present  in  the 
local  lesions,  blood  or  lymph. 

Syphilis  in  the  Nurse. — In  view  of  the  possibility  of  a  wet  nurse 
•claiming  that  she  has  acquired  the  disease  from  the  infant,  it  is  important  to 


868  Chapter  LXII. 

consider  the  evidence  pro  and  con.  A  chancre  takes  at  least  21  days  to 
develop  and  secondary  symptoms  appear  in  about  45  days.  Hence,  the- 
stage  of  the  disease  may  be  too  advanced  for  it  to  have  been  caught  from 
the  child.  The  position  of  the  primary  sore  should  be  conformable,  e.g- 
on  the  breast.  There  must  be  further  evidence  such  as  induration,  a  bubo,, 
mucous  plaques,  rash,  condylomata,  etc.  It  must  be  quite  clear  that  the- 
child  showed  priority  of  infection.  Either  the  child  or  the  nurse  may  have 
acquired  the  disease  from  each  other  or  independently.  Examine  the- 
nurse's  child  and  husband.  If  the  child  is  unaffected,  the  nurse  has  not  had 
recent  syphilis.  The  nurse  may  have  been  giving  the  breast  to  other  infants 
or  may  have  acquired  a  mammary  chancre  from  venereal  contamination. 

Syphilis  of  the  Third  Generation. — It  is  generally  accepted  that  the= 
children  of  those  who  have  had  congenital  syphilis  are  not  affected.  Before- 
regarding  any  case  as  affording  reliable  evidence  of  transmission  to  the 
third  generation,  many  sources  of  error  must  be  taken  into  account.  Either 
parent,  though  congenitally  syphilitic,  may  have  acquired  the  disease  in 
later  life.  Both  primary  and  secondary  syphilis  may  be  mild  and  overlooked. 
The  husband  is  not  necessarily  the  father.  Boeck  (1904)  reported  3  cases~ 
The  grandmother  had  secondary  syphilis  ;  the  mother  congenital  syphilis  in 
1860  at  2  years  of  age,  and  many  signs  thereof  in  1889  when  she  brought 
her  child,  aged  4  months,  with  typical  congenital  syphilis.  The  mother 
showed  no  evidence  of  the  acquired  disease,  had  had  no  miscarriages,  and 
had  had  a  healthy  first-born  child.  The  husband  gave  no  evidence  of 
syphilis.  Possibly  the  father  was  syphilitic  or  the  mother  had  been 
re-infected  after  the  birth  of  her  first  child.  In  the  second  case  the  grand- 
mother had  acquired  syphilis  in  1873.  The  mother  showed  scars  about  the- 
mouth  in  1897  and  had  a  congenitally  syphilitic  child.  The  father  was  not- 
examined.  In  a  third  instance  the  grandmother  showed  tertiary  syphilis,, 
the  mother  had  scars  about  the  mouth  and  Hutchinson's  teeth,  and  her  first 
2  children  were  syphilitic.  Here  too  the  possibility  of  re-infection  of  the 
mother  or  a  syphilitic  father  was  not  excluded.  In  a  case  recorded  by 
C.  F.  Marshall  the  evidence  of  congenital  syphilis  was  weak  and  the  father- 
was  not  examined.  The  grandmother  had  scars  of  gummata  about  the 
knees.  The  mother,  at  age  16,  had  gummata  in  the  popliteal  space  and 
extensive  destruction  of  the  palate.  Her  first  child  had  saddle  nose  and 
frontal  bosses,  the  second  died  of  bronchitis,  and  the  third  was  healthy  _ 
There  were  no  miscarriages. 

Fournier  collected  116  cases  of  which  59  in  his  opinion  fulfilled  the 
conditions  required.  He  states  that  the  disease  manifests  itself  by  dys- 
trophic stigmata  like  those  of  the  second  generation,  and  by  virulent  syphilis, 
in  14  per  cent.  Tarnowsky  (1904)  agrees  with  Fournier  as  regards  the 
transmission  of  dystrophic  effects  but  not  of  virulent  syphilis.  Possibly  a 
dystrophic  influence  is  transmitted  in  the  form  of  a  tendency  to  pre- 
maturity, delicacy  and  malnutrition.     As  a  rule  congenital  syphilis  has. 


Syphilis  :    Acquired  and  Congenital.  869 

•ceased  to  be  virulent  by  the  time  procreative  age  is  reached.  Fournier 
investigated  the  results  of  the  marriages  of  46  patients  with  congenital 
syphilis.  Out  of  145  pregnancies  there  were  39  still-boms, 43 abortions  and 
63  living  children.  Nearly  all  showed  stigmata  of  degeneration,  especially 
defects  of  the  eyes  and  teeth.  According  to  him  certain  diseases  may  be 
syphilitic  in  origin  but  not  in  nature.  To  this  condition  he  gives  the  name 
•of  "  parasyphilis."  Syphilitic  affections  are  closely  allied  to  and  simulate 
non-specific  ones.  There  is  no  strict  line  of  demarcation.  The  so-called 
parasyphilitic  affections  are  anaemia,  marasmus,  rashes,  choroiditis,  inter- 
stitial keratitis,  leucoderma  and  notched  teeth.  They  can  occur  indepen- 
dently of  syphilis  and  may  be  unaffected  by  specific  drugs.  Parasyphilis, 
as  a  distinct  affection,  needs  more  evidence  in  its  favour. 

On  the  whole  we  must  regard  transmission  of  the  disease  to  the  third 
generation  as  not  proven.  There  is  not  the  least  evidence  of  such  trans- 
mission when  the  transmitter  of  the  second  generation  did  not  have 
congenital  syphilis. 

Pathology. — A  diffuse  blood  infection  sets  up  a  diffuse  cell  proliferation, 
i.e.  an  inflammation,  in  the  perivascular  connective  tissue  of  the  minute 
blood  vessels.  The  lesions  are  multiple,  similar  in  type,  but  modified  by  the 
structures  in  which  they  occur.  Blood  vessels  may  be  obliterated  by  con- 
traction of  the  perivascular  connective  tissue  or  by  secondary  endar- 
teritis, spreading  from  without.  The  organs  are  much  increased  in  weight 
but  may  show  no  macroscopic  evidence  of  disease.  The  parenchyma  is 
sometimes  unrecognisable.  There  is  a  tendency  to  cirrhotic  changes,  and 
to  aggregation  of  newly-formed  cells  in  masses  as  syphilomata.  Minute 
•areas  of  anaemic  necrosis,  the  size  of  a  large  pin's  head,  are  found  in  the 
liver,  kidneys,  adrenals  and  epiphyses.  The  liver  is  always  affected  in  the 
foetus  and  generally  in  all  infants.  The  skin,  lungs,  pancreas,  kidneys, 
adrenals,  spleen  and  epiphyses  are  attacked.  The  inflammatory  changes 
in  the  skin  start  as  a  proliferation  in  the  blood  vessels  of  the  sweat  glands. 
According  to  some  authorities  the  intestinal  glands  of  the  foetus,  formed 
in  the  third  and  fourth  months  of  pregnancy,  first  exhibit  this  diffused 
syphilitic  inflammation.  The  blood  signs  are  deficiency  of  red  cells  and 
haemoglobin,  the  presence  of  nucleated  red  cells,  and  a  leucocytosis, 
•especially  of  myeloblasts  and  eosinophiles.  Secondary  arrests  of  develop- 
ment are  liable  to  occur  in  affected  organs. 

Symptomatology. —  Foetal  syphilis  is  a  visceral  and  bone  affection. 
Hepatic  enlargement  and  osteochondritis  are  the  chief  signs  in  the  foetus 
and  still-born  child.  The  bone  changes,  especially  at  the  epiphysial  lines, 
are  the  most  constant.  There  is  a  tendency  to  diffuse  infiltrations  in  the 
viscera  of  the  foetus  and  the  cutaneous  tissues  of  the  infant,  notably  the 
palms  and  soles.  The  changes  are  most  marked  in  the  structures  which,  at 
the  time  of  infection,  are  undergoing  the  most  rapid  development.  The  skin 
is  of  somewhat  later  development,  as  regards  its  glandular  structures,  than 


870  Chapter  LXII. 

other  organs  and  is  consequently  affected  in  the  later  months  of  pregnancy, 
shortly  before  birth,  or  not  until  after  birth.  Although  its  glands  are 
formed  at  the  fifth  month,  their  blood  vessels  do  not  develop  until  the  seventh 
month  of  foetal  life.  The  palms  and  soles  are  particularly  liable  because  of 
their  multiple  sweat  glands. 

Syphilis  at  Birth. — Pregnancy  may  end  in  the  expulsion  of  a  macerated 
foetus,  a  dead  foetus,  a  still-born  babe,  a  premature  and  feeble  infant  which 
survives  a  few  hours  or  days,  a  babe  showing  signs  of  the  disease,  or  one 
which  is  apparently  healthy.  Death  of  the  foetus  is  most  common  between 
the  fourth  and  seventh  months,  and  is  due  to  placental  disease  or  severe- 
general  infection.  Though  maceration  of  the  foetus  is  not  conclusive  of 
syphilis,  it  is  strongly  suggestive  for  it  is  due  to  this  cause  in  about  two- 
thirds  of  the  cases. 

The  presence  of  signs  at  birth  is  indicative  of  grave  infection.  The 
babe  is  feeble,  dull,  torpid  and  ill-nourished,  with  wrinkled  skin,  old-age 
aspect  and  subnormal  temperature.  It  usually  exhibits  an  eruption  of 
papules,  pustules  or  bulla?,  snuffling,  jaundice  due  to  intercellular  hepatitis, 
enlargement  of  the  liver  and  spleen,  epiphysitis  and  perhaps  choroido- 
retinitis.    Death  ensues  in  1-4  weeks. 

Later  Signs. — Frequently  there  is  no  indication  at  birth  and  the 
symptoms  appear  during  the  first  two  months  of  life,  less  often  in  the 
third  month  and  rarely  later.  In  about  half,  the  signs  appear  in  the  second 
to  fourth  week.  They  are  most  marked  in  the  skin  and  mucous  membranes.. 
Mild  cases  are  often  unrecognised. 

Wasting  is  an  important  sign  and,  if  present  in  the  first  three  months 
without  an  apparently  reasonable  cause,  is  very  suggestive.  It  may  be  of  a 
very  severe  type,  beginning  shortly  after  birth,  with  no  definite  relationship 
to  the  severity  of  the  syphilitic  signs  and  not  improving  as  these  signs 
subside.  There  may  be  no  demonstrable  changes  after  death.  Wasting, 
in  proportion  to  the  severity  of  the  symptoms,  is  of  less  grave  prognostic 
import.  At  birth  the  child  may  be  a  fine  baby.  If  breast-fed  and  not 
gravely  infected  it  may  maintain  its  nutrition.  More  commonly  it  is  not 
so  fed,  or  the  breast  milk  is  insufficient  in  quality  and  quantity,  and  it 
wastes  progressively  until  it  reaches  the  stage  of  marasmus  in  which  the 
facial  aspect  is  that  of  wrinkled  old  age,  with  the  skin  hanging  in  folds  all: 
over  the  body  and  deficient  in  elasticity,  in  colour  like  that  of  cafe  au  lait 
through  infiltration  and  pigmentation  of  the  rete  Malpighii,  and  in  texture 
thin  and  dry.  The  child  is  whining,  irritable,  peevish,  restless  and  sleeps 
badly  and  may  be  feverish  from  enteric  disturbance,  epiphysitis,  etc. 

Rhagades. — The  lips  are  stiffened  by  infiltration  and  crack  at  the 
angles,  forming  radial  fissures.  Similar  fissures  are  found  at  the  edges  of 
the  nostrils  and  eyes  and  in  the  genito-anal  region.  The  tongue  has  a, 
shaven  appearance   the  filiform  papilla?  being  stripped  off,  the  fungiform* 


Syphilis  :     Acquired  and  Congenital.  871 

left,  and  the  circumvallate  enlarged.    Papules  and  mucous  plaques  are  seen 
on  the  baccal  mucosa. 

Snuffles  (p.  374),  a  subacute  or  chronic  coryza,  is  present  in  §--£  and  is 
one  of  the  first  signs.  It  usually  begins  before  the  rash  in  the  first  month, 
commonly  in  2-3  weeks,  and  may  be  present  at  or  shortly  after  birth. 
It  gives  rise  to  mouth-breathing,  loud  snuffling  and  difficulty  in  suckling. 
In  severity  it  varies  from  slight  stuffiness  up  to  acute  obstructive  hyper- 
trophic rhinitis,  ulceration  of  the  nasal  mucosa  and  necrosis  of  bone. 

In  babies  the  discharge  is  primarily  serous,  later  yellow  and  irritating, 
and  may  become  profuse,  muco-purulent  and  bloody.  It  may  only  be 
visible  in  the  pharynx.  The  nose  is  blocked  by  swollen  mucous  membrane 
and  thick  crusts.  The  bridge  becomes  thickened  and  depressed,  the  tip 
swollen  and  tilted  up,  and  its  appearance  describable  as  "  pug  nose  "  or 
"  saddle  nose."  The  pug  nose  is  due  to  contraction  of  the  tissues  and 
cartilage,  and  the  nostrils  look  upward.  Sometimes  the  bridge  never 
develops  although  there  has  been  no  definite  external  evidence  of  disease 
and  bone  destruction.  Snuffles  must  be  differentiated  from  other  causes 
of  nasal  discharge  (p.  371). 

Its  course  is  chronic,  more  than  2  weeks.  The  catarrh  frequently 
extends  to  the  pharynx  and  larynx,  interfering  with  swallowing  and 
respiration,  and  affecting  the  voice. 

Gummatous  deposit  in  the  submucosa  and  periosteal  thickening  may 
lead  to  ulceration,  caries  and  extensive  necrosis,  even  in  the  early  months 
of  life.  It  is  more  frequent  in  later  childhood  and  causes  ozama,  destructive 
ulceration  of  the  nasal  structures,  necrosis  and  falling  in  of  the  nasal  bridge. 
The  nose  may  be  almost  destroyed  in  a  few  weeks. 

Rashes. — The  skin  eruption  is  more  or  less  synchronous  with  the  coryza, 
usually  a  few  days  to  a  week  later.  It  may  come  out  independently  if  the 
coryza  is  absent,  slight  or  overlooked.  It  is  present  in  two-thirds,  uncommon 
after  6  months,  and  exceptionally  delayed  until  the  end  of  the  first  year. 
The  common  sites  are  the  soles  and  palms,  the  glabella  or  triangular  space 
between  the  eyebrows,  the  bathing  drawers  area,  the  legs,  trunk  and  arms, 
and  the  muco-cutaneous  junctions.  Itching  is  rare.  Polymorphism  is  a 
marked  characteristic.  Spots  tend  to  coalesce  into  extensive  areas  and  in 
situations  like  the  napkin  region  are  liable  to  superficial  ulceration.  Second- 
ary pus  inoculation  may  occur.  Many  varieties,  diffuse  or  circumscribed, 
have  been  noted  independently  or  in  combination,  and  occasionally 
associated  with  non-specific  rashes,  such  as  erythema,  intertrigo,  seborrhoea, 
lichen  urticatus,  eczema  and  pustular  dermatitis.    The  chief  varieties  are  : — 

1.  Simple  erythema  of  the  buttocks  and  perineum,  extending  down  the 
inner  side  of  the  thighs,  on  to  the  scrotum  or  vulva,  and  even  on  to  the 
abdomen  and  down  to  the  feet.  This  rash  is  not  evidence  of  syphilis,  unless 
it  distinctly  spreads  beyond  the  area  of  friction  (bathing  drawers  area), 


872  Chapter  LXII. 

affects  the  palms  and  soles,  and  is  smooth  and  scaleless.     The  tint  is 
variable. 

2.  A  dry  desquamative  rash  is  characteristic.  It  particularly  affects 
the  palms  and  soles,  causing  the  epidermis  to  peel  off  in  great  flakes  and 
leave  a  smooth,  dusky  red,  glazed  or  glossy  surface  of  sclerosed  and 
thickened  skin. 

3.  The  common  rash  is  macular  or  papulo-macular  in  type,  such  as  is 
seen  in  acquired  syphilis,  and  sometimes  pustular.  The  macular  rash  is 
the  mildest  and  the  pustular  one  the  most  serious.  The  rash  is  often 
polymorphous.  Macules  are  more  or  less  circular,  disc-shaped  patches  of  a 
roseolous,  pale  rose  red,  dusky  red,  raw  ham  or  coppery  colour.  They 
appear  on  any  part  of  the  body  but  have  a  special  predilection  for  the 
junction  of  the  forehead  and  hairy  scalp,  the  glabella,  cheeks,  chin,  neck, 
buttocks,  hands,  feet  and  the  flexor  surfaces  of  the  upper  and  lower 
extremities.  There  is  evidence  that  a  roseola  never  appears  on  the  trunk  in 
congenital,  only  in  acquired  syphilis.  Papules  are  most  frequent  on  the 
palms  and  soles.  The  macules  become  covered  with  fine  scales.  Finally 
smooth  coppery  discs  are  left  and  persist  for  some  time.  They  may 
desquamate,  or  fade  from  the  centre,  and  leave  pigmented  spots.  The  rash 
develops  fully  in  1-3  weeks  and  lasts  1-2  months. 

A  frequent  combination  is  a  diffuse  erythema  of  the  bathing  drawers 
area,  with  roseolous  macules,  papules  or  coppery  discs  on  the  adjacent  skin 
and  distributed  fairly  generally  over  the  rest  of  the  body,  least  on  the 
trunk.  The  rash  is  never  as  bright  red  as  true  intertrigo,  and  the  skin  feels 
stiff  from  the  infiltration  but  is  not  swollen.  The  scrotum  is  often  swollen, 
opdematous  and  peeling.  Condylomata  are  fairly  common.  Ulceration  is 
rare  except  in  moist  areas. 

4.  Pemphigus  is  a  bullous  rash  with  a  special  affinity  for  the  palms 
and  soles  where  it  first  appears.  It  is  not  seen  in  acquired  syphilis.  It  is 
a  sign  of  severity  and  may  be  present  before,  at  or  shortly  after  birth,  and  is 
rare  after  the  fifth  week.  The  bullae  are  as  big  as  peas  or,  by  coalescence, 
reach  the  size  of  marbles.  Their  contents  are  sero-pus  or  bloodstained 
serum.  The  base  is  infiltrated,  excoriated  and  copper  coloured.  Ulceration 
and  even  gangrene  of  the  skin  may  supervene.  On  the  face  and  head  the 
rash  becomes  pustular.  Papules  appear  on  other  parts.  It  must  be 
distinguished  from  pemphigus  neonatorum  (p.  142),  a  rash  which  is  never 
present  at  birth  and  has  no  infiltration  of  the  bases  of  the  bullae. 

5.  Secondary  ulceration  of  the  mucosa,  usually  superficial,  is  apt  to 
occur  and  spread  to  the  skin  or  the  thickened  skin  is  liable  to  crack  and 
fissure  (rhagades).  These  ulcers  are  multiple,  linear,  bleed  readily,  and 
form  fissures  radiating  outward  from  the  angles  of  the  mouth,  nose,  eyes  and 
anus.    They  leave  behind  radiating  scars. 

6.  Mucous  patches  and  condylomata  are  papules  modified  by  peculiari- 
ties of  situation.    Mucous  patches  are  found  on  the  buccal  mucosa,  tonsils 


Syphilis  :     Acquired  and  Congenital.  873 

and  soft  palate.  Condylomata  develop  from  papules  situated  in  moist 
^contiguous  places  such  as  the  anus  and  perineum,  folds  of  the  buttock, 
scrotum,  vulva,  behind  the  ears  and  sometimes  in  the  axilhe.  They  are 
Taised,  flat- topped,  moist,  whitish  discs,  £-4  in.  diameter.  They  are  rarely 
seen  before  6  months  of  age  ;  may  be  found  in  the  genito-anal  region 
from  the  second  to  the  sixth  year,  rarely  after  the  fourth  year ;  and  are 
much  more  frequent  in  the  acquired  disease.  Both  mucous  plaques  and 
•condylomata  are  apt  to  end  in  superficial  ulceration,  especially  in  the 
mouth  and  genitals. 

7.  Ringed  eruptions,  vesicles,  pustules  and  serpiginous  rash  are 
uncommon  varieties.  Ulcers  are  occasionally  deep  and  serpiginous.  The 
infiltration  of  the  buttocks  may  be  dense  and  gummatous. 

8.  Cutaneous  gummata,  sometimes  described  as  "  blind  boils  "  or 
a  "  furuncular  syphilide  "  (C  Carpenter),  are  by  no  means  rare  during 
the  first  year.  Apparently  they  are  not  a  true  gummata.  The  skin  is 
■dusky,  coppery  or  bluish,  and  contains  nodular  infiltrations.  These  attain 
the  size  of  peas,  are  raised  above  the  surface,  and  may  have  a  vesicular, 
pustular  or  scabbed  apex.  Occasionally  they  are  larger  or  aggregated  into 
groups.  They  often  break  down  by  central  softening  and  necrosis,  dis- 
•charging  their  contents  and  leaving  a  small  deep  ulcer  which  soon  heals. 
They  are  most  common  on  the  head,  buttocks  and  thighs. 

9.  Subcutaneous  gummata  are  rare  in  infancy  but  may  occur  at  any 
later  age.  They  are  often  single,  at  first  movable,  and  form  dome-shaped, 
projecting,  dusky  red  or  purplish,  rather  soft  nodules  of  variable  size. 
Later  they  adhere  to  the  skin  which  is  infiltrated,  hypersemic,  and  breaks 
down,  forming  a  deep,  clean  cut  or  serpiginous  ulcer.  The  usual  site  is  the 
head  or  the  neighbourhood  of  a  joint.  A  white  scar  is  left  on  healing. 
Muscular  gummata  are  very  rare. 

The  Hair  and  Nails. — A  profuse  growth  of  hair,  straight,  dark  in 
•colour  and  fine  in  texture,  has  been  regarded  as  specific  and  named  the 
""  syphilitic  wig."  The  evidence  in  its  favour  is  inconclusive.  Usually  the 
hair  becomes  very  thin  and  scanty  in  a  few  months,  especially  on  the 
vertex  and  eyebrows.  Permanently  bald  patches  may  develop.  Absence  of 
occipital  hair  is  due  to  many  causes  and  not  of  diagnostic  value.  Absence 
of  eyebrows  is  more  suggestive.  Eruptions  on  the  scalp  may  stimulate 
■sebaceous  activity  and  the  formation  of  seborrheic  crusts.  The  subjacent 
skin  does  not  ulcerate  and  patches  of  the  rash  may  be  seen  at  the  edges 
of  the  crusts. 

The  nails  may  show  a  paronychia  sicca  vel  ulcerosa,  or  a  true  suppurative 
inflammation  of  the  matrix,  generally  in  conjunction  with  a  desquamative 
rash.  The  adjacent  skin  at  the  bases  is  discoloured,  thick,  glossy,  scaly 
and  crusted.  The  nails  become  discoloured,  opaque  or  dusky  ;  shrivelled, 
furrowed,  arched  or  claw-like,  or  narrowed  at  the  base  and  fan-shaped  at 
the  free  edge  ;  dry  and  brittle  ;  and  may  be  exfoliated,  perhaps  repeatedly. 


874  Chapter  LXII. 

A  transverse  furrow  or  ridge  divides  the  new,  more  or  less  healthy  nail,, 
from  the  thin  soft  diseased  portions.  The  finger  nails  are  more  affected 
than  the  toes. 

The  Bones  and  Joints. — These  are  secondary  rather  than  tertiary 
symptoms,  multiple,  symmetrical,  early  in  onset,  and  transitory.  Epiphy- 
sitis, a  cause  of  pseudo-paralysis,  is  present  in  10-20  per  cent.  It  is  described 
together  with  the  later  manifestations  of  joint  disease,  in  a  previous  chapter 
(pp.  817-8).  Periostitis  may  occur  independently  of  epiphysitis  and  form 
nodes,  rarely  under  6  months  of  age.  The  humerus  and  tibia  are  chiefly 
affected  in  infants,  and  the  tibia  in  older  children.  It  is  more  frequent  about 
puberty,  at  which  age  osteitis  may  occur.  The  diaphysis  becomes  spindle- 
shaped  from  thickening  of  the  periosteum  and  the  joint  may  be  involved. 
Subsequently  it  leaves  a  thickened,  rounded  tibial  crest  and  an  antero- 
posterior sabre-like  curvature,  chiefly  of  the  middle  third.  Fournier  has 
consequently  named  the  tibia  the  os  revelateur. 

Dactylitis  may  affect  the  fingers  and,  to  a  less  extent,  the  toes.  It  is 
a  gummatous  periostitis  and  the  interior  of  the  bone  is  unaffected  or 
sclerosed.  It  occurs  in  the  first  few  years  of  life,  even  as  early  as  the  third 
month.  It  begins  in  and  chiefly  affects  the  proximal  phalanges,  especially 
the  index  finger,  rarely  attacks  the  metacarpals  and  metatarsals,  and  never 
involves  the  joints.  In  a  girl,  3  months  old,  the  first  metatarsals  were  alone 
diseased.  It  may  be  limited  to  one  finger,  or  be  multiple  and  often  sym- 
metrical. The  affected  parts  are  painless,  swollen,  red  and  fusiform.  The 
inflammation  is  subacute,  tends  to  recovery  and  does  not  break  down.  It 
must  be  distinguished  from  tuberculous  dactylitis,  closely  resembling  it  in 
appearance,  due  to  a  caseous  focus  in  the  bone  and  secondary  periostitis, 
and  tending  to  suppuration.  In  this  the  metacarpals  and  metatarsals  may 
be  affected. 

Gummatous  cranial  syphilis  is  uncommon  in  early  childhood.  Hoch- 
singer  saw  4  cases  in  600  syphilitic  nurslings.  It  ends  in  absorption,  the 
formation  of  a  cranial  boss,  ulceration,  or  necrosis  and  exfoliation,  perhaps 
leaving  a  large  gap  in  the  frontal  or  parietal  region.  Parrot's  nodes  is  a 
name  given  to  the  cranial  bosses  or  hyperostoses  of  the  skull,  due  to  excessive 
formation  of  bone  in  the  frontal  and  parietal  regions  surrounding  the 
anterior  fontanelle,  giving  the  skull  a  "  hot-cross  bun  "  aspect,  the  sulci 
being  the  sutures.  The  forehead  is  square  and  upright,  the  frontal  emi- 
nences prominent,  and  the  bones  very  hard.  These  bosses  develop  after  birth. 
They  are  frequently  absent  in  syphilis,  present  in  rickets  with  no  evidence 
of  syphilis,  and  still  more  often  absent  in  rickets.  Possibly  they  are  rachitic 
in  origin  (p.  184),  or  the  result  of  syphilis  as  an  additional  factor.  They 
must  be  regarded  as  specific  if  they  are  present  in  the  first  few  months  of 
life  in  a  child  with  a  small  anterior  fontanelle  and  hard  bone.  The  nodes 
have  a  bluish  colour  as  seen  through  the  thin  scalp.  Frontal  bosses  and  a 
prominent  square  forehead  are  rachitic.     Craniotabes  has  been  described 


Syphilis  :     Acquired  and  Congenital.  875- 

as  a  rachitic  sign  (p.  184).  The  type  in  which  there  are  numerous,  small 
areas  of  softening,  crackling  on  pressure,  chiefly  in  the  parietal  bones,  in 
the  first  4  months  of  life  is  probably  syphilitic  in  origin. 

Necrosis  leads  to  depression  of  the  bridge  of  the  nose,  exfoliation  of  the- 
vomer  and  turbinals,  perforation  or  destruction  of  the  septum  nasi  and  hard 
palate,  and  destruction  of  the  cranial  bones.  Perforation  of  the  nasal- 
septum  has  occurred  at  6  months  (Goldreich,  1908).  These  effects  are  rare 
before  the  onset  of  the  first  dentition  and  are  commonly  delayed  until 
about  puberty.    Most  of  them  are  secondary  to  gummatous  infiltration. 

The  Circulatory  System  and  Blood.— Developmental  errors  (p.  466)' 
may  be  present.  Duguy  ascribed  many  cases  of  mitral  stenosis,  of  which 
several  were  associated  with  other  defects,  to  this  cause.  Myocardial  and 
endocardial  changes,  gummatous  aortitis,  and  endarteritis  are  late  affections. 
Arteriosclerosis  may  be  due  to  the  specific  toxin.  Endarteritis  is  rare  in  the 
viscera  ;  it  may  be  found  in  the  brain  and  in  chronic  meningitis,  and  cause 
softening. 

Interstitial  myocarditis  may  occur  in  infancy  and  cause  sudden 
death  while  in  apparent  health.  It  is  indicated  by  paroxysmal  dyspnoea, 
cough  and  intense  cyanosis.  Foci  of  anaemic  necrosis  in  the  heart  are 
liable  to  be  mistaken  for  gummata. 

Anaemia  is  proportionate  to  the  severity.  The  blood  picture  is  that  of 
secondary  anaemia  or  of  a  more  infantile  stage  of  development.  Severe 
anaemia,  independent  of  splenic  hyperplasia,  may  appear  in  the  second 
year,  without  other  evidence  of  syphilis  or  after  the  symptoms  have 
subsided.  Haemorrhages  arise  from  ulceration  of  the  mucous  membranes. 
Umbilical  bleeding  depends  on  vascular  disease  impairing  contractility. 
Some  cases  of  haemorrhagic  disease  of  the  newborn  (p.  127),  and  possibly 
haemoglobinuria,  are  syphilitic  in  origin. 

The  Glands  and  Spleen. — The  glands  in  the  axillae,  groins  and  occipital 
region  are  often  palpable  and  a  little  enlarged,  hard,  separable  and 
movable  ;  usually  in  conjunction  with  anaemia  and  enlargement  of  the 
liver  "and  spleen. 

The  spleen  is  palpable  in  about  half  the  cases  but  clinically  should  not 
be  accepted  as  definitely  enlarged  unless  it  extends  h  in.  below  the  costal 
margin.  Marfan  (1903)  agrees  with  Birch-Hirschfeld  that  the  spleen  of 
non-syphilitic  stillborn  babies  is  0'33  per  cent.,  and  that  of  the  syphilitic 
is  0-76  per  cent,  of  the  body  weight.  Hochsinger  gives  the  relative  pro- 
portions as  ^5  and  Ty  8  of  the  body  weight.  Marfan  states  that  75 
per  cent,  of  enlarged  infantile  spleens  are  due  to  syphilis  and  almost  all  the 
rest  to  rickets.  Out  of  376  infants  under  2  years  old  40  had  large  spleens  : — 
undoubted  congenital  syphilis  18,  probable  13  (with  rickets  in  12),  rickets, 
without  syphilis  6,  tuberculosis  1,  and  no  definite  cause  2.  The  hyperplasia 
is  an  interstitial  splenitis  with  fibrous  overgrowth,  chiefly  affecting  the 


•876  Chapter  LXII. 

Malpighian  bodies  and  vessel  walls.  Perisplenitis  is  not  uncommon  and 
may  cause  adhesions. 

The  Respiratory  System. — Catarrhal  laryngitis  is  a  common  early 
symptom,  causing  hoarseness  and  aphonia,  and  is  liable  to  be  mistaken  for 
■croup.  The  chronic  form  is  generally  a  late  symptom  and  adult  in  type. 
It  causes  chronic  cough  and  hoarseness,  perhaps  aphonia,  and  occasionally 
•attacks  of  dyspnoea  which  may  be  so  severe  as  to  necessitate  tracheotomy. 
The  various  parts  are  swollen  or  ulcerated.  The  epiglottis  may  be  deeply 
fissured,  the  ary-epiglottic  folds  ulcerated  and  the  vocal  cords  thickened. 
Some  cases  have  condylomata  or  papillomata  on  the  epiglottis  and  vocal 
cords.  Older  children  may  show  perichondritis,  papillomatous  excrescences, 
ulceration  of  the  larynx,  destruction  of  the  uvula  and  epiglottis  ;  scarring, 
ulceration,  gummata  or  perforation  of  the  palate  ;  gummatous  affections  of 
the  larynx  and  trachea,  and  even  tracheal  fistula.  Acute  laryngitis,  oedema 
of  the  glottis  and  laryngeal  stenosis  may  occur.  A  case  of  Frankl's  died  at 
3  months  from  acute  stenosis  due  to  necrosis  of  the  cricoid  cartilage  and  left 
arytenoid.  Mattosso  (1905)  reported  stenosis  at  4  months  of  age.  From 
birth  the  boy  had  stridor,  increasing  difficulty  in  breathing  and  nursing, 
retraction  of  the  chest,  suffocative  attacks  and  wasting.  Recovery  followed 
injections  of  biniodide  of  mercury.  Stenosis  of  the  trachea  or  bronchus  is  a 
rare  sequel  of  gummatous  infiltration.  The  symptoms  (p.  393)  are 
uninfluenced  by  posture. 

In  the  foetus  the  lungs  may  show  gummata  or  white  hepatisation, 
the  "  white  'pneumonia  "  of  Virchow,  a  fibrous  induration  with  grey  areas 
of  consolidation.  Microscopical  examination  reveals  infiltration  with 
lymphoid  cells  ;  cylindrical  or  cubical  masses,  the  remains  of  foetal  lung 
tissue  ;  and  fatty  degeneration  of  the  alveolar  septa.  Its  general  appear- 
ance is  much  like  sarcoma.  Possibly  the  supposed  gummata  are  remnants 
of  foetal  lung  tissue.  Gummata  have  occasionally  been  found  in  the  first 
year  of  life  and  later.  They  may  soften  and  produce  bronchiectasis.  Some 
of  the  chronic  fibroid  changes,  interstitial  pneumonia,  in  the  lungs  of  infants 
are  possibly  of  syphilitic  origin.  Both  fibroid  changes  and  gummata  may 
be  present. 

The  Alimentary  System. — Apart  from  mucous  patches  and  rare  faucial 
affections,  there  is  nothing  characteristic  of  the  disease  in  infancy.  Subse- 
quently the  tongue  may  show  rough,  corrugated  patches,  suggestive  of 
leucoplakia  and  perhaps  due  to  recurrent  condylomata  ;  and  in  later  child- 
hood may  be  enlarged,  thickened  and  contain  indurated  nodules,  or 
a  single  unilateral  gumma.  Deep  ulceration  of  the  palate,  pharynx  and 
naso-pharynx  is  rarely  seen  in  the  first  year.  It  usually  occurs  about 
puberty,  is  followed  by  caries  and  necrosis,  and  is  remarkably  rapid  and 
destructive  in  its  progress. 

The  milk  teeth  show  no  special  changes.  They  may  appear  unduly  early 
and  are  prone  to  decay.    Hutchinson  described  certain  peculiarities  of  the 


Syphilis  :     Acquired  and   Congenital.  877" 

permanent  teeth,  notably  a  semilunar  erosion  of  the  upper  central  incisors,, 
and  peg-like  lateral  incisors.  The  central  incisors  are  the  most  liable  to  show 
defects.  They  are  dwarfed,  rounded  and  peg-like,  short  and  strong  ;  and 
sometimes  present  a  central  crescentic  notch  and  chisel  shaped  section,  a 
concave  free  edge,  bevelled  anterior  surface  and  rounded  corners.  The 
deformity  is  present  before  they  are  cut.  It  is  due  to  impaired  nutrition  of 
the  dental  germ  from  various  causes.  The  bicuspids  are  often  peg-like.. 
The  first  molars  are  "reduced  in  size  and  dome-shaped,  through  the 
dwarfing  of  the  central  tubercle  of  each  cusp  "  (H.  Moon,  1884)  ;  or  show 
4  yellowish  cusps  or  protuberances  which  are  excavated  and  not  covered  by 
enamel  (Suker,  1905).  These  are  the  first  teeth  of  the  second  dentition  to 
calcify  and  the  most  liable  to  be  damaged  by  mercurial  stomatitis  in 
infancy.  The  other  teeth  escape  unless  mercury  is  given  in  later  infancy, 
and  then  the  first  bicuspids  may  be  affected  (Hutchinson)  and  horizontal 
furrows  form  across  the  incisors  and  near  the  apex  of  the  canines.  Fournier 
attaches  importance  to  a  horizontal  white  streak  on  the  surface  of  the  incisors. 
Enamel  defects  are  not  always  due  to  congenital  syphilis  or  mercury,  and 
the  absence  of  such  defects  cannot  be  relied  on  as  evidence  of  non-mercurial 
treatment  in  infancy  (p.  223).  Sound  first  molars  are  in  favour  of  no  such 
treatment.  The  malformation  of  the  upper  central  incisors  is  the  one 
dental  defect  to  which  importance  can  be  attached  as  a  sign  of  congenital 
syphilis. 

The  alimentary  tract  may  show  perivascular  hyperplasia  in  the  mucosa, 
causing  diffuse  thickening  and  injury  to  glandular  structures.  The  pancreas 
may  present  an  indurative  enlargement,  a  sclerosis  with  fatty  degeneration 
of  the  cells  and  obliteration  of  the  lobules.  The  liver  is  the  most  frequently 
affected  visceral  organ.  According  to  Hochsinger  the  relative  weight  of 
the  liver  to  that  of  the  body  is  1  :  21-5  normally,  and  1  :  14  in  congenital 
syphilis.  It  is  large,  soft  at  first,  and  later  uneven  and  indurated  (p.  365). 
The  indurative  type  is  sometimes  associated  with  jaundice  and,  less  often, 
with  ascites,  splenic  enlargement  and  engorgement  of  the  abdominal  veins. 
It  responds  better  than  the  spleen  to  anti-syphilitic  remedies. 

The  Genito-Urinary  System. — Nephritis  is  acute  interstitial,  inter- 
stitial and  parenchymatous,  or  chronic  interstitial.  Areas  of  amemic  necrosis 
may  be  present.  An  acute  interstitial  nephritis  has  been  described  by 
Coupland  (1876),  Stroebe  (1891),  and  by  Sutherland  and  Thomson  Walker 
(1903).  The  interstitial  connective  tissue  is  infiltrated  with  round  cells. 
Stoerk  of  Vienna  (1901)  maintains  that  syphilis  retards  the  renal  develop- 
ment, so  that  at  birth  the  outer  layer  of  the  cortex  contains  imperfect 
tubules  and  glomeruli.  Speiss  (1877)  collected  34  cases  of  the  disease  and 
found  renal  changes  in  10.  Possibly  there  is  a  diffuse  perivascular  con- 
nective tissue  infiltration,  causing  imperfect  development  of  the  cortex, 
Malpighian  bodies  and  tubules.  Gummata  are  rare.  Chronic  interstitial 
nephritis  (p.  581)  has  been  ascribed  to  syphilis  and  cases  in  favour  of  this 


878  Chapter  LXII. 

view  have  been  reported  by  Massalongo,  Guthrie  and  Carpenter.  Superficial 
affections  of  the  genitals  (pp.  871-3)  and  orchitis  (p.  596)  have  been  described. 
The  Nervous  System. — The  developmental  defects  include  hydro- 
cephalus due  to  arrest  of  cerebral  development  with  degeneration  of  the 
optic  thalami,  to  meningitis  or  to  ventricular  ependymitis.  It  is  rarely  as 
great  as  in  non-specific  cases,  may  be  present  at  birth  or  comes  on  in  the 
first  3  months  of  life,  and  is  incurable.  Other  defects  are  spina  bifida  ;  and 
■congenital  club-foot,  due  to  atrophy  of  the  cells  of  the  anterior  cornua  and 
Clarke's  column.  Pachymeningitis,  simple  or  hemorrhagic,  and  cortical 
sclerosis  may  occur  in  the  first  year  of  life  and  be  associated  with  gummata. 
It  is  less  rare  at  6-15  years  of  age,  and  gives  rise  to  headache,  mental 
deterioration,  fits,  wasting  and  death  from  asthenia.  Meningitis  is  rare  and 
ill-defined,  diffuse  and  basal ;  localised,  chronic  and  gummatous,  perhaps 
hemorrhagic.  Ventricular  ependymitis  is  the  most  common  sign  in  infancy, 
giving  rise  to  rapidly  increasing  hydrocephalus,  squint,  tremor  and  con- 
vulsions. Cerebral  arteritis  is  common  at  the  base  of  the  brain  and  in  the 
small  vessels  of  the  brain  and  cord.  Both  arteritis  and  meningitis  give  rise 
to  encephalitis  and  myelitis,  with  softening  or  secondary  sclerosis  and 
atrophy,  and  imbecility.  Hemiplegia  may  depend  on  local  encephalitis 
■  or  gummatous  meningitis,  but  is  rarely  syphilitic.  Gummata  are  rare  in  the 
brain  and  cord ;  less  so  in  meningitis  and  inflammation  of  the  cranial 
nerves.  Barlow  reported  gummatous  neuritis  of  several  nerves  at  4  months 
of  age.    The  third,  fifth  and  seventh  are  most  liable  to  be  affected. 

The  onset  and  progress  of  cerebral  syphilis  are  subacute,  and  the 
symptoms  multiple  and  complex.  One  variety  usually  predominates  at 
the  onset  and  throughout,  e.g.  Motor  signs  such  as  tremor,  athetosis,  palsies, 
rigidity  and  affections  of  speech  and  the  cranial  nerves  ;  Visual  symptoms, 
especially  Argyll-Robertson  pupils,  squint,  optic  neuritis  and  atrophy,  and 
choroido-retinitis  ;  or  Psychical  phenomena,  viz.  changes  in  disposition, 
diminished  intellectual  power,  backwardness,  irritability,  depression  or 
excitement,  and  causeless  fits  of  grief  or  anger.  Insomnia  and  sensory 
symptoms  are  rare.  Headache,  occasionally  hemicrania,  is  common,  early, 
and  not  severe.  Temporary  disorders  of  speech  or  vision,  vertigo  and 
sudden  syncope,  may  depend  on  circulatory  disturbance.  Restlessness, 
irritability,  sleeplessness  and  fits  may  be  due  to  slightly  increased  cerebral 
tension  or  hydrocephalus  in  the  eruptive  period.  The  fontanelle  is  then 
tense  or  bulging. 

Either  the  congenital  or  acquired  disease  may  give  rise  to  cerebral 
syphilis  as  above  described,  epilepsy,  Jacksonian  epilepsy,  cerebral  palsy, 
cerebral  sclerosis,  multiple  sclerosis,  tabes,  general  paralysis  of  the  insane, 
backwardness,  imbecility  and  idiocy,  spinal  palsies,  myelitis  and  rarely 
multiple  neuritis.  Grinker  (1904)  reported  a  good  illustration  of  the 
transmission  of  nervous  instability.  The  mother  had  syphilis  4  years  before 
.  marriage  and  developed  the  first  symptoms  of  tabes  9  years  after  the  birth 


Syphilis  :     Acquired  and   Congenital.  879 

•of  her  third  child.  The  first  child,  a  boy,  had  typical  juvenile  tabes  at 
15  years  ;  the  second,  a  boy,  had  general  paralysis  during  adolescence  ; 
and  the  third,  a  girl,  showed  signs  of  cerebral  syphilis  soon  after  birth. 
Intervals  of  2  years  occurred  between  each  birth. 

The  Eyes. — Iritis  is  occasionally  seen  in  the  first  18  months  and  is 
bilateral  in  about  50  per  cent.  It  is  said  to  occur  even  in  utero  but  the 
evidence  thereof  is  unreliable.  It  is  not  uncommon  in  late  congenital  syphilis 
as  a  complication  of  keratitis.  It  is  simple,  mild  and  slowly  progressive, 
perhaps  with  exudation  ;  or  gummatous,  with  small  yellowish  nodules  at 
or  near  the  margin  of  the  iris.  Interstitial  keratitis  occurs  at  6-15  years  of 
age,  sometimes  earlier  or  later.  It  is  common,  most  frequent  in  the  eldest 
child  and  in  females,  and  insidious  and  painless  in  onset.  The  child  may  be 
in  excellent  health.  It  begins  in  the  ciliary  body  of  one  eye  and  affects  the 
other  in  a  few  weeks.  Occasionally  one  recovers  before  the  other  is  attacked. 
The  cornea  has  the  appearance  of  ground  glass  and  the  episcleral  vessels 
•are  injected.  Later,  vascularisation  of  the  cornea  gives  it  a  salmon,  cherry 
red  or  dark  red  colour.  Pain,  photophobia  and  blepharospasm  are  present ; 
ulceration  and  suppuration  are  rare.  About  two-thirds  to  three-quarters  of 
these  cases  are  due  to  congenital  syphilis  and  the  remainder  to  acquired 
syphilis,  malnutrition  or  tuberculosis.  Under  efficient  treatment  recovery 
is  generally  complete,  but  may  take  months.  The  opacity  may  become 
white,  dense  and  persist  as  a  leukoma.  Choroido-retinitis  is  present  in 
15  per  cent,  in  the  first  year  (Still).  It  is  usually  discovered  accidentally 
unless  specially  sought  for,  and  is  not  proof  of  syphilis,  for  it  occurs  inde- 
pendently. In  one  variety  there  are  white  or  pale  yellow  patches  of 
atrophy,  often  surrounded  or  spotted  with  pigment.  In  another,  the 
•condition  is  like  that  of  retinitis  pigmentosa  and  often  associated  with 
nyctalopia.     Optic  neuritis  is  rare,  atrophy  more  common. 

The  Ears. — Otitis  media,  secondary  to  the  pharyngitis,  may  become 
chronic  and  cause  deafness.  Acute  attacks,  sometimes  painless  and 
■apyrexial,  end  in  perforation  of  the  drum  and  otorrhcea.  It  is  a  cause  of 
deaf-mutism.  It  is  doubtful  whether  specific  inflammation  occurs  in 
infancy.  Bilateral  deafness  of  rapid  development  is  much  more  common  in 
girls  than  boys,  aged  8-25  years.  It  is  due  to  disease  of  the  auditory 
nucleus,  nerve  or  labyrinth.  The  common  type  is  a  chronic  osteitis  or 
periostitis,  causing  more  or  less  complete  occlusion  of  the  cavities  of  the 
internal  auditory  meatus  and  labyrinth,  just  as  in  the  tertiary  form  of 
■acquired  syphilis.  This  sets  up  an  acute  or  subacute  inflammation  of  the 
nerve  or  its  terminals.  It  begins  insidiously,  without  pain  or  vertigo,  in  one 
•ear  and  later  on  in  the  other.  Complete  permanent  deafness  may  result 
in  a  few  weeks.  If  the  labyrinth  is  affected  the  onset  is  somewhat  acute  and 
there  is  vertigo  for  the  equilibrating  apparatus  is  involved,  perhaps  at  first 
by  increased  tension  from  effusion.  Incurable  tinnitus  may  be  present.  It  is 
Jess  common  than,  and  frequently  precedes,  though  it  may  follow,  keratitis. 


880  Chapter  LX1I. 

Diagnosis. — Foetal  syphilis  can  be  recognised  by  osteochondritis, 
demonstrable  by  X-rays  after  the  fifth  month  of  intra-uterine  life.  Infantile 
syphilis  may  be  very  easy  or  extremely  difficult  of  recognition.  Diagnosis- 
is  based  on  the  aspect  of  the  child,  the  symptoms  and  physical  signs,  and 
to  a  certain  extent  on  the  response  to  mercurial  treatment.  A  family 
history  of  miscarriages  and  still-births  is  suggestive  but  not  conclusive. 
Evidence  of  the  disease  in  older  children  is  of  more  value.  Much  tact  must 
be  exercised  in  eliciting  the  family  history.  To  ask  the  father  whether  he 
has  had  the  disease  may,  if  he  has  not  had  it  or  is  unaware  that  he  may 
have  been  infected,  lead  to  unwarranted  suspicion  of  the  mother.  The 
absence  of  evidence  of  infection  in  the  maternal  history  or  the  previous 
children  does  not  exclude  the  possibility  of  recent  infection.  On  the  whole 
it  is  of  little  use  troubling  much  about  a  history.  A  negative  one  is  valueless, 
a  positive  one  is  not  conclusive  proof  that  the  particular  illness  is  of 
syphilitic  origin.  Other  diseases  occur  in  syphilitic  children  and  there  is 
much  too  great  a  tendency  to  ascribe  such  diseases,  when  present,  to  the 
specific  taint. 

Valuable  points  in  diagnosis  are  wasting  without  obvious  cause,  the 
association  of  snuffles  and  rash,  anaemia,  and  splenic  and  hepatic  hyper- 
plasia.   Epiphysitis  is  almost  conclusive. 

Late  congenital  syphilis  is  equivalent  to  the  tertiary  stage  of  the 
acquired  disease.  The  ulceration  of  the  skin  and  mucous  membranes,  and 
the  affections  of  the  bones  and  joints,  must  be  differentiated  from  those  of 
tuberculous  origin.  The  late  signs  develop  after  the  third  year,  usually  at 
6-15,  and  most  commonly  at  12  years  of  age.  Stigmata  in  the  form  of  radial 
scars  at  the  angles  of  the  mouth,  etc.,  are  the  most  reliable  sign  of  past 
disease.  The  general  signs  are  a  greyish  earthy  pallor,  sallow  skin,  anaemia, 
delicacy,  malnutrition,  physical  and  mental  backwardness,  dwarfism, 
infantilism,  and  a  delay  of  1-4  or  more  years  at  puberty.  These  children 
walk  and  talk  late.  The  natiform  or  hot-cross  bun  type  of  head,  deformed 
nose,  Hutchinson's  teeth  and  curved  tibia  may  be  present.  The  chief 
active  signs  are  keratitis,  progressive  deafness,  hyperplastic  osteitis  and 
periostitis,  joint  affections,  destructive  ulceration  of  the  nose,  naso-pharynx 
and  larynx,  gummata  and  gummatous  enlargement  of  the  liver  or  spleen. 

A  sunken  nasal  bridge  is  strong  evidence,  and  the  destruction  of  the 
soft  palate,  perforation  of  the  palate  or  vomer,  and  ulceration  of  the 
epiglottis  and  larynx  are  practically  certain  proof  of  the  disease.  Gummata 
are  conclusive.  They  chiefly  affect  the  tibia,  bones  of  the  upper  limbs, 
sternum  and  cranium.  They  have  been  found  in  the  third  year  but  are 
rare  before  puberty.  It  is  often  difficult  to  be  certain  whether  the  late  signs 
are  due  to  congenital  disease  or  syphilis  acquired  in  early  life. 

Course  and  Prognosis. — Congenital  syphilis  after  birth  must  be  looked 
upon  as  the  secondary  stage  of  the  disease  acquired  in  intra-uterine  life. 
Usually  it  is  progressive,  except  in  so  far  as  the  skin  affections  tend  to 


Syphilis  :    Acquired  and  Congenital.  881 

become  less  marked.  Mucous  patches  may  recur  in  the  mouth  up  to  the 
sixth  year;  and  condylomata,  especially  in  the  genito-anal  region,  not 
infrequently  recrudesce,  even  repeatedly.  An  imperfectly  treated  rash 
may  return  in  the  second  year.  Specific  intracranial  affections  may  arise 
independently  of  other  evidence  of  infection.  Many  of  the  symptoms 
described  might  be  spoken  of  as  relapses,  but  are  rather  evidence  of  the 
persistence  of  infection,  although  there  are  periods  of  latency  in  which  the 
special  symptoms  are  absent. 

The  outlook  depends  on  the  severity  at  birth.  A  puny,  marasmic 
infant  with  a  pustular  or  bullous  rash  is  almost  certain  to  die.  Much  wasting 
in  the  first  3  weeks  is  a  bad  sign.  The  earlier  the  symptoms  appear,  the 
worse  is  the  prognosis.  Late  rash  is  a  sign  of  mild  infection.  Marked 
enlargement  of  the  liver  and  spleen  is  unfavourable.  Visceral  lesions  at 
birth  are  of  bad  prognosis  ;  skin  and  bone  affections  are  curable.  The 
degree  of  nutrition,  mode  of  feeding,  nursing  and  hygiene  influence  the 
result.  A  well  nourished,  breast-fed  infant,  who  develops  mild  symptoms 
in  the  second  month  of  life,  will  recover.  An  ill-nourished,  bottle-fed  baby 
with  severe  symptoms  in  the  second  or  third  week  will  probably  die.  Apart 
from  the  immediate  effects  of  the  disease,  the  child  is  more  liable  to  rickets, 
bronchitis  and  broncho-pneumonia,  intestinal  disorders,  and  septic  infection. 
Its  vital  resistance  is  low.  It  readily  contracts  infantile  disorders  and  dies 
from  them,  and  is  liable  to  convulsions.  Often  it  presents  developmental 
defects  incompatible  with  life  or  decreasing  the  chance  of  existence.  The 
prognosis  is  worse  in  hospital  than  in  private  cases  for  there  is  less  likelihood 
that  the  mother  has  been  treated  during  pregnancy.  The  later  infants 
have  a  better  chance  for  they  are  less  severely  affected.  Early  and  pro- 
longed treatment  will  completely  cure  many  children.  Kecrudescences  may 
occur  between  infancy  and  puberty.  The  prognosis  in  the  acquired  disease 
is  generally  favourable. 

Choroidal  atrophy  does  not  tend  to  get  worse.  Late  affections  are 
curable  if  prolonged  treatment  is  adopted  sufficiently  early.  Kecovery 
from  keratitis,  choroiditis  and,  less  often,  deafness,  is  good  and  usually 
permanent.  Nervous  complications  and  sequels  are  more  serious  ;  the 
outlook  being  best  in  gummatous,  worse  in  arterial,  and  very  bad  in 
degenerative  lesions. 

Treatment. — Prevention  is  better  than  cure.  No  syphilitic  man  should 
marry  until  at  least  2  years  have  elapsed  since  the  appearance  of  active 
symptoms.  Hochsinger  insists  on  efficient  treatment,  4  years  interval  from 
the  primary  infection,  and  entire  freedom  from  signs  for  6  months.  The 
interval  should  be  even  longer  in  women.  The  mother  must  be  treated 
during  pregnancy  if  she  has  recently  acquired  syphilis,  if  she  has  had  it 
some  considerable  time  previously  but  no  recent  treatment,  if  there  has 
been  any  recrudescence,  or  if  the  father  has  had  the  disease  within  2  years 
previous  to  the  mother's  conception. 

3    L 


882  Chapter  LXIL 

If  the  child  is  healthy  at  birth  the  risk  of  transmission  of  the 
disease  to  an  attendant  is  trivial.  Syphilitic  parents  must  be  warned 
that  there  is  a  risk  and  proper  precautions  adopted.  Maternal  nursing 
is  essential  if  practicable  ;  otherwise  recourse  must  be  had  to  artificial 
feeding. 

If  there  is  strong  reason  to  suppose  infection  give  a  course  of  treatment 
for  4-6  weeks.  Otherwise  wait  for  the  first  symptoms.  Blue  ointment  is 
the  most  reliable  preparation.  Oleate  of  mercury  1,  ung.  rosa?  4  parts,  or 
mercury  vasogen,  may  be  used.  Wash  the  child  with  warm  water  and 
soap,  dry,  and  rub  in  about  grs.  15,  a  lump  of  ointment  the  size  of  a  pea,  for 
5  minutes  nightly  into  the  skin  of  the  abdomen,  chest  or  limbs.  Or  spread  a 
larger  quantity  on  a  binder,  from  the  ensiform  to  the  pubes,  and  leave  it  on 
for  2  days.  If  the  skin  gets  sore,  apply  a  simple  ointment,  and  rub  the  blue 
ointment  into  the  axillse  or  groins.  In  addition  give  grey  powder  gr.  |-1, 
with  aromatic  chalk  powder,  t.d.s.  Add  to  this  Dover's  powder  gr.  ^-f, 
if  there  is  any  diarrhoea  ;  or  bismuth,  carb.,  creta}  prep,  aa  grs.  2-4.  Other 
suitable  mercurials  are  liq.  hyd.  perchlor.  m.  3-10  ;  Van  Swieten's  fluid 
(hyd.  perchlor.  1,  alcohol  100,  aq.  destill.  900)  m.  3-10  ;  hyd.  protiod. 
(yellow  iodide)  ;  liq.  hyd.  perchlor.,  with  pot.  iod.  gr.  5  in  each  drachm  ; 
tannate  of  mercury  ;  and  calomel  gr.  -fo-  Hochsinger  prefers  the  yellow 
iodide  1  part  in  pulv.  acacia?  50  parts,  as  more  efficacious  than  grey  powder 
or  Van  Swieten's  fluid,  and  states  that  it  rarely  causes  transient  diarrhoea. 
Calomel  produces  rapid  effects  but  is  likely  to  set  up  diarrhoea.  For  severe 
pustular  rashes  a  daily  bath  of  hyd.  perchlor.  grs.  5-10  in  5  gallons  may  be 
used.  On  the  whole  mercurial  inunction  and  grey  powder  are  the  safest 
measures  and  generally  sufficiently  efficacious. 

In  all  cases  watch  for  gangrenous  stomatitis  and  cancrum  oris.  Keep 
the  mouth  clean.  Salivation  is  absent  for  the  glands  are  not  developed. 
The  duration  of  treatment  should  depend  on  the  severity  of  the  case. 
Continue  it  energetically  until  symptoms  have  disappeared,  and  gradually 
omit  it  in  the  course  of  the  next  3-4  months.  A  case  of  medium  severity 
requires  full  treatment  for  2  months  ;  grey  powder  only  for  another 
2  months  t.d.s.  ;  then  twice  and  finally  once  a  day.  It  must  be  repeated  if 
there  is  the  least  relapse.  In  the  late  manifestations  it  is  essential  to  get 
the  child  as  quickly  as  possible  under  the  influence  of  mercury.  Mercurial 
plasters  are  good,  but  liable  to  cause  troublesome  skin  irritation.  Daily 
injections  of  biniodide  of  mercury  (gr.  tV)  for  2-3  weeks  at  a  time  act  rapidly. 
Intra-muscular  injections  are  unsuitable  for  children,  painful  and  un- 
necessary, but  have  proved  successful. 

Grey  oil,  40  per  cent,  strength,  is  injected  in  doses  of  1  c.gm.  for  the 
newborn  deeply  into  the  buttock  under  strict  antisepsis  every  8-15  days. 
A  long,  firm  platinum  needle  is  used..  The  induration,  if  any,  is  said  to 
disappear  quickly.  I  have  no  experience  of  this  treatment.  Iodides  are 
necessary  in  late  stages,  and  occasionally  useful  in  infants,  especially  if 


Syphilis :    Acquired  and  Congenital.  883 

there  are  gummata.     From  gr.  J-l  J  per  year  of  life  can  be  given  daily  in 
water  and  milk. 

For  sores  on  the  buttocks  and  mucous  patches  on  the  vulva  apply 
•calomel  1,  zinc.  oxid.  1,  amyli  2-4  parts  ;  iodoform,  or  lotio  nigra.  Use  pure 
calomel  for  condylomata  and  mucous  warts;  ung.  hydrarg.  arnmon.,  33  per 
•cent,  strength,  for  ulcers.  The  latter  ointment  is  beneficial  for  nasal  sores, 
being  inserted  into  the  nostrils  after  removal  of  crusts.  Or  cotton  tampons 
-covered  with  red  precipitate  ointment  are  placed  alternately  in  each  nostril 
for  an  hour  at  a  time,  after  cleaning  with  a  cotton  swab.  Or  the  yellow 
•oxide  of  mercury  ointment,  1  in  8,  can  be  used.  Adrenalin  drops  relieve 
nasal  obstruction.  Phagedamic  ulcers  of  the  nose  or  palate  are  cauterised 
with  nitric  acid  or  the  acid  nitrate  of  mercury.  For  gummatous  ulcers 
apply  ung.  hyd.  anim.,  ung.  hyd.  oxid.  rub.,  or  lotio  nigra,  and  cover  with 
sublimate  gauze.  For  interstitial  keratitis  prescribe  a  shade,  fomentations 
and  an  ointment  of  cocaine  gr.  5,  atropine  gr.  5,  vaseline  oz.  1  ;  and 
.mercurial  inunctions  or  intra-muscular  injections,  together  with  pot.  iod. 
internally.  Arsenic  and  extract  of  thyroid  gland  are  beneficial  in  some 
•cases.  Pilocarpine  injections  gr.  -^-i  may  do  good  in  early  stages  of 
•deafness. 

The  maintenance  of  the  general  health  by  syr.  fer.  iod.,  ol.  mor.  and 
-other  tonics  is  a  factor  sometimes  more  conducive  to  cure  than  treatment 
hy  specific  remedies. 


CHAPTER    LXIII 

DIPHTHERIA. 

Diphtheria  is  a  specific  infectious  disease  with  a  local  lesion  in  which  the- 
specific  bacillus  is  found.  The  infection  is  almost  always  in  the  upper- 
respiratory  passages  and  the  local  mischief  only  mechanically  dangerous  to 
life.  The  systemic  effects  on  nervous  and  muscular  tissues  are  due  to> 
soluble  toxins.  The  bacillus  was  found  by  Klebs  in  1883  and  isolated  by 
Loffler  in  1884.    Subsequently  Roux  and  Yersin  separated  the  toxin. 

The  disease  is  regarded  as  primarily  local,  because  of  the  mild  cases  in 
which  it  produces  few  or  no  constitutional  effects.  It  spreads  through  the- 
blood  and  lymph  channels  to  internal  organs.  It  is  regarded  as  primarily 
constitutional,  because  of  its  incubation  period  of  1-7  days  ;  the  early 
occurrence  of  albuminuria  or  nephritis,  within  24  hours  in  malignant  cases  ^ 
and  the  cases  of  severe  and  fatal  nephritis  and  profound  systemic  infection 
although  the  local  disease  may  be  trivial. 

The  affection  is  faucial,  pharyngeal,  laryngeal,  nasal,  and  exceptionally 
in  other  situations,  such  as  the  conjunctiva,  vulva,  skin  or  wounds.  Mem- 
branous sore-throat  is  not  invariably  diphtheria  for  it  may  be  due  to 
a  pneumococcus,  streptococcus,  staphylococcus  or  yeast.  Often  there  is  a 
mixed  infection.  The  presence  of  the  specific  organism  in  the  false  membrane 
is  conclusive,  but  its  absence  is  inconclusive.  Negative  results  are  of" 
comparatively  little  value.  A  swab  may  have  been  badly  taken,  few  bacilli, 
may  be  actually  present,  their  vitality  may  have  been  weakened  by  recent 
antiseptic  applications,  and  they  may  fail  to  grow  on  the  culture  media.. 
If  a  case  is  clinically  diphtheria,  it  should  be  treated  as  such  and  notified,, 
although  the  bacteriological  report  is  negative.  The  organism  usually 
disappears  from  the  throat  of  convalescents  within  6  weeks  of  the  onset. 

Bacteriology. — Three  kinds  of  organisms  are  generally  recognised,, 
though  as  many  as  20  morphological  varieties  have  been  described.  The 
true  bacillus  is  Gram-positive,  produces  acid  in  glucose  broth,  and  stains, 
readily  with  Neisser's  stain.  It  is  a  slender  rod,  uniformly  cylindrical  or 
slightly  curved,  dotted  or  beaded,  sometimes  club-shaped,  and  non-motile.. 
The  characters  vary  with  the  culture  media.  It  is  easily  destroyed  by  heat 
and  chemicals,  but  resists  cold  and  drying.  Hofmann's  bacillus,  or  the- 
pseudo-diphtheria  bacillus,  is  often  present  in  normal  throats.  Some  assert 
that  it  is  an  attenuated  form  of  the  true  bacillus  and  that  its  virulence  can  be 
increased  by  successive  passage  through  small  birds,  rendering  it  pathogenic. 


Diphtheria.  885 

■to  guinea-pigs  and  rabbits.  More  probably  it  is  a  totally  different  organism. 
It  is  innocuous  to  animals  producing  no  pathological  lesions,  forms  no  acid 
in  glucose  broth,  and  can  be  distinguished  by  its  morphological,  cultural  and 
biological  features.  A  third  group  consists  of  much  less  virulent  diphtheria 
bacilli  found  in  healthy  throats  or  in  convalescence,  especially  during 
epidemics,  their  lack  of  virulence  being  due  to  some  anti-action  of  the 
tissues  or  secretions.  The  bacilli  vary  in  virulence  in  different  cases.  They 
;are  widely  distributed,  and  possibly  some  additional  factor  is  required  for 
their  development.  The  toxin  causes  local  necrosis,  destruction  of  red 
■cells  and  diminution  of  haemoglobin,  subnormal  temperature,  primary  nerve 
•degeneration  and  paralysis,  and  degeneration  of  cardiac  nerve  centres  and 
muscle  fibres.  The  membrane  is  due  to  the  toxin,  for  it  can  be  produced  by 
injection  of  germ- free  toxin.  It  is  somewhat  doubtful  whether  diphtheria 
Avithout  membrane  formation  exists. 

Mode  of  Infection. — The  disease  is  spread  by  direct  contact,  sputum, 
infected  hands  and  articles,  and  by  animals.  Little  is  known  of  the  life  of 
the  bacillus  outside  the  body.  The  disease  is  more  common  in  rural  districts 
and  isolated  farmhouses  than  in  towns.  It  has  become  more  prevalent  in 
towns  in  recent  years.  Probably  the  germs  can  be  propagated  independently 
•of  the  sick,  when  they  are  deposited  in  suitable  places.  In  New  York  City 
the  drains  were  foul  and  insanitary  conditions  prevalent,  yet  there  was  no 
•diphtheria  before  1850.  After  that  the  organism  was  introduced  and  now 
the  affection  is  widespread.  Improved  sanitation  appears  to  have  little 
•effect.  It  is  very  contagious,  though  the  contagion  is  limited  to  the 
immediate  neighbourhood  of  the  patient.  It  may  be  limited  to  one  side  of  a 
•class  room,  if  it  is  separated  from  the  other  by  a  fairly  wide  passage  ;  to 
a  single  house,  street  or  parish  ;  and  spreads  very  slowly.  Mild  ambulatory 
:and  unrecognised  cases  are  the  main  source  of  its  spread,  especially  where 
the  population  is  dense  and  aggregated  in  schools,  churches  and  places  of 
•amusement.  The  school  habits  of  licking  slates,  pencils,  and  sucking  the 
same  sweets  are  very  dangerous.  Children  may  be  "  carriers  "  of  infection 
though  themselves  uninfected.  Infective  organisms  can  be  carried  long 
■distances  in  trains,  cabs  and  other  conveyances  and  by  garments  or  articles 
-of  merchandise.  Big  outbreaks  have  been  traced  to  infected  milk.  Diph- 
theria in  the  cow  is  generally,  if  not  always,  due  to  human  infection. 

Avian  diphtheria  affects  pigeons,  fowls,  turkeys,  pheasants,  partridges, 
•quails,  parrots  and  sparrows.  A  big  epidemic  occurred  in  the  Thames 
Valley  district  in  1907.  The  prevalence  of  an  offensive  membranous  sore 
throat  in  pigeons  has  been  followed  by  an  outbreak  of  malignant  diphtheria 
in  the  inhabitants  of  the  district,  probably  through  eating  the  pigeons. 
Possibly  the  infection  may  be  carried  by  eggs  for  false  membrane  has  been 
found  in  the  oviducts  of  fowls,  ducks  and  pheasants.  Cats,  sheep  and  pigs 
have  suffered  from  a  disease  of  the  throat  in  several  localities  in  which 
•diphtheria  was  prevalent.    Cattle,  horses,  dogs  and  rabbits  are  also  liable. 


886  Chapter  LXIII. 

Some  of  these  epidemics  are  not  due  to  the  Klebs-Lofner  bacillus,  but  are* 
caused  by  the  bacillus  of  necrosis,  protozoa  or  by  organisms  producing; 
septiesemia.  Calf  diphtheria  and  that  form  common  in  lambs  are  due  to  the- 
bacillus  of  necrosis.  It  must,  however,  be  accepted  that  cats,  rabbits  and 
birds  may  get  diphtheria  and  convey  the  infection.  Or  the  cat  may  be- 
merely  a  "  carrier." 

Pathology. — The  toxin  is  allied  to  snake  venom  in  character.  Ehrlich 
maintains  that  it  is  composed  of  2  substances  : — (1)  Toxin,  to  which  anti- 
toxin is  an  antidote,  causing  acute  symptoms  of  poisoning  ;  (2)  Toxone,. 
causing  degeneration  of  peripheral  nerves.  Sidney  Martin  has  shown  that 
the  bacillus  secretes  a  toxin  :  and  can  digest  proteins,  forming  albumoses  and 
an  acid  body,  both  poisonous.  Others  maintain  that  only  one  poisonous- 
substance  is  produced.  There  are  two  stages  of  the  disease,  toxic  and 
paralytic,  with  no  line  of  demarcation  between  them.  The  paralytic  may 
be  regarded  as  due  to  the  action  of  the  toxin  rather  than  to  an  independent 
poison.  The  toxin  produces  fatty  changes  in  the  diaphragm,  heart  muscle,, 
kidneys,  adrenals  and  liver,  and  to  a  less  extent  in  other  organs.  Later  on 
the  vagus,  phrenics  and  other  nerves  are  affected.  Antitoxin  neutralises- 
the  toxin  and  will  prevent  this  fatty  protoplasmic  change,  if  it  is  given 
early.  The  pathological  change  is  in  active  progress  by  the  fourth  day- 
Fatty  change  in  the  heart  muscle  may  be  found  on  the  third  day  as  the 
cause  of  acute  cardiac  failure.  It  antedates  any  nerve  affection.  The  heart 
shows  no  macroscopical  change  and  no  "  tabby-cat  "  striation  (Dudgeon)r 
but  minute  granules  of  fat  are  visible  on  staining  with  Sudan  III.  or 
Scharlach  R.  In  later  stages  of  the  disease  the  heart  shows  interstitial 
changes.  The  muscles  undergo  hyperplasia,  swelling,  loss  of  striation  and 
fatty  change.  Fatty  changes  may  be  found  in  the  diaphragm  before  the 
heart,  although  there  are  no  symptoms.  In  the  kidneys  it  chiefly  affects  the 
convoluted  tubules,  and  there  is  no  interstitial  or  vascular  change,  even 
though  there  is  albuminuria.  The  liver  is  extremely  prone  to  fatty  change 
and  may  even  float  in  water.  Dudgeon  (1908)  has  also  shown  that  extensive 
fatty  changes  occur  in  the  adrenals,  causing  deficient  production  of  adrenalin 
with  early  acute  congestion  and  hemorrhage  in  guinea  pigs,  as  well  as  fatty 
changes  in  the  medulla.  In  cases  fatal  from  acute  toxseniia  degenerative 
changes  have  been  found  in  the  motor  nucleus  of  the  vagus  and  in  the 
anterior  cornua  of  the  spinal  cord,  as  well  as  cardiac  degeneration.  In- 
later  stages  there  is  usually  considerable  change  in  the  peripheral  nerves. 

The  local  condition  is  a  coagulation  necrosis  of  the  epithelium  due  to  the 
toxin,  vascular  engorgement  of  the  mucosa,  exudation  of  cells,  and  coagu- 
lation of  the  exudate.  Hence  the  membrane  is  composed  of  coagulated 
fibrin,  leucocytes,  epithelial  cells,  debris  and  bacilli  in  groups  or  nests. 
If  quite  superficial,  it  can  be  peeled  off.  More  often  it  involves  deeper- 
structures,  and  secondary  necrosis  causes  ulceration  or  gangrenous 
changes. 


Diphtheria.  887 

Etiology. — A  familial  susceptibility  has  been  noted.  The  predisposing 
factors  are  lowered  vitality  from  any  cause,  abrasion  or  impaired  vitality 
of  the  epithelium,  and  catarrh  of  the  mucous  membrane.  It  is  especially 
apt  to  follow  measles,  scarlet  fever  and  whooping  cough.  Meteorological 
conditions  are  unimportant,  except  as  a  cause  of  catarrh.  The  disease  is 
rather  more  common  in  girls,  perhaps  because  they  are  fond  of  pets.  It  is 
rare  in  infants  under  6  months,  most  common  at  2-10  years,  and  causes  the 
greatest  number  of  deaths  in  the  third  and  fourth  years.  Nasal  diphtheria 
has  been  recorded  at  2  weeks  of  age  (Kiihn),  and  faucial  diphtheria  on  the 
eighth  day  of  life  (Auden,  1902). 

Symptoms  of  Faucial  Diphtheria. — The  onset  is  insidious  with  general 
malaise.  Epistaxis,  as  a  prodromal  symptom,  indicates  gravity.  Vomiting 
is  a  rare  initial  symptom.  Occasionally  the  onset  is  acute,  with  throat 
symptoms,  T.  101-102°  F.,  and  the  usual  signs  of  fever.  Severe  attacks  may 
be  ushered  in  by  rigors,  vomiting  or  convulsions,  and  a  temperature  up  to 
101°  F.  or  more,  or  Avith  marked  prostration.  Very  extensive  membranous 
inflammation  of  the  fauces  may  exist  in  a  child,  without  the  least  complaint 
or  discomfort.  Sometimes  there  is  pain  in  the  neck  and  on  swallowing. 
Pallor,  offensive  breath,  listlessness,  depression  and  languor  are  often 
marked  early  signs.  There  is  complete  disinclination  for  food  or  play,  with 
fretfulness  and  irritability,  and  the  voice  may  be  hoarse  or  nasal. 

The  appearance  of  the  throat  at  the  onset  and  throughout  is  sometimes 
that  of  follicular  tonsillitis.  There  may  be  little  or  no  exudation,  a  little 
cheesy  follicular  deposit,  or  small  necrotic  areas  on  the  tonsils.  The 
membrane  may  start  so  low  down  on  the  tonsils  as  to  escape  detection. 
Usually  there  is  seen  on  one  or  both  tonsils,  or  on  the  pharynx,  patches  of 
membrane  which  rapidly  spread  and  coalesce.  The  membrane  is  tough, 
adherent,  and  leaves  a  bleeding  surface  if  detached.  It  varies  in  colour 
from  a  greyish  white  to  dirty  yellow  or  even  black.  It  is  smooth,  flattened, 
and  depressed  below  the  surrounding  mucous  membrane,  which  overlaps 
it  as  the  rim  of  a  watch-glass  overlaps  the  glass.  It  tends  to  spread  toward 
the  air  passages  and  on  to  the  uvula  and  soft  palate.  A  primary  patch  on 
the  uvula  is  almost  certainly  diphtheria.  The  membrane  indicates  the 
intensity  of  the  local  process  but  is  no  measure  of  the  toxaemia.  It  peels  off 
or  is  liquefied  by  the  action  of  antitoxin  in  24-48  hours.  In  severe  cases, 
there  is  great  faucial  oedema,  much  membrane  and  horrible  fcetor.  The 
tongue  is  covered  with  a  thick,  creamy  fur.  The  tonsils  and  uvula  are 
greatly  swollen,  red  and  oedematous  ;  and  there  is  general  extension,  with 
much  swelling  of  glands  and  subcutaneous  tissues  (angina  Ludovici).  The 
submaxillary  lymph  glands  are  usually  a  little  enlarged,  not  to  the  great 
extent  so  often  seen  in  follicular  and  other  forms  of  tonsillitis.  There  is 
frequently  pain  in  the  ear  on  the  affected  side. 

In  pure  faucial  diphtheria  the  mucous  membrane  is  rather  pale,  not 
inflamed,  and  there  is  no  muco-purulent  secretion.     The  child  looks  ill, 


888  Chaper  LX1II. 

with  a  pale  leaden  aspect  and  small  frequent  pulse.  Albuminuria  is  slight 
or  absent,  T.  100-101°  F.  for  a  short  time,  and  the  glands  are  a  little  or  not 
at  all  enlarged.  The  chief  danger  is  that  of  extension  to  the  larynx  and 
bronchi.  If  antitoxin  is  injected  there  is  marked  improvement  on  the 
following  day,  local  recovery  in  2-3  days,  and  convalescence  in  a  week. 

In  diphtheria  associated  with  streptococcal  or  staphylococcal  infection 
the  mucous  membrane  is  red  and  sometimes  bleeds,  the  inflammation 
limited  or  generalised,  and  the  secretion  muco-purulent.  The  temperature 
ranges  from  101-104°  F.  The  breath  has  a  saprophytic  odour.  The  tonsils 
are  always  swollen,  glands  almost  invariably  enlarged,  and  the  nose  generally 
attacked.  The  membrane  is  not  characteristic  but  may  be  very  thick  and 
extensive,  if  due  to  staphylococci.  It  is  apt  to  give  rise  to  broncho- 
pneumonia, otitis,  and  septicaemia. 

Pharyngeal  Diphtheria  is  localised,  follicular,  spreading,  or  malignant. 
The  milder  types  give  rise  to  dysphagia,  occasionally  angina  Ludovici,  and 
constitutional  symptoms,  and  usually  get  well  under  antitoxin  treatment  in 
a  week.  The  larynx  generally  escapes.  Sometimes  anaemia  is  extreme  and 
ulceration  extensive.  The  malignant  type  is  rare  under  4  years  of  age. 
It  is  due  to  excessive  virulence,  mixed  infection,  or  increased  susceptibility. 
It  produces  extensive  and  deep  lesions  with  severe  toxsemia.  It  may 
gradually  supervene  on  the  localised  or  spreading  variety,  or  be  ushered 
in  acutely  with  fever,  vomiting  and  epigastric  tenderness.  The  skin  is 
dusky,  features  bloated  or  drawn,  and  the  neck  and  pharynx  swell 
enormously.  The  mucous  membrane  exhibits  intense  redness,  much 
membrane  and  mucus,  with  fcetid  odour  and  black  tongue.  The  mental 
condition  is  one  of  restlessness,  excitement,  insomnia  and  slight  delirium  ; 
or  prostration  and  apathy.  The  temperature  is  low,  perhaps  high  at  the 
onset,  and  albuminuria  is  present. 

Laryngeal  Diphtheria  maybe  due  to  gradual  extension  but  more  often 
comes  on  suddenly  about  the  fourth  day  of  the  illness,  or  is  primary  in 
the  larynx.  It  may  be  limited  to  the  ventricles  of  Morgagni.  The  early 
symptoms  are  those  of  simple  laryngitis,  with  less  fever  and  more  general 
depression.  A  gradual  or  sudden  onset  is  followed  by  all  the  signs  of 
increasing  laryngeal  obstruction,  viz.  hoarse  or  muffled  voice  ;  tickling 
cough,  becoming  dry,  harsh,  brassy,  hollow  or  barking  ;  inspiratory  stridor  ; 
and  attacks  of  asphyxia.  In  these  the  child  thrusts  its  fingers  into  its 
mouth,  tears  at  the  throat,  and  becomes  livid,  convulsed,  drowsy  and 
comatose.  Or  they  are  milder  in  type,  lasting  for  a  few  seconds,  with 
anxious  look,  staring  eyes,  sweating  forehead,  cyanosis  and  crowing  inspira- 
tion. Casts  of  the  trachea  and  bronchi  may  be  coughed  up.  The  symptoms 
may  become  acute  in  24  hours,  or  severe  obstruction  may  not  develop  for 
some  days.  It  terminates  in  asphyxia  with  cyanotic  pallor,  pinched  nose,, 
drawn  features,  sweating  forehead,  cold  extremities,  rapid  superficia 
breathing,  thready  pulse  and  ominous  calm. 


Diphtheria.  889 

Nasal  Diphtheria,  sometimes  called  membranous  or  fibrinous  rhinitis, 
is  primary  or  secondary.  It  often  follows  scarlatina.  Nine-tenths  of  the 
cases  are  under  10  and  few  under  3  years  of  age.  In  some  cases  there  is  no 
membrane,  although  pure  cultures  of  the  bacillus  are  obtained.  In  others 
the  symptoms  are  mild  and  yet  there  is  much  membrane.  At  first  the 
•discharge  is  acrid,  clear,  watery  and  irritating,  perhaps  sanious.  Later, 
it  becomes  muco-purulent  or  purulent,  and  may  contain  shreds  of  mem- 
brane. Sometimes  it  is  peculiarly  offensive.  It  is  unilateral  in  about 
20  per  cent.  It  causes  redness  and  excoriation  of  the  alae  nasi,  congestion 
and  nasal  obstruction,  and  often  epistaxis.  In  a  day  or  two  there  may  be 
iound  a  white  film  or  a  tough  gelatinous  yellowish  membrane  in  the  anterior 
nares.  This  may  be  limited  to  the  anterior  end  of  the  septum  or  cover  the 
whole  of  the  mucous  membrane  ;  or  limited  to  the  naso-pharynx  and  found 
•only  on  the  choanse  and  orifices  of  the  Eustachian  tubes.  Finally,  only 
blood  and  pus  are  exuded. 

A  mild  type,  limited  to  the  nose,  gives  rise  to  slight  constitutional 
symptoms,  such  as,  pallor,  languor,  anorexia  and  moderate  fever.  The 
glands  are  rarely  enlarged.  It  runs  a  benign  chronic  course,  rarely  causes 
epistaxis  or  sepsis,  is  only  mildly  infectious  but  may  spread  the  disease  in 
schools.  The  organism  does  not  seem  to  produce  enough  toxin  to  impair 
the  general  health  to  any  great  extent.  A  more  severe  type  is  generally 
secondary  to  faucial  infection.  A  gangrenous  form  begins  in  the  nose  with 
•oedema,  swelling,  shiny  overlying  skin,  marked  pallor,  foetid  secretion  and 
epistaxis.  Eenal  and  nervous  complications  are  uncommon  in  nasal 
diphtheria,  and  the  disease  rarely  spreads  to  the  pharynx  and  larynx.  It 
is  not  followed  by  paralysis,  although  it  lasts  from  1-3  months.  In  the 
newborn  it  causes  nasal  obstruction,  asphyxia  while  suckling,  anremia, 
prostration  and  adenitis. 

Cutaneous  Diphtheria  follows  some  excoriation  or  injury.  It  may  be 
wide-spread  and  very  severe.  A  definite  membrane  with  surrounding  zone 
of  inflammation  is  present,  or  a  gangrenous  slough  with  subjacent  ulceration, 
not  at  all  like  the  diphtheritic  process  and  only  diagnosed  by  bacteriological 
■examination.    Vulvar  diphtheria  is  similar  in  type. 

Conjunctival  Diphtheria  is  most  frequent  under  4  years  of  age,  and  is 
either  primary  or  due  to  extension  up  the  lachrymal  ducts.  It  begins  on  the 
palpebral  conjunctiva.  Typical  membrane  is  formed  or  the  appearance  is 
more  like  gonorrhoeal  ophthalmia,  with  patchy  deposit  on  the  surface.  It 
may  spread  to  the  bulbar  conjunctiva,  involve  the  cornea,  and  cause 
destruction  of  the  eye. 

Aural  Diphtheria  is  due  to  extension  to  nasal  passages  and  then  up  the 
Eustachian  tubes,  occasionally  to  the  tympanum  and  mastoid  ;  or  the 
•orifices  of  the  tubes  are  blocked  by  swelling.  The  otitis  is  very  painful, 
■causes  violent  headache,  sometimes  delirium  or  coma,  and  rapid  tympanic 
necrosis. 


890  Chapter  LXIII. 

Diphtheritic  Stomatitis  is  rarely  primary.  Thin,  greyish  white  patches,, 
like  aphthous  stomatitis,  are  found  on  the  mucosa  and  may  become  con- 
fluent and  thick.  It  may  begin  on  the  lips  and  spread  to  the  tongue  and 
larynx.  More  frequently  it  is  secondary  to  faucial  infection  and  may  spread 
even  to  the  skin.  The  oral  cavity  is  lined  with  membrane,  salivation 
increased  and  foetor  marked.  Membranous  stomatitis  is  sometimes  due  to^ 
other  organisms. 

Hemorrhagic  Diphtheria,  confined  to  children,  is  a  malignant  variety 
with  severe  bleeding  from  the  nose,  mouth  and  pharynx;  into  the  stomach,, 
intestines  and  urinary  tract ;  and  into  the  skin.  A  purpuric  rash  during 
convalescence,  or  epistaxis  or  faucial  bleeding  only,  is  not  sufficient  for 
such  diagnosis.  It  is  most  common  in  cases  in  which  early  treatment  has 
been  neglected.  They  react  less  readily  to  antitoxin.  It  causes  vomiting, 
foetid  diarrhoea  and  profound  anaemia  ;  and  death  from  coma  or  con- 
vulsions, in  a  few  hours  or  days,  in  over  80  per  cent. 

Hypertoxic  Diphtheria  causes  heart  failure,  cyanosis,  unconsciousness 
and  death  from  toxaemia,  although  the  local  signs  are  slight. 

Latent  Diphtheria  is  a  name  given  to  cases  with  no  local  lesion  or  sign  of 
ill  health,  viz.  "  contacts "  ;  cases  with  local  lesions  and  no  general 
symptoms  ;  and  those  in  which  there  is  ansemia,  indefinite  malaise,  and 
some  rhinitis,  otorrhcea,  faucial  catarrh,  cutaneous  sore,  etc.,  which  is 
bacteriologically  diphtheritic.  It  is  an  unsuitable  name,  except  for  the 
first  variety. 

Toxaemia  is  indicated  first  by  an  irregular  and  intermittent  pulse,  with 
or  without  signs  of  cardiac  dilatation,  and  progressive  cardiac  failure  ;: 
diminution  in  the  amount  of  albuminous  urine,  occasionally  anuria ;: 
vomiting,  without  nausea  and  independent  of  food.  It  comes  on  early, 
usually  in  the  first  week  while  membrane  and  adenitis  are  still  present.  The 
child  becomes  greyish,  pale  and  cold,  listless,  and  refuses  food.  Tem- 
perature falls  and  the  pulse  fails,  although  there  may  be  no  signs  of: 
obstruction  to  breathing  and  local  manifestations  may  be  subsiding.  Drow- 
siness often  comes  on,  though  consciousness  persists  to  the  end.  Restless- 
ness is  common,  delirium  an  occasional  symptom,  and  sometimes  there  are 
convulsions  or  coma.  Breathing  may  be  sighing  or  laboured,  and  pulmonary 
oedema  is  not  infrequent.  The  symptoms  are  due  to  the  action  of  the 
poison  on  the  heart,  motor  nerve  cells  in  the  spinal  cord,  and  the  vasomotor 
system.  It  is  probable  that  the  rapid  fall  in  biood  pressure,  collapse  and 
death  are  due  to  the  deficient  secretion  of  adrenalin,  from  the  action  of  the 
poison  on  the  adrenal  glands.  The  pulse  rate  is  a  valuable  measure  of  the 
toxaemia,  especially  if  it  is  out  of  proportion  to  the  fever.  The  prognosis 
becomes  steadily  worse  as  the  rate  exceeds  100  per  minute. 

The  Heart. — Endocarditis  and  pericarditis  are  very  rare,  while  affections; 
of  the  myocardium  and  its  innervation  are  common  and  serious.    The  toxin. 


Diphtheria.  891 

acts  on  the  cardiac  muscle  and  nerves.  The  earliest  sign  is  irregularity. 
Later  there  develop  dilatation,  cardiac  murmurs,  gallop-rhythm,  weak 
action,  short  and  weak  first  sound,  reduplication  of  the  first  sound,, 
approximation  of  the  first  and  second  sounds,  vomiting,  and  occasionally 
epistaxis,  subcutaneous  haemorrhages,  collapse  and  sudden  death.  Heart 
failure  may  occur  in  the  acute  stage  of  bad  cases,  even  without  warning.. 
The  pulse  must  be  watched  very  carefully,  for  it  varies  in  frequency  and 
regularity  at  different  periods  of  the  same  day.  Three  fairly  defined  types 
of  myocardial  mischief  are  seen.  The  first  is  usually  fatal  in  2  or  3  weeks 
and  is  characterised  by  gallop-rhythm,  vomiting,  epigastric  pain  and 
tenderness.  In  the  second  variety,  not  often  fatal,  rapid  regular  or 
irregular  action  of  the  heart  may  last  for  months.  It  is  increased  by 
exertion  and  gradually  becomes  normal.  In  the  rarest  type  the  pulse,  at 
the  end  of  the  second  or  beginning  of  the  third  week,  becomes  very  infre- 
quent and,  when  it  falls  to  40  per  minute,  is  associated  with  signs  of  pros- 
tration. The  heart  sounds  are  weak  and  there  is  a  moderate  degree  of 
dilatation. 

Murmurs,  sometimes  loud  and  musical,  are  more  frequent  at  the 
apex  than  base  and  are  due  to  relative  insufficiency  of  the  mitral  valve. 
They  are  of  little  value  in  prognosis  and  occasionally  persist  after  recovery. 
Dilatation  may  be  quite  sudden.  The  onset  of  serious  heart  complications 
i.3  nearly  always  in  the  first  3  weeks.  Vomiting,  restlessness,  subnormal 
temperature  and  an  unaffected  mind  are  characteristic  features.  Heart 
failure  and  persistent  vomiting  rarely  appear  before  the  seventh  day  and  are 
due  to  extensive  fatty  degeneration.  In  later  stages  a  certain  amount  of 
dilatation  is  due  to  anaemia. 

Thrombosis  may  take  place  in  an  auricular  appendage,  renal  vein  or 
cerebral  vessel.  Cardiac  thrombosis  is  an  occasional  source  of  death.  It 
causes  slow  heart  failure,  pallor,  cyanosis,  cold  extremities,  restlessness  and 
precordial  pain,  probably  due  to  dilatation.  The  pulse  is  small,  thready,, 
quick  and  irregular.  Death  takes  place  without  loss  of  consciousness.  The 
thrombus  may  contain  the  bacillus  and  various  cocci,  and  may  break  down, 
giving  rise  to  infarction.  Sudden  death  may  occur  in  convalescence  or 
even  mild  diphtheria,  after  slight  exertion  or  a  good  meal,  either  from 
syncope  or  vasomotor  palsy.  Cardiac  paralysis  is  most  frequent  from 
2-9  years  of  age.  Its  duration  is  variable  ;  1-14  days  if  due  to  vagus 
paralysis,  but  much  more  prolonged  if  there  is  actual  myocardial, 
degeneration. 

The  Kidneys. — The  renal  changes  are  a  measure  of  the  toxaemia  which 
falls  on  the  renal  epithelium.  Albumin  is  present  in  30-50  per  cent,  of  all 
cases,  generally  on  the  fourth  to  the  seventeenth  day.  Its  frequency  varies 
in  different  epidemics.  The  quantity  increases  with  the  severity  of  the 
attack.  It  is  more  frequent  in  fatal  than  non-fatal  cases,  and  in  paralytic 
than  in  non-paralytic  ones.    It  is  present  in  nearly  all  tracheotomy  eases,. 


•892  Chapter  LX11I. 

gangrenous  attacks,  serious  sepsis,  and  cases  sufficiently  severe  to  cause 
paralysis  of  the  pharynx  and  otitis  media.  It  is  not  caused  or  affected  by 
the  injection  of  antitoxin.  In  toxaemia  the  amount  of  urine  is  diminished  in 
■quantity,  and  that  of  albumin  varies  directly  as  the  intensity  of  the 
toxaemia.  In  mild  cases  it  may  only  be  present  for  2  or  3  days.  Hyaline  and 
granular  casts  are  uncommon. 

It  is  sometimes  due  to  actual  nephritis  and  may  then  end  in  uraemia. 
Nephritis  is  rare  and  hardly  ever  becomes  chronic.  Anuria  is  due  to 
toxaemia  or  to  degenerative  renal  changes.  Suppression  is  generally  fatal. 
Urobilinuria  and  indicanuria  are  almost  constant,  phosphaturia  often  well 
marked,  and  acetonuria  fairly  common.  Severe  cases,  especially  if  there  is 
acute  nephritis,  may  give  the  diazo-reaction. 

Complications  are  due  to  toxaemia,  the  spread  of  inflammation  down- 
ward and  its  effects  on  the  lungs,  local  mischief,  and  the  action  of  the 
toxin  on  the  nervous  system.  Epistaxis  is  a  bad  sign  when  it  occurs  early, 
•on  the  fourth  or  fifth  day,  and  is  a  warning  of  probable  toxaemia  and 
haemorrhage  into  the  skin.  It  is  an  initial  symptom  in  malignant  angina, 
and  of  grave  import  if  it  precedes  coryza.  It  indicates  severity  of  infection 
and  liability  to  cardiac  failure  from  toxaemia.  Sometimes  it  is  due  to 
separation  of  the  membrane  or  sloughing. 

Skin  rashes  may  occur  apart  from  antitoxin  treatment,  usually  after 
the  third  day.  They  are  urticarial,  diffuse  erythematous  or  measliform,  and 
last  for  a  few  hours  to  2  days.  Skin  haemorrhages  are  most  common  under 
7  and  exceptional  after  12  years  of  age.  They  are  due  to  toxaemia  ;  in 
•cases  not  treated  early  by  antitoxin,  and  in  severe  faucial  or  nasal  diph- 
theria. They  come  out  on  the  fifth  to  the  tenth  day,  and  are  purpuric  in 
■character,  like  large  bruises  or  purple  spots,  especially  on  areas  subject  to 
pressure.  They  may  be  found  on  the  trunk,  extremities,  face,  neck  and 
•ears  ;  and  are  almost  always  of  fatal  significance,  if  there  are  more  than 
two  or  three.  They  are  associated  with  the  usual  signs  of  toxaemia,  per- 
sistent vomiting,  cardiac  failure,  epistaxis  and  occasionally  hsematemesis. 

The  respiratory  complications  are  glottic  spasm,  bronchitis,  broncho- 
pneumonia, collapse,  gangrene  and  interlobular  emphysema.  Diphtheritic 
membrane  may  extend  down  the  pharynx  and  oesophagus  and  affect  the 
-stomach,  or  the  latter  organ  may  be  involved  without  any  evidence  of 
direct  spread  (p.  257).  Renal  and  cardiac  affections  must  be  regarded 
rather  as  symptoms  than  complications,  except  perhaps  nephritis  which  is 
rare.  The  liver  is  often  enlarged  in  fatal  cases  ;  and  shows  fatty  degenera- 
tion in  the  acute  disease  or  congestion  from  cardiac  failure. 

Various  nervous  symptoms  have  been  noted,  such  as  ataxy  due  to 
"neuritis  or  inco-ordination,  tetany,  hemiplegia  and  other  forms  of  palsy. 
Optic  neuritis  is  rare.  Progressive  debility  without  actual  paralysis  may 
prove  fatal.  Otitis  media  is  not  uncommon.  Adenitis  may  result  in  abscess 
iormation. 


Diphtheria.  893 

Diphtheritic  paralysis  is  a  sequel  rather  than  a  complication,  though 
it  may  occur  very  early  in  the  disease.  If  it  begins  during  the  toxsemic  stage 
it  is  due  to  the  toxin  causing  degenerative  changes  in  the  central  nervous 
system.  Changes  have  been  induced  in  the  motor  cells  by  injection  of 
diphtheria  toxin  into  rabbits  (Rainy,  1900).  Subsequently  the  symptoms 
are  ascribed  to  toxone.  The  toxin  has  been  neutralised  and  the  nerve 
cells  have  recovered,  but  the  nerve  fibres  show  parenchymatous  inflam- 
mation, and  the  heart  shows  interstitial  changes.  Probably  these  con- 
ditions are  more  or  less  combined.  Thus,  the  cardiac  symptoms  are  due 
to  impaired  innervation  of  a  fatty  heart,  in  consequence  of  acute  degenera- 
tive changes  in  cells  of  the  lower  nerve  centres  producing  an  irritative  and 
a  paralytic  effect  on  the  vagus.  Later  on,  they  are  due  to  peripheral  nerve 
degeneration  and  interstitial  cardiac  changes.  Motor,  sensory  and 
sympathetic  nerves  are  affected  with  a  parenchymatous  inflammation. 

The  paralysis  is  more  common  in  children  than  in  adults,  and  in  males 
than  females.  Insufficient  food,  bad  nursing  and  lack  of  care  during 
convalescence  are  predisposing  factors.  It  affects  10-20  per  cent,  of  all  cases,, 
and  30  per  cent,  of  severe  ones,  but  there  is  no  constant  relation  between 
the  severity  of  the  attack  and  paralysis.  Nevertheless  it  is  a  toxic  mani- 
festation and  varies  directly  as  the  dose  of  the  toxin,  the  extent  of  the 
membrane  and  severity  of  the  disease,  both  in  frequency  and  fatality. 
It  is  most  frequent  after  faucial  attacks.  In  malignant  cases  it  may  come 
on  almost  immediately.  Albuminuria  is  much  more  common  in  paralytic 
cases.  The  proportion  of  cases  is  high,  if  loss  of  knee  jerks  alone  is  taken 
as  proof  of  paralysis.  Antitoxin  treatment  has  not  diminished  its  frequency  ; 
and  indeed  it  is  probably  more  frequent,  if  less  severe,  because  of  the- 
recovery  of  many  more  of  the  severe  cases. 

It  begins  insidiously  1-3  weeks  after  the  local  symptoms  have  subsided,, 
rarely  as  late  as  the  seventh  week.  The  early  signs  are  weakness,  feeble  and 
irregular  pulse,  tendency  to  cough  and  splutter  when  fed,  regurgitation  of 
food,  nasal  voice,  impaired  vision,  tingling  and  numbness  in  the  lower 
limbs  and  loss  of  knee  jerk.  At  first  there  is  merely  a  little  hesitation  in  the 
performance  of  motor  functions.  Palatal  palsy  is  the  most  common 
symptom,  and  the  earliest  in  about  two-thirds  of  the  cases.  It  may  be 
limited  to  the  soft  palate,  half  or  all  of  which  hangs  down,  is  motionless,, 
insensitive,  and  does  not  respond  to  electrical  stimuli.  This  gives  rise  to  the 
nasal  voice,  regurgitation  of  fluid  through  the  nose,  difficulty  in  swallowing 
and  unintelligible  speech.  If  unilateral,  the  fluid  only  regurgitates  through 
one  side  of  the  nose  and  the  uvula  is  drawn  to  one  side. 

Paralysis  of  accommodation  is  due  to  cycloplegia  and  occurs  in  most 
cases,  though  it  cannot  always  be  recognised  because  of  the  difficulty  in 
testing  young  children.  Jaeger  type  and  needle  threading  are  the  best 
tests.  It  is  bilateral,  rarely  comes  on  before  the  third  or  after  the  seventh 
week,  and  lasts  from  1-6  weeks.      Other  ocular  affections  are  amblyopia,. 


894  Chapter  LXIII. 

amaurosis,  mydriasis,  inequality  of  the  pupils  and  convergent  squint. 
Almost  all  the  ocular  muscles  may  be  affected  in  turn.  Exceptionally  the 
pupils  react  to  accommodation  but  not  to  light. 

Difficulty  in  swallowing,  due  to  pharyngeal  paralysis,  begins  almost 
always  in  the  first  to  the  third  week.  Most  cases  in  which  the  onset  is 
delayed  to  the  third  week  recover,  but  two-thirds  of  those  of  earlier  onset 
die.  Food  can  only  be  swallowed  after  repeated  attempts  which  fatigue 
the  patient,  and  nasal  feeding  is  necessary.  It  partly  accounts  for  regur- 
gitation of  fluid  through  the  nose,  entrance  of  liquids  into  the  air  passages 
and  cough.  It  lasts  for  a  few  days  to  6-8  weeks.  In  laryngeal  paralysis  the 
adductors  are  affected  and  cough  is  toneless.  It  only  occurs  after  laryngeal 
diphtheria,  and  gives  rise  to  aphonia,  irritating  cough  and  dysphagia. 

The  early  disappearance  of  the  knee  jerk  is  a  bad  sign.  It  is  often 
enfeebled  without  being  actually  lost,  and  occasionally  it  may  be  a  little 
exaggerated  at  first.  It  usually  disappears  in  6-8  weeks,  or  at  any  time 
within  6  months,  and  returns  gradually  in  from  1-12  months.  The  Tendo 
Achilles  jerk  is  affected  less  frequently  than  the  knee  jerk.  Usually  both 
are  completely  abolished  in  paralysis,  and  their  absence  may  be  the  only 
indication  of  the  loss  of  motor  power  in  the  lower  limbs.  They  may  remain 
absent  for  long  after  recovery  and  on  one  side  longer  than  on  the  other. 

Paralysis  of  the  extremities  is  seldom  complete.  It  is  ushered  in  by 
gradually  increasing  weakness,  numbness  and  formication.  The  gait 
becomes  uncertain  and  the  patient  has  incomplete  perception  of  what  he 
walks  on.  There  is  difficulty  in  the  dark  and  in  going  up  and  down  stairs. 
The  legs  are  more  often  and  more  severely  affected  than  arms.  Sometimes 
the  palsy  precedes  the  loss  of  knee  jerk.  It  usually  begins  in  the  fifth  to 
seventh  week,  and  may  begin  in  the  second  or  be  delayed  until  the  sixteenth. 

Inco-ordination  may  occur  without  paralysis,  and  amount  to  stag- 
gering suggestive  of  cerebellar  disease.  Children  stumble  and  fall  about, 
bruising  themselves,  for  the  knees  suddenly  give  way  under  them.  Ataxic 
symptoms,  combined  with  loss  of  reflexes  and  ocular  troubles,  give  rise  to 
the  form  of  pseudo-tabes.  The  hands  are  clumsy,  awkward  and  drop  things, 
or  may  exhibit  tremors  like  those  of  paralysis  agitans.  Inco-ordination 
generally  comes  on  when  the  knee  jerks  disappear  and  lasts  for  a  few  weeks. 
It  is  nearly  always  associated  with  more  or  less  paresis  and  may  occur  first. 
Sensory  disturbance  may  be  absent. 

Various  other  palsies  occasionally  occur.  Head-drop  is  due  to  weakness 
of  the  muscles  of  the  neck,  and  inability  to  sit  up  to  weakness  of  the  back 
muscles.  Acute  inflammation  of  the  nuclei  may  cause  permanent  palsy  of 
one  or  more  cranial  nerves.  Sometimes  the  tongue,  lips,  cheeks  and  larynx 
are  affected  as  in  labio-glosso-laryngeal  palsy.  In  rare  instances  the 
paralysis  is  mono-,  hemi-,  or  paraplegic.  Hemiplegia  is  generally  due  to  a 
vascular  lesion.  Paralysis  of  the  diaphragm  and  the  intercostals  is  serious 
and  often  fatal. 


Diphtheria.  895 

Bulbar  Crises. — Bulbar  palsy  is  due  to  the  action  of  the  toxin  on  the 
bulbar  centres  and  is  a  cause  of  cardio-pulmonary  paralysis,  dyspnoea 
and  rapid  death.  It  comes  on  within  6  weeks  of  the  onset  of  paralysis. 
Guthrie  has  called  the  dyspneeic  attacks  "  bulbar  crises."  According  to 
his  description  the  premonitory  signs  are  restlessness  and  apathy,  a  weak 
hoarse  nasal  voice,  irregular  sighing  respiration,  loose  weak  cough,  accumu- 
lation of  mucuS  in  the  air  passages  and  rapid  pulse.  The  crisis  is  a  sudden 
and  acute  exacerbation  of  the  above  symptoms  due  to  excitement,  physical 
exertion  or  no  apparent  cause.  It  produces  sudden  and  complete  paralysis 
of  deglutition,  aphonia,  alarming  dyspnoea  and  extreme  restlessness.  The 
alae  nasi  are  distended,  mouth  open,  pupils  dilated,  colour  bluish  and  skin 
sweating.  The  respiration  is  gasping,  sighing  and  irregular,  and  there 
is  general  accumulation  of  mucus.  The  pulse  rate  is  150  or  more  ;  T. 
102-103°  F.  Sometimes  there  is  violent  vomiting  which  may  relieve  the 
symptoms  ;  occasionally  the  diaphragm  is  paralysed.  These  attacks  last 
lor  a  few  minutes  to  hours,  are  recurrent,  and  may  end  in  death  from 
exhaustion,  syncope,  asphyxia  or  cardiac  thrombosis.  The  first  attack  is 
rarely  fatal. 

Sensory  Affections. — Anaesthesia  of  the  soft  palate  is  common, 
-occasionally  it  is  preceded  by  hyperesthesia.      The  lips,  nose,  cheeks  and 

limbs  may  be  affected.  Frequently  it  does  not  extend  above  the  knees  and 
•elbows,  but  it  may  be  general  and  associated  with  analgesia.  Pains  in  the 
■calves  are  common.    Tingling,  pins  and  needles,  and  numbness  may  be  felt 

in  the  hands  and  feet.  The  bladder,  rectum  and  special  senses  are  affected 
:in  the  worst  cases.    Incontinence  is  due  to  the  general  state  rather  than  to 

sphincter  paralysis.  It  may  occur  for  a  few  days  in  a  transient  form  during 
•convalescence   from   lack   of   controlling   power.      The   muscles   give   the 

reaction  of  degeneration  and  there  is  augmentation  of  galvanic,  and 
•diminution   of  faradic   contractility.      Slight  contractures  may  occur   in 

the  most  severe  cases. 

Diagnosis. — Diphtheria  is  overlooked  on  account  of  forgetting  the 
:golden  rule  to  examine  the  throat  of  every  sick  child.  Early  diagnosis  is 
•  of  extreme  importance  and  very  difficult.  The  bacteriological  report  may 
he  misleading.  In  some  of  the  worst  cases  the  bacillus  may  not  be  found. 
Other  exudates  may  simulate  that  of  diphtheria.  The  faucial  affection  has  to 
be  distinguished  from  certain  mouth  affections  (p.  219)  and  many  varieties 
•of  sore-throat  (pp.  231-233)  ;  and  the  laryngeal  obstruction  from  that  due 
to  other  causes.  Secretion,  as  opposed  to  membrane,  may  be  found  on  the 
uvula  and  soft  palate  in  septic  and  ulcerative  sore-throats.  Follicular  ton- 
sillitis associated  with  laryngitis  is  almost  invariably  diphtheria.  The 
scarlatinal  sore-throat  is  liable  to  be  erroneously  diagnosed  as  diphtheria, 
if  exposure  to  cold  has  caused  temporary  disappearance  of  the  rash.  As  a 
rule  diphtheria  comes  on  insidiously  without  vomiting  ;  while  scarlet  fever 
is  ushered  in  violently  with  severe  vomiting  and  high  fever,  and  there  is 


896  Chapter  LXIII. 

more  of  an  appearance  of  sloughing  and  ulceration  of  the  tonsils,  or  vivid 
redness  at  the  onset.  If  there  is  neither  laryngitis  nor  adenitis,  the  pseudo- 
membranous sore-throat  of  scarlet  fever  may  be  regarded  as  not  diphtheritic 
unless  the  bacteriological  report  is  to  the  contrary.  As  a  general  principle- 
the  presence  of  anaemia,  depression  and  lassitude  greater  than  the  severity  of 
the  signs  would  account  for,  in  any  throat  case,  with  moderate  fever  and 
slight  adenitis,  are  strongly  in  favour  of  diphtheria.  More  especially  is  this- 
the  case  if  there  is  unilateral  rhinitis,  coherent  and  tenacious  membrane- 
limited  to  one  tonsil,  or  extending  on  to  the  uvula  and  soft  palate,  and 
albumin  in  the  urine.  In  mild  and  doubtful  cases  the  clinical  symptoms  may 
be  limited  to  slight  nasal  catarrh,  faucial  trouble  and  otorrhcea,  with  or 
without  constitutional  symptoms,  such  as  ansemia,  increased  pulse  rate 
and  general  malaise.  Occasionally  there  is  no  sign  of  ill-health  or  local 
lesion,  but  the  typical  bacilli  are  found  on  bacteriological  examination. 
Morphological  characteristics  are  insufficient  for  certain  diagnosis.  Cultural 
and  inoculation  tests  take  4-7  days. 

Primary  laryngeal  diphtheria  in  young  infants  is  very  difficult  to 
distinguish  from  acute  laryngitis,  for  nothing  special  may  be  noted  until 
there  are  signs  of  laryngeal  obstruction.  The  laryngitis  at  the  onset  of 
measles  is  apt  to  be  mistaken  for  diphtheria,  and  in  the  course  of  the 
disease  mav  be  due  to  secondary  diphtheritic  infection.  The  constitutional 
symptoms  are  more  severe  than  in  simple  laryngitis,  and  the  diagnosis  may 
be  confirmed  by  the  presence  of  a  faucial  secretion  or  the  coughing  up  of 
membrane.  Though  membranous  laryngitis  is  not  always  diphtheritic,, 
it  is  advisable  that  such  cases  should  be  treated  with  antitoxin  at  the 
onset. 

Diphtheritic  paralysis  is  diagnosed  by  the  history  of  recent  sore- 
throat,  laryngitis  or  nasal  catarrh  ;  and  the  presence  of  anaesthesia  and 
immobility  of  the  soft  palate,  nasal  voice,  regurgitation  of  food  through  the 
nose,  defective  accommodation,  loss  of  knee  jerks,  etc.  It  may  closely 
simulate  acute  anterior  poliomyelitis.  In  one  case  the  two  affections  were 
apparently  combined.  The  child  had  a  history  of  recent  laryngitis,  the 
diphtheritic  bacillus  was  recovered  from  the  fauces,  and  there  was  some 
slight  inequality  of  the  pupils,  a  little  palatal  and  pharyngeal  palsy,  and 
marked  paralysis  of  the  lower  intercostals.  Gradually  the  knee  jerks, 
disappeared  and  paralysis  developed  in  the  muscles  of  the  neck,  back  and 
limbs.  In  the  course  of  his  illness  he  had  dilatation  of  the  heart,  tachy- 
cardia, submaxillary  adenitis  and  otitis  media.  He  recovered  with  partial 
paralysis  of  both  legs  and  was  a  good  deal  wasted. 

Multiple  neuritis  due  to  typhoid  fever,  measles,  scarlet  fever,  small  pox, 
syphilis,  beri  beri,  etc.,  and  poisons  such  as  lead,  arsenic,  alcohol,  etc.,. 
is  almost  unknown  in  infants  and  rare  in  children.  Atrophy,  rigidity  and 
deep-seated  muscular  tenderness  are  said  to  be  characteristic  of  the  alcoholic 
type  and  absent  in  diphtheria.    In  one  case  of  the  latter  variety  they  were 


Diphtheria.  897 

all  present.     Paralytic  chorea,  cerebellar  tumour  and  Landry's  paralysis 
are  possible  sources  of  wrong  diagnosis. 

Prognosis. — Under  antitoxin  treatment  patients  get  well  in  a  week. 
Otherwise  the  disease  spreads  easily,  then  remains  stationary  for  some  days, 
and  subsides  in  2-3  weeks.  Epidemics  differ  greatly  in  severity,  and  the 
mortality  varies  in  different  epidemics  and  with  the  mode  of  treatment. 
The  reduction  in  mortality  depends  upon  early  diagnosis,  the  early  adminis- 
tration of  antitoxin,  and  a  sufficient  dosage.  The  older  the  patient  and  the 
earlier  antitoxin  is  given,  the  better  is  the  prognosis.  The  mortality  is  very 
small  in  children  over  2  years  of  age  treated  by  antitoxin  on  the  first  day  of 
the  disease.  Under  2  there  is  great  liability  to  septic  complications  and 
under  5  years  to  respiratory  ones.  In  the  first  5  years  of  life  the  mortality 
is  10-15  per  cent.  ;  in  the  next  5  years  5-6  per  cent.  ;  and  then  it  falls  to 
2-4  per  cent.  Laryngeal  diphtheria  is  the  most  dangerous  type  in  infants 
because  of  the  small  larynx,  the  yielding  character  of  its  walls,  the  spread 
of  the  infection  and  membrane  downwards,  or  capillary  bronchitis  and 
broncho-pneumonia.  Tracheotomy  is  an  added  danger,  for  it  only  relieves 
the  obstruction  and  the  membrane  may  continue  spreading.  Large  tonsils, 
adenoids  and  nasal  infection  increase  the  risk.  The  constitutional 
symptoms  vary  greatly  in  severity  and  are  most  serious  in  the  secondary 
nasal  and  the  malignant  faucial  types.  Mixed  infections  are  more  severe 
than  pure  diphtheria,  and  staphylococcal  more  dangerous  than  strepto- 
coccal ones.  The  dangers  and  degree  of  toxaemia,  mechanical  obstruction 
and  carbonic  acid  poisoning  must  be  estimated. 

The  gravest  symptoms  are  early  vomiting,  abdominal  pain,  much 
albumin,  anuria,  restlessness,  apathy,  signs  of  profound  toxaemia  and  its 
effects  on  the  heart  and  circulation,  weak  first  sound,  gallop-rhythm, 
frequent  and  irregular  pulse,  vagus  paralysis,  and  paralysis  of  the  inter- 
costals,  diaphragm  and  pharyngeal  muscles.  A  slow  irregular  pulse  is  a 
very  bad  sign  in  the  acute  toxic  stage.  Death  is  generally  due  to  cardiac  or 
respiratory  paralysis,  toxaemia,  broncho-pneumonia  or  asphyxia.  Broncho- 
pneumonia and  the  cardiac  complications  each  accounts  for  about  25-50  per 
cent,  of  the  fatal  cases.  Toxaemia  must  not  be  confused  with  cardiac 
paralysis.  It  occasionally  produces  respiratory  paralysis  and  breathing 
ceases  for  some  time  before  the  heart  stops.  Tracheotomy  in  a  case  of  this 
kind  was  useless.  If  due  to  toxaemia  death  takes  place  during  the  first 
2  weeks,  occasionally  during  the  third  week,  and  never  before  the  third  day. 
The  diazo-reaction  and  haemorrhages  are  unfavourable  signs. 

Vomiting  is  a  bad  omen.  The  earlier  it  occurs  the  worse  is  the  prognosis. 
It  may  be  present  from  the  onset,  start  at  the  middle  or  the  end  of  the 
second  week,  or  begin  after  some  weeks.  Occasional  vomiting,  about  7-10 
days  after  injection  of  antitoxin,  may  be  due  to  certain  properties  in  the 
serum  ;  to  food  getting  into  the  larynx  in  consequence  of  palsy  ;  or  to 
partially  detached  membrane  irritating  the  fauces.    Persistent  vomiting  is 

3    M 


898  Chapter  LXIII. 

grave  and  comes  on  at  any  period.  In  early  cases  it  is  a  measure  of  the 
toxaemia  and  in  trie  first  2  weeks  is  nearly  always  a  fatal  indication. 
Frequently  it  is  associated  with  cardiac  symptoms.  It  is  induced  by  food, 
usually  accompanied  by  nausea,  may  consist  entirely  of  bile,  and  may  be 
conjoined  with  increased  peristalsis  and  loss  of  sphincter  control,  making  it 
impossible  to  give  food  per  rectum.  Occasionally  it  depends  on  uraemia, 
diphtheria  of  the  stomach,  or  direct  irritation  from  inflammation  and  fatty 
changes  ;  or  on  vagus  irritation,  an  incipient  neuritis,  in  which  case  it 
should  be  associated  with  bradycardia. 

Sudden  death  during  convalescence  is  rare.  It  may  occur  as  late  as  the 
third  month,  and  during  apparently  normal  progress,  even  without  warning 
signs.  It  is  generally  caused  by  excitement,  vomiting,  getting  up  too  soon, 
or  strain.  Usually  there  is  irregularity  of  the  pulse,  and  no  patient  is 
absolutely  safe  while  the  pulse  remains  irregular.  Arrhythmia  may  last 
for  a  few  days  to  6  months,  and  a  latent  weakness  of  the  heart  muscle  may 
persist  for  years  and  develop  under  strain.  Fainting  attacks  with  vomiting 
may  occur  for  3  or  4  years. 

Other  bad  prognostic  features  are  failure  of  the  appearance  of  a  rash 
after  antitoxin  treatment ;  progressive  hepatic  enlargement  preceding  and 
accompanying  cardiac  failure,  partly  due  to  congestion  and  partly  to  fatty 
degeneration  ;   and  a  punctate  rash  on  the  knees  (Marfan). 

The  prognosis  of  diphtheritic  paralysis  is  good,  unless  there  is  early 
•cardiac  palsy.  It  is  good  in  the  localised  and  generalised  varieties,  and  bad 
in  the  cardio-pulmonary  type.  Bulbar  crisis  is  usually  fatal.  Involvement  of 
the  muscles  of  the  pharynx,  the  intercostal  muscles  and  diaphragm  increases 
the  liability  to  food  getting  into  the  larynx,  asphyxia,  inspiration-pneu- 
monia and  broncho-pneumonia,  and  the  difficulty  of  getting  rid  of  bronchial 
secretions.  Unfavourable  signs  are  paralysis  of  the  cervical  muscles  and 
marked  ataxia.    No  case  is  hopeless.    There  is  no  permanent  palsy. 

Relapses  occur  in  1-2  per  cent,  and  are  difficult  to  explain.  A  relapse 
comes  on  after  the  second  week,  with  fresh  membrane  and  milder  symptoms 
and  without  complications.  It  must  be  diagnosed  from  late  tonsillitis  and 
scarlet  fever  ;  and  from  the  throat  condition  or  pseudo-relapse,  due  to 
antitoxin,  which  comes  on  within  2  weeks  with  rash  on  the  tonsils  and  skin, 
adenitis,  arthritic  pain  and  fever. 

Treatment. — The  mortality  of  diphtheria  has  decreased  from  40  to  10 
per  cent,  since  the  introduction  of  antitoxin  treatment.  The  disease  is 
not  fatal,  if  antitoxin  is  given  on  the  first  day. 

Antitoxin  is  a  true  antidote,  combining  with  the  toxin  as  long  as  it  is 
free  and  rendering  it  harmless.  It  must,  therefore,  be  given  early,  for  it  has 
little  effect  if  the  toxin  has  become  chemically  fixed  in  the  tissue  cells.  It 
exerts  no  bactericidal  or  regenerative  action  on  the  cells,  and  does  not 
influence  septic  complications.     If    given    late,    it  only  neutralises  the 


Diphtheria.  899 

uncombincd  toxin.  In  malignant  cases  the  poison  gets  too  great  a  start. 
The  importance  of  administering  it  early  is  well  illustrated  by  the  reduction 
in  mortality  of  post-scarlatinal  diphtheria  in  the  Asylums  Board  Hospitals 
from  50  per  cent,  to  nil,  and  in  laryngeal  cases  from  70  to  30  per  cent.,  and 
the  reduced  frequency  of  tracheotomy.  We  have  to  be  careful  in  estimating 
its  value  since  epidemics  vary  in  virulence.  Many  mild  cases  are  diagnosed 
on  bacteriological  grounds,  and  sometimes  only  the  very  severe  ones  are 
treated  by  antitoxin.  It  is  advisable  to  give  antitoxin  to  children  without 
waiting  for  a  bacteriological  confirmation  of  the  diagnosis.  A  single  culture 
does  not  give  infallible  results.  If  the  case  is  slight,  limited  to  the  throat 
which  is  clearing  up  quickly  as  the  result  of  local  applications,  and  with 
few  or  no  constitutional  symptoms,  it  is  not  always  necessary ;  but  it 
requires  much  experience  and  considerable  courage  to  decide  against  its 
administration,  for  mild  cases  may  become  severe  and  individual  sus- 
ceptibility varies.  It  must  be  used  if  there  are  any  laryngeal  symptoms. 
It  has  no  injurious  effect  on  the  kidneys  and  does  not  prevent  diphtheritic 
paralysis.  The  objections  to  its  use  are  its  cost,  the  opposition  of  relatives, 
and  the  production  of  serum  disease. 

Simon  states  that  a  temporary  reduction  of  leucocytes  in  the  blood 
after  antitoxin  injection  is  followed  in  3-4  hours  by  an  increase.  If  this 
increase  does  not  occur  and  the  number  exceed  that  present  before  injection, 
it  indicates  failure  of  the  serum  to  act  and  is  a  bad  sign. 

Mode  of  Administration. — Use  serum  not  more  than  3  months  old  of 
strength  of  500  units  to  1  c.c.  Administration  by  the  mouth  or  rectum  is 
useless.  Inject  it  slowly  into  the  subcutaneous  tissues  of  the  abdominal  wall 
or  side  of  the  chest  under  strict  antiseptic  precautions.  It  acts  more 
quickly  intra-muscularly  and  intra-venously  but,  if  used  in  this  way,  it 
must  not  be  carbolised.  The  dose  should  be  large  and  in  proportion  to  the 
type  and  severity  of  the  case  ;  for  faucial  diphtheria  3000-6000  units,  for 
nasal  and  laryngeal  6000-9000.  Give  2000  units  only  in  suspicious  cases, 
and  larger  doses  still  in  virulent  cases  or  if  treatment  has  been  delayed  to 
the  third  day.  The  dose  must  be  repeated  in  24  hours  if  there  is  no  improve- 
ment, and  even  before  if  the  symptoms  are  getting  worse,  especially  in 
laryngeal  attacks.  Half-doses  may  be  given  every  12  hours  until  the 
membrane  is  separated.  Doses  up  to  30,000  units  at  a  time  have  been  given, 
but  do  not  appear  of  more  value  than  those  recommended.  More  should 
be  given  within  10  days  if  there  is  any  relapse,  if  toxic  symptoms  persist, 
or  if  diphtheritic  bronchitis  develops.  Intra-venous  inj  ection  of  20,000-30,000 
units  has  been  given  by  Cairns  (1902)  in  malignant  cases  with  toxrcmia, 
considerable  involvement  of  lung  and  a  moribund  state.  After  the  fifth 
day  of  the  disease  antitoxin  appears  of  little  value.  Caiger  reported  that 
the  mortality  of  3000  cases  at  the  Brook  Hospital,  during  1896-1899 
inclusive,  rose  from  nil  in  those  inoculated  on  the  first  day  to  3-6  per  cent. 
-on  the  second  day,  6*7  on  the  third  day,  14-9  on  the  fourth  day  and  21-2  on 


900  Chapter  LX1II. 

the  fifth  day.  In  a  second  period  of  6  years,  1897-1902,  the  mortality  wa* 
under  5  per  cent,  of  those  inoculated  on  the  second  day,  over  10  per  cent,  of 
those  on  the  third  day,  and  about  20  per  cent,  of  those  inoculated  later. 

The  Effects  of  Antitoxin. — The  membrane  ceases  to  spread,  becomes- 
sharply  demarcated,  separates  more  readily,  is  reduced  to  half  on  the- 
second  day  and  gone  on  the  third  day.  The  throat  swelling  and  adenitis- 
quickly  subside,  rhinorrhcea  is  checked,  the  toxin  is  neutralised,  and  the 
child  becomes  more  comfortable.  The  fever  subsides,  blood  pressure 
rises,  and  the  pulse  becomes  stronger  and  less  frequent.  Complications  are- 
rare  and  less  severe. 

Serum  Disease. — The  sequels  of  antitoxin  injection  are  due  to  the- 
horse  serum  and  not  to  the  antitoxin.  They  may  follow  small  as  well  as 
large  doses.  The  serum  acts  as  a  foreign  substance  and  should  be  used  in 
a  highly  concentrated  form.  The  serum  of  some  horses  is  more  irritant  than 
that  of  others.  Children  are  less  liable  than  adults  to  these  sequels  and 
more  liable  to  paralyses.  The  serum  disease  begins  with  a  rash  in  7-14  days, 
fever,  local  or  even  general  adenitis,  oedema,  occasional  joint  pains, 
leucopenia  and  slight  albuminuria.  It  lasts  for  3-4  days.  It  occurs  very 
frequently  and  on  smaller  dosage  after  re-injections,  unless  within  10  days- 
The  symptoms,  especially  local  ones,  are  more  severe,  and  there  is  intense- 
oedema  round  the  site  of  injection.  The  rash  comes  out  within  a  few  hours 
and  may  be  associated  with  oedema,  rigors,  vomiting  and  collapse 
(v.  Anaphylaxis,  p.  905). 

Sudden  death  and  fatal  collapse  have  followed  antitoxin  injection, 
probably  due  to  the  status  lymphaticus  or  to  the  injection  of  serum  into 
a  vein.  The  latter  may  give  rise,  because  of  rapid  dissemination,  to  toxic 
symptoms  within  a  few  minutes,  viz.  rash,  rigors,  pyrexia,  convulsions, 
vomiting  and  collapse.  Pain  at  the  site  of  injection,  within  an  hour  or  two, 
is  relieved  by  hot  fomentations.  Local  abscess  or  cellulitis  appears  on  the 
third  to  the  twenty-first  day,  and  is  most  liable  to  follow  large  injections.  It 
is  not  always  due  to  lack  of  care.  Profuse  sweating  in  a  few  hours  indicates 
constitutional  reaction  to  the  drug,  whereas  a  dry  skin  is  a  bad  sign. 

Eashes  appear  in  from  30-80  per  cent.  Many  are  transient,  slight  and 
liable  to  be  overlooked.  Primary  rashes  are  usually  urticarial,  and  begin 
about  the  wrists  and  ankles  or  in  the  neighbourhood  of  the  injection, 
becoming  generalised  in  a  few  days.  The  rash  generally  appears  on  the 
seventh  or  eighth  day,  or  the  first  to  the  fourteenth  day,  and  lasts  1-10  days. 
It  gives  rise  to  local  itching,  and  rarely  fever  or  malaise.  Erythematous 
rashes  may  be  so  marked  in  diphtheria,  apart  from  antitoxin  injection,  as  to 
suggest  scarlet  fever.  The  antitoxin  erythema  may  start  at  the  site  of 
injection  within  a  few  days.  Both  varieties  are  more  like  blotchy  erythema 
than  scarlet  fever.  They  may  be  delayed  until  the  second  or  third  week, 
and  be  accompanied  by  rise  of  temperature  and  throat  affection,  but  no 
pin-hole  desquamation.   Circinate  erythema,  the  common  type  of  secondary 


Diphtheria.  901 

rash,  may  follow  urticaria  after  a  short  interval,  or  be  preceded  by  a 
measliform  eruption.  From  a  prognostic  point  of  view  the  urticarial 
rash  indicates  response  to  the  antitoxin ;  so,  too,  a  secondary  rash.  The 
greater  such  response,  the  smaller  is  the  liability  to  cardiac  or  other 
paralysis.  Petechia?  and  ha3matoma  sometimes  occur  at  the  site  of 
injection. 

Joint  pains,  and  pains  in  the  muscles  and  fascia,  especially  of  the 
thighs  and  forearms,  may  occur  in  the  second  or  third  week  and  last  for  a 
few  days.  The  larger  joints  are  affected  and  there  may  be  some  effusion 
with  fever.  Albuminuria  is  not  infrequent  and  adenitis  is  fairly  common, 
but  they  are  not  due  to  the  antitoxin. 

General  treatment  consists  of  rest,  isolation  and  bed  for  at  least  3  weeks, 
■even  in  the  mildest  cases.  The  horizontal  position  must  be  maintained  for 
■a  fortnight ;  and  longer,  if  there  is  irregularity  or  undue  rapidity  of  the 
heart  or  the  least  evidence  of  dilatation.  The  child  should  not  be  allowed 
to  sit  up  for  any  purpose.  Rest  preserves  the  strength  and  reduces  the 
liability  to  sudden  cardiac  failure  during  convalescence.  In  very  mild 
•cases  treated  by  antitoxin  the  child  may  be  up  in  a  week,  if  the  pulse  and 
colour  are  quite  good.  Young  children  will  require  some  mechanical 
restraint  to  prevent  them  suddenly  jumping  up  in  bed.  In  cases  of  nasal 
•diphtheria,  intubation  and  tracheotomy,  cylindrical  cardboard  splints  are 
fixed  to  the  arms  to  prevent  the  child  infecting  the  eyes,  pulling  out  the 
"tube  or  interfering  with  the  bandages. 

The  diet  must  be  nutritious  and  easily  digestible,  chiefly  milk.  It 
should  be  given  by  mouth  in  small  quantities  about  every  3  hours,  for 
•distension  of  the  stomach  may  cause  fatal  syncope  and  must  be  guarded 
against  even  during  convalescence.  Children  are  often  too  well  fed  at  this 
time.  For  regurgitation  give  jellies  and  thick  fluids,  and  feed  slowly. 
Solid  food  must  not  be  given  if  it  causes  cough.  Nasal  feeding  is  not 
•often  necessary,  even  after  intubation  or  tracheotomy.  It  must  be  used 
•cautiously,  if  at  all,  in  cardiac  and  diaphragmatic  paralysis.  It  is  indicated 
by  inability  to  swallow,  due  to  pain,  swelling,  regurgitation  or  pharyngeal 
palsy ;  coughing  due  to  food  getting  into  the  larynx ;  troublesome 
regurgitation,  continued  vomiting,  or  exhaustion  following  mouth  feeding 
and  the  refusal  of  food.  Recourse  is  had  to  rectal  feeding  during 
pharyngeal  palsy,  and  for  vomiting,  difficulty  in  passing  the  nasal  tube, 
•epistaxis,  fright  and  struggling  against  nasal  feeding. 

Stimulants  are  generally  necessary,  except  in  the  mildest  cases,  and 
should  be  distributed  over  the  whole  24  hours,  a  reserve  dose  being  kept  for 
the  early  hours  of  the  morning,  2-4  a.m.,  when  vitality  is  lowest.  Brandy, 
strychnia,  nux  vomica,  ether,  ammonia,  caffeine  and  digitalis  are  all  useful, 
•especially  the  first  two.  They  must  be  used  with  caution,  if  there  is  fatty 
•degeneration  of  the  heart.  The  poison  of  diphtheria  appears  to  be  directly 
antagonistic  to  strychnia,  which  can  be  given  in  considerable  doses.    It  is 


902  Chapter  LXIII. 

most  efficacious  subcutaneously.  Atropine  has  been  recommended  to 
counteract  the  effect  of  the  poison  on  the  heart  muscle.  It  paralyses  the 
ends  of  the  vagus,  reduces  its  inhibitory  action  and  often  accelerates  the 
heart.     Tonics,  especially  iron  and  strychnia,  are  given  internally. 

Local  treatment  is  hardly  necessary  if  antitoxin  is  given,  especially  in 
very  young  children  whom  it  worries  and  wearies,  and  may  do  more  harm 
than  good.  Membrane  must  never  be  forcibly  removed,  unless  very  loose 
and  almost  separated.  The  ordinary  local  remedies  recommended  for  septic 
conditions  of  the  throat  (p.  234)  can  be  used,  choosing  by  preference  liq. 
sod.  chlorinatae,  chlorine  water,  liq.  hyd.  perchlor.,  peroxide  of  hydrogen,, 
and  permanganate  of  potash  or  zinc.  For  nasal  diphtheria  syringe  or 
douche  gently  with  alkaline  antiseptic  solutions  (p.  373).  Treat  laryngeal 
diphtheria  on  the  same  lines  as  laryngitis. 

Intubation  or  tracheotomy  may  be  imperative.  For  intubation  use  a 
tube  as  large  as  can  be  conveniently  inserted,  made  of  hard  rubber  or 
vulcanite.  Wrap  the  child  in  a  blanket,  with  his  arms  by  the  side  and 
head  extended,  and  place  him  on  his  back  with  a  small  pillow  under  the  neck. 
Insert  a  gag  covered  with  rubber  tubing  at  the  left  side  of  the  mouth,  do 
not  open  it  widely,  and  remove  it  between  the  attempts  at  intubation.  The 
tube  is  sterilised  in  a  warm  saturated  solution  of  boric  acid  and  smeared  with 
a  lubricant.  It  is  fixed  into  the  introducer  and  held  in  the  right  hand. 
The  left  index  finger  is  hooked  round  the  epiglottis  and  the  tube  inserted, 
along  this  as  a  guide,  in  the  median  line.  The  attempts  at  introduction 
must  be  made  quickly  and  very  little  force  is  needed.  Some  operators 
prefer  the  sitting  posture,  with  the  head  held  erect  and  well  lifted  up  to 
prevent  approximation  of  the  epiglottis  to  the  glottis.  When  the  tube  is 
in  the  pharynx,  violent  cough  is  induced  but  it  soon  subsides  ;  the  respira- 
tion is  hissing  in  character,  breathing  tubular,  and  the  dyspnoea  is  relieved. 
It  may  enter  the  oesophagus  and  be  swallowed.  The  general  difficulties 
of  insertion  are  oedema,  a  thick  membrane  in  the  larynx,  spasm  of  the 
glottis,  the  end  of  the  tube  entering  the  ventricle  of  the  larynx,  and  a  ring 
of  sub-glottic  oedema  about  the  level  of  the  cricoid.  Spasm  gives  way  on 
inspiration,  if  gentle  pressure  is  kept  up.  A  silk  string  is  fixed  to  the  tube 
and  fastened  by  plaster  in  the  neighbourhood  of  the  ear,  thus  enabling  the 
tube  to  be  removed  at  a  moment's  notice.  The  tube  is  kept  in  for  24  hours., 
removed  daily  for  cleaning,  kept  out  a  short  time  at  the  end  of  36  hours,  and 
can  generally  be  dispensed  with  in  3  or  4  days.  It  may  be  rejected  on  cough- 
ing ;  may  increase  the  dyspnoea  by  pushing  down  loose  membrane  or 
tenacious  mucus,  or  by  becoming  slowly  or  suddenly  blocked  ;  or  may 
induce  vomiting.  If  the  breathing  is  not  immediately  relieved,  the  tube 
must  be  removed.  It  may  give  rise  to  abrasion  or  ulceration  (pressure 
ulcers)  of  the  mucus  membrane,  "  thread  ulcer  "  due  to  the  silk,  may  slip 
into  the  bronchus  or  trachea,  or  cause  stenosis  of  the  larynx.  If  it  increases- 
the  dyspnoea,  do  tracheotomy.     When  no  string  is  attached  the  tube  is- 


Diphtheria.  903 

removed  by  an  extractor,"  or  by  backward  and  upward  pressure  on  the 
trachea  below  its  lower  end.  On  several  occasions  it  has  been  swallowed 
and  evacuated  without  difficulty. 

The  disadvantages  of  intubation  are  obvious.  It  requires  considerable 
experience  and  affords  less  complete  relief  ;  false  membrane  is  less  easily 
got  rid  of  ;  and  subsequent  feeding  is  more  difficult.  The  patient  needs 
constant  skilled  attention,  while  the  tube  is  in  position,  for  at  any  moment 
it  may  be  coughed  up  or  have  to  be  removed,  and,  as  it  can  only  be 
replaced  by  a  skilled  person,  there  is  constant  risk  of  sudden  asphyxia  unless 
an  expert  is  always  at  hand.  Sudden  asphyxia  from  blockage  of  the  tube 
may  necessitate  its  immediate  removal,  and  even  tracheotomy. 

On  the  other  hand  it  is  advantageous  in  that  no  anaesthetic  is  required, 
and  no  cutting  operation.  There  is  no  liability  to  wound  infection,  no 
subsequent  scar,  less  risk  of  lung  infection,  and  it  need  not  be  postponed  until 
imperative.  It  can  be  done  quickly  without  assistance  and  in  a  bad  light. 
There  is  less  risk  of  subsequent  hoarseness,  and  recovery  is  quicker.  The 
voice  may  remain  husky  for  a  few  weeks. 

After-treatment  of  intubation  consists  in  careful  feeding,  usually  by 
the  mouth  or  by  nasal  tube.  If  given  by  mouth,  the  food  should  be  semi- 
solid ;  there  is  comparatively  little  risk  of  any  getting  into  the  larynx. 
The  child  should  be  kept  on  the  side,  not  on  the  face,  to  facilitate  the 
escape  of  mucus,  and  cough  is  induced  by  sips  of  water  every  2-3  hours  to 
clear  the  tube.  Nasal  feeding  is  sometimes  needed  after  the  tube  has  been 
removed. 

Tracheotomy  is  required  if  the  obstruction  is  rapidly  increasing, 
recession  more  marked,  temperature  rising,  respiration  and  pulse  rate  more 
frequent,  and  if  the  child  is  more  restless  and  cyanotic.  It  can  be  done 
almost  as  rapidly  as  intubation,  but  it  increases  the  risk  of  broncho-pneu- 
monia and  creates  an  absorbing  surface.  If  possible,  time  should  be 
allowed  for  antitoxin  to  act.  It  is  advisable  to  avoid  the  use  of  feathers, 
steam  tents  and  overfeeding.  Do  not  keep  the  tube  in  longer  than  is 
necessary.  Kemove  it  frequently  and  re-insert  if  required,  and  leave  it 
permanently  out  in  48  hours  if  possible.  The  chief  difficulty  in  removal  of 
the  tube  is  that  it  may  be  followed  by  severe  dyspnosa,  which  may  come  on 
at  once,  in  a  few  hours  or  even  during  sleep.  This  is  sometimes  caused  by 
injury  to  the  cricoid  cartilage,  interfering  with  proper  action  of  the  crico- 
arytenoid muscles,  spasm  of  the  glottis  or  granulations  of  the  mucosa. 
Granulations  must  be  treated  by  astringents  or  removal.  Sometimes  the 
inability  to  do  without  the  tube  is  due  to  mere  nervousness,  occasionally  to 
abductor  paralysis,  and  rarely  to  a  ring-like  stricture  of  the  trachea.  Active 
interference  is  of  doubtful  value.  Attempts  should  be  made  to  remove 
the  tube  when  obstruction  is  least  marked,  and  repeated  every  3  or  4  weeks. 
Early  removal  of  the  tube,  in  48-72  hours,  is  the  best  preventive. 


904  Chapter  LX11L 

Stenosis  of  the  larynx  may  follow  either  intubation  or  tracheotomy. 
It  is  usually  due  to  granulations  but  may  result  from  cicatricial  contraction, 
swelling  and  infiltration  of  the  mucous  membrane  of  the  arytenoids,  or  a 
chronically  inflamed  condition  of  the  sub-glottic  region.  Occasionally  there 
is  only  a  pin-point  orifice  or  practically  complete  atresia.  It  is  treated  by 
tents  and  bougies  ;  dilators  and  intubation  tubes  ;  intra-laryngeal  division 
of  the  stricture ;  and  other  surgical  measures.  Polypoid  granulations 
may  occur  although  tracheotomy  has  been  quickly  and  easily  performed 
and  the  tube  left  in  only  a  few  days.  They  give  rise  to  increasing  dyspnoea, 
after  a  period  of  health,  and  necessitate  further  operation. 

Treatment  of  Special  Symptoms. — Paralysis  is  partially  prevented 
by  complete  rest  at  the  onset  of  the  disease,  recumbency  during  its  course, 
and  rest  during  convalescence.  Antitoxin  has  occasionally  seemed  of  value 
but  may  cause  aggravated  serum  disease,  because  of  anaphylaxis.  It  is 
given  every  3-5  days.  Pood  must  be  warm,  not  hot,  liquid  or  semi-solid, 
and  given  in  small  mouthfuls.  Nasal  feeding  and  nutrient  enemata  may 
be  needed.  See  that  the  bladder  and  bowels  are  evacuated.  The  chief 
measures  for  curing  the  neuritis  are  rest,  liberal  diet,  tonics  and  moderate 
stimulation.  Galvanism,  massage  and  strychnia  can  be  used,  provided  there 
is  no  acute  tenderness.  For  cardiac  and  respiratory  symptoms  try  oxygen 
inhalations,  faradism  of  the  vagus  and  injections  of  camphorated  oil, 
■sparteine  or  strychnia.  Atropine  and  strychnia  are  given  for  pseudo- 
bulbar crises.  In  early  cardiac  palsy  avoid  drugs  likely  to  cause  vomiting, 
and  use  enemata  for  constipation.  If  the  diaphragm  is  paralysed,  causing 
cyanosis  and  accumulation  of  mucus  in  the  pharynx  and  bronchial  tubes, 
give  large  doses  of  belladonna  or  atropine  by  mouth  and  strychnia  sub 
cutem.  Adrenalin  is  probably  of  no  value,  unless  injected  into  a  vein,  and 
it  is  doubtfully  advisable  to  raise  peripheral  blood  pressure  if  there  is  the 
least  sign  of  degeneration  of  cardiac  muscle. 

For  vomiting  in  early  stages,  due  to  deglutition  or  nervousness,  rely 
on  nasal  feeding,  nutrient  enemata,  and  large  doses  of  belladonna  and 
bromide.  In  late  stages  it  may  be  relieved  by  saline  enemata,  bromides 
per  rectum  and  morphia  sub  cutem.  Saline  injections  relieve  thirst,  increase 
diuresis  and  assist  in  evacuation  of  the  toxin,  reduce  restlessness  and  raise 
blood  pressure.  Anuria  is  relieved  by  hot  packs,  and  saturated  solution  of 
mag.  sulph.  in  drachm  doses  as  a  diuretic. 

Convalescence  and  Prophylaxis. — Gradually  the  child  is  allowed  to 
sit  up  in  bed  by  increasing  the  number  of  supporting  pillows,  and  so  he 
progresses  to  the  use  of  a  bed  rest,  to  sitting  up  in  bed  without  support, 
on  a  sofa,  walking  about  the  room  and  then  out-of-doors.  Convalescence 
is  greatly  aided  by  fresh  air,  so  in  suitable  weather  the  bed  may  be  placed  near 
an  open  window.    Tonics,  notably  iron  preparations,  are  necessary. 

The  period  of  quarantine  is  an  open  question.  If  no  bacteriological 
examination  is  made,  the  child  should  be  isolated  for  3  weeks  after  the 


Diphtheria.  005 

membrane  has  gone.  Probably  in  most  cases  there  is  no  infectivity  a  few 
•days  after,  and  the  child  may  be  allowed  to  go  to  school  in  another  week. 
It  is  safer  to  insist  on  6  weeks  quarantine.  Swabs  should  yield  no  specific 
bacilli  on  culture,  but  they  have  been  recovered  from  the  throat  even  on  the 
363rd  day,  though  they  are  not  likely  to  be  virulent  as  late  as  this.  The 
usual  methods  of  isolation  and  disinfection  of  all  utensils,  discharges,  etc., 
are  necessary.  Antiseptic  treatment  of  the  nose  and  throat  reduces  the 
infectivity.  These  structures  should  be  examined  bacteriologically  in  all 
"  contacts  "  and,  in  schools,  children  in  whom  the  result  is  positive  or  doubt- 
ful should  be  isolated  and  treated  with  hydrogen  peroxide  spray  or  gargle. 
A  "  contact  "  can  spread  the  disease  without  developing  it.  The  injection  of 
200-500  units  of  antitoxin  every  3  weeks  has  been  recommended,  but  is  not 
advisable  on  account  of  the  risks  of  anaphylaxis  and  the  possibility  of  having 
to  treat  an  actual  attack  of  the  disease. 

Anaphylaxis. — This  is  a  curious  constitutional  state  set  up  in  a  patient 
by  the  injection  of  antitoxin,  rendering  him  liable  to  serious  and  even  fatal 
symptoms  if  a  further  injection  is  given  after  an  interval  of  10  days,  say 
within  another  2-3  weeks.  It  is  due  to  the  protein  substance  in  the  serum 
and  has  been  known  to  last  more  than  a  year.  A  similar  condition  follows 
the  injection  of  milk  and  egg  albumin.  The  symptoms  are  those  of  aggra- 
vated serum  disease.  It  is  an  important  peculiarity,  for  it  makes  it  essential 
to  exercise  great  care  in  the  repeated  administration  of  the  drug.  If  given 
"within  10  days  the  effect  is  not  produced. 


Chapter  LXIV. 

INFLUENZA. 

Influenza  is  an  acute  specific  infective  febrile  disorder  of  variable 
severity  and  extremely  difficult  of  diagnosis  in  its  milder  manifestations. 
Children  of  all  ages  are  liable  to  it,  less  so  than  adults,  but  they  are  com- 
paratively immune  from  its  complications  and  dangers.  Attacks  are 
generally  mild  and  followed  by  slight  catarrh  and  profuse  sweating.  Cases 
have  been  recorded  on  the  first  and  second  days  of  life,  possibly  of  con- 
genital origin,  and  occur  occasionally  in  the  early  months.  A  certain 
amount  of  immunity  is  conveyed  to  breast-fed  infants. 

Pathology. — It  is  due  to  Pfeiffer's  bacillus.  This  organism  is  not 
invariably  present  and  has  been  found  in  other  diseases.  It  resembles 
the  bacillus  found  by  Sprengel  and  Eppendorf  in  pertussis  and  the  Koch- 
Weeks  bacillus,  and  is  readily  stained  by  carbol-fuchsin  and  Canon's  dye. 
Many  attacks  of  so-called  influenza  are  due  to  organisms  belonging  to  the 
same  group  but  differing  in  slight  morphological  and  cultural  details. 
The  organism  has  been  found  in  the  nasal  secretion,  sputa,  cerebrospinal 
fluid,  pus  from  the  ears,  etc.,  and  occasionally  in  the  blood.  It  probably 
enters  through  the  nose  or  naso-pharynx.  Its  effects  are  mainly  due  to  a 
toxin  which  acts  primarily  on  the  nervous  system.  In  some  cases  the 
chief  effects  fall  on  the  gastro-intestinal,  respiratory  or  blood-forming 
organs. 

Symptoms. — The  incubation  period  is  uncertain,  probably  1-3  days. 
The  onset  is  variable,  and  often  sudden  with  fever,  headache,  general  malaise 
and  pains.  Lassitude  and  slight  fever  may  be  the  only  signs.  Sometimes 
it  is  ushered  in  by  epistaxis,  sore-throat,  coryza  or  gastro-intestinal  symp- 
toms. Furred  tongue,  loss  of  taste,  anorexia,  flatulence,  nausea,  vomiting 
and  constipation  are  common  symptoms.  Occasionally  an  evanescent 
erythema  is  noted.  The  pulse  is  unduly  rapid,  rarely  slow  and  irregular. 
Cases  may  be  grouped  according  to  the  predominant  symptoms.  In 
practice  it  is  common  to  find  various  combinations  of  the  different  symptoms 
but  sometimes  the  attack  can  be  definitely  labelled  as  belonging  to  one  or 
other  group.  The  febrile  type  is  frequent  in  children.  The  temperature  is 
raised  for  a  day  or  two,  rising  suddenly,  perhaps  to  105°  F.,  and  subsiding 
rapidly  or  coming  down  gradually  by  lysis  in  the  course  of  a  week.  Such  a 
temperature  is  common  in  every  kind  of  attack.  The  child  is  ailing  and 
languid,  with  loss  of  appetite,  and  sweats  readily. 


Influenza.  907 

The  gastro-intestinal  type  is  also  common  in  children,  and  liable  to  be 
misconstrued  for  it  simulates  acute  febrile  gastro-intestinal  catarrh.  The 
symptoms  are  marked  colic,  restlessness,  constipation  and  moderate  fever  ; 
or  vomiting  and  convulsions,  suggestive  of  the  onset  of  tuberculous 
meningitis.  In  other  instances  there  are  loss  of  appetite,  furred  tongue, 
vomiting  and  constipation,  followed  by  diarrhoea  in  a  few  days.  Or  there 
may  be  much  diarrhoea  and  abdominal  pain,  sometimes  hrematemesis  and 
melama.     The  spleen  may  be  enlarged. 

The  catarrhal  type  may  be  naso-pharyngeal  in  origin  or  simulate  the 
onset  of  measles.  Retro-pharyngitis  is  common  at  the  onset  and  a  local 
fibrinous  exudation  forms  later.  Sometimes  there  is  a  tonsillitis  which  may 
be  membranous  ;  or  pronounced  coryza  and  epistaxis  ;  or  coryza,  con- 
junctivitis and  cough.     Earache  is  often  present. 

In  the  pulmonary  type  the  air  passages  are  rapidly  affected.  Inspiratory 
crepitations  are  heard  throughout  the  lungs,  especially  over  the  posterior 
parts.  There  is  no  dulness.  Cough  is  dry,  paroxysmal  and  difficult.  This 
cedematous  state  of  the  lungs  is  apt  to  wander  from  one  part  to  another, 
and  is  followed  by  profuse  muco-purulent  catarrh. 

The'  nervous  type. — Infants  may  exhibit  a  marked  somnolence,  due  to 
the  toxgemia  and  lasting  for  even  7-10  days.  It  may  be  associated  with 
high  fever.  It  is  not  infrequent  in  older  children,  but  in  these  the  more 
common  nervous  symptoms  are  headache,  sleeplessness,  severe  depression, 
aching  bones,  sensitive  spine,  general  pains,  and  perhaps  mental  aberration 
and  various  forms  of  neuritis  and  palsy.  Meningeal  irritation  is  easily  set 
up,  and  possibly  an  influenzal  meningitis  or  encephalitis  may  occur. 
Retraction  of  the  head,  irritability  and  fever  are  usually  toxic  and  of  a 
few  days'  duration.  More  prolonged  cases  are  inflammatory,  due  to  the 
specific  bacillus  or  secondary  infection,  and  may  end  fatally.  Occasionally 
cerebral  and  peritoneal  irritation  are  combined.  Thus,  an  infant  developed 
a  pseudo-peritonitic  attack  and  well  marked  symptoms  of  basal  menin- 
gitis after  influenza,  but  recovered  in  a  few  days.  Another  boy,  aged  7 
years,  was  dazed  and  listless  on  the  eighth  day,  had  abdominal  pain  on  the 
eleventh,  and  paroxysmal  pain  with  inability  to  pass  water  and  constipation 
two  days  later.  He  was  drowsy  with  dilated  pupils,  furred  tongue,  and 
retention.  On  the  sixteenth  day  he  was  noisy  and  presented  general 
hyperesthesia,  pain  in  the  back  of  the  neck  and  slight  retraction  of  the 
head.  On  the  following  day  he  was  irritable  and  complained  of  pins  and 
needles  down  the  legs  and  pains  in  the  back  as  of  "  fleas  biting  him." 
After  this  he  steadily  recovered.  There  was  no  fever  throughout,  except 
possibly  at  the  onset.  In  another  case  there  was  considerable  muscular,, 
nervous  and  psychical  derangement  one  month  after  influenza.  The 
girl,  2|  years  old,  was  unable  to  hold  up  her  head,  weak  on  her  legs,  and  fell 
on  attempting  to  walk  or  exhibited  a  gait  like  cerebellar  ataxia.  She 
moaned  all  day,  made  faces,  did  not  talk,  was  not  interested  in  toys  or 


908  Chapter  LXIV. 

games,  and  kept  picking  her  face  and  throwing  the  head  and  trunk  about. 
She  was  strange  in  her  manner  and  had  got  very  spiteful,  biting  the  other 
children  if  she  had  the  chance.  Twitching  of  the  face,  eyes  and  hands 
was  present  during  sleep.  The  pulse  rate  was  120  and  the  knee  jerks 
Avere  exaggerated.     Recovery  was  complete. 

Occasionally  the  toxin  acts  powerfully  on  the  heart,  causing  tachy- 
cardia, arrhythmia,  attacks  of  collapse  with  small  thready  pulse,  or  even 
angina.  These  are  apt  to  occur  even  under  1  year  of  age  and  may  be 
regarded  as  complications.  Asthenia  and  general  hyperesthesia  are 
sometimes  very  marked.  Headache  is  usually  frontal  and  may  be  temporal. 
It  is  often  severe  in  older  children  and  slight  or  absent  in  infants. 

Complications  are  mainly  those  of  the  pulmonary,  cardiac  and  nervous 
systems.  They  occur  at  the  onset,  during  the  course,  or  after  the  fever. 
Attacks  of  syncope,  anginal  in  character,  are  not  infrequent.  The  child 
becomes  very  pale,  cold  and  almost  pulseless,  or  the  pulse  is  frequent,  small 
and  thready.  Similar  attacks  may  follow  the  old-fashioned  influenza  cold. 
Tachycardia  and  arrhythmia  are  common  at  any  period  of  the  disease. 
At  the  onset  the  pulse  is  unduly  rapid  in  proportion  to  the  fever,  just  as  in 
scarlet  fever.  The  cardiac  symptoms  are  due  to  the  action  of  the  toxin 
on  the  cardiac  muscle  or  nerves,  or  secondary  to  neuritis  of  the  cardiac 
nerves.  Parenchymatous  degeneration  may  be  found  after  death. 
Sometimes  there  is  dilatation  of  the  heart,  with  cyanosis  and  collapse. 

Catarrh  of  the  air  passages  is  part  of  the  pulmonary  type  of  the 
disease.  There  may  be  a  wandering  patchy  oedema  of  the  lungs,  general 
capillary  bronchitis,  or  broncho-pneumonia.  In  rare  instances  the 
pneumonic  affection  is  insidious  and  atypical,  creeping  about  the  lungs  and 
in  time  affecting  practically  the  whole  of  them,  one  portion  becoming 
involved  as  another  recovers.  Pneumonia  is  usually  lobular,  if  due  to  the 
specific  bacillus,  and  often  not  recognised  as  influenzal.  Each  kind  of 
pneumonia  may  be  primary  or  secondary  to  pneumococcal  infection. 
Pleurisy  is  not  uncommon,  lobar  pneumonia  may  occur  during  convalescence, 
and  asthma  is  an  occasional  sequel. 

Convulsions  are  not  infrequent  in  babies  and  may  recur  for  several 
days.  In  the  early  stages  headache,  neuralgic  pains,  delirium,  somnolence 
and  coma  are  due  to  the  action  of  toxin  on  the  central  nervous  system. 
Later  on,  toxic  Or  inflammatory  affections  may  develop,  e.g.  meningitis  of 
the  brain  or  cord,  encephalitis,  neuritis,  degenerative  changes  in  the 
nerves  analogous  to  those  in  diphtheria,  myalgias,  and  neuralgias  of 
various  kinds,  functional  or  organic.  Mental  disturbances,  varying  from 
simple  fatuity  to  acute  mania  and  insanity,  may  occur  at  any  period  but 
most  often  in  convalescence.  At  this  period  hallucinations,  lethargy,  stupor 
and  loss  of  memory  are  not  uncommon.  Sometimes  epilepsy,  hysteria  and 
neurasthenia  date  from  an  attack  of  cerebral  type.     The  cranial  nerves  are 


Influenza.  9091 

apt  to  suffer,  especially  the  sixth  and  third  nerves.     Profuse  sweating  is  a 
frequent  nervous  symptom. 

Otitis  media  (p.  995)  is  common  and  the  organism  may  be  found  in  the 
pus.  It  is  unilateral  in  75  per  cent,  and  sometimes  followed  by  mastoiditis. 
Albuminuria  is  present  in  5-10  per  cent.,  and  acute  glomerulo-nephritis 
is  an  occasional  complication.  Retention  is  due  to  paresis  of  the  bladder 
and  secondary  pyelitis  may  ensue.  Dudgeon  and  Adams  (1907)  reported  a 
case  of  pysemia,  multiple  arthritis  and  meningitis  in  a  10-year  old  girl.. 
The  primary  lesion  was  an  epiphysitis  of  the  upper  end  of  the  radius. 

Diagnosis. — Much  importance  must  be  attached  to  a  history  of  exposure- 
to  infection  and  the  presence  of  other  cases  in  the  house.  At  the  onset 
the  cough  may  suggest  measles  and  later  on  be  like  that  of  pertussis.  The 
diagnosis  from  the  simple  influenzal  cold  depends  on  bacteriological 
examination  and  is  relatively  unimportant,  for  the  same  treatment  is 
necessary.  Cases  ushered  in  with  erythema,  rapid  pulse  and  vomiting,. 
are  difficult  to  diagnose  from  scarlet  fever,  if  there  is  any  sore-throat.  The 
pulmonary  type  may  simulate  incipient  phthisis.  Gastro-intestinal  attacks. 
are  like  (1)  acute  appendicitis,  perforated  gastric  ulcer  or  intestinal 
obstruction  ;  (2)  typhoid  fever,  acute  enteritis  or  colitis  ;  (3)  Henoch's 
purpura.  The  nervous  type  simulates  meningitis  or  encephalitis,  especially 
if  associated  with  an  infrequent  irregular  pulse,  somnolence,  and  cranial 
nerve  palsy.  But  it  ends  in  recovery,  though  the  squint  may  take  3  months 
to  disappear. 

Prognosis. — Death  rarely  occurs  in  the  young,  except  from  cardiac 
failure  or  secondary  pneumonia.  The  outlook  is  good  unless  the  heart 
is  affected.  In  babies  it  must  be  guarded,  for  sudden  failure  may  develop 
at  any  period  within  a  week  of  the  onset,  especially  if  the  pulse  is  unduly 
rapid  or  irregular.  Usually  recovery  takes  place  in  a  few  days,  but  some 
uncomplicated  cases  last  for  weeks.  Possibly  the  infection  is  a  cause  of 
prolonged  anomalous  fever.  Convalescence  is  slow  and  marked  by  lack  of 
appetite,  debility,  sweating,  cough,  fractiousness,  cardiac  weakness  and 
liability  to  secondary  infections.  There  is  no  special  tendency  to 
tuberculosis. 

Treatment. — Isolate  the  child  and  give  a  mixture  of  ammoniated 
quinine,  acetate  of  ammonia,  and  syrup  of  orange.  Keep  the  patient 
in  bed,  and  avoid  cold  and  exposure.  Order  a  reduced  diet  and  plenty  of 
fluid  in  the  febrile  stage,  but  encourage  the  appetite  and  feed  the  patient 
as  soon  as  possible.  A  dose  of  calomel  or  castor  oil  is  beneficial.  In  the 
early  stages  give  phenacetin  as  a  sedative,  antipyretic,  and  for  the  relief 
of  headache.  Phenacetin  gr.  ^,  caffein  citrate  gr.  \  and  sod.  bicarb,  gr.  1 
can  be  given  every  2  hours  at  1  year  of  age,  and  in  double  quantities  at 
3-4  years,  for  6-8  doses.  For  older  children  aspirin  or  salicylate  of  soda 
can  be  used  instead  of  the  bicarbonate.  At  all  ages  aspirin  may  be  given 
alone  in  small  fraquent  doses.     The  heart  must  be  carefully  watched  and 


S10  Chapter   LX1  V. 

stimulated  with  strychnia,  caffeine,  strophanthus  or  digitalis,  if  necessary. 
Euquinine,  quinine  and  salicylate  of  quinine  are  also  useful.  Amyl  nitrite 
has  been  advocated  for  profuse  sweating.  For  high  fever  and  delirium 
apply  ice  to  the  head  and  give  tepid  baths.  Other  treatment  is  symptomatic. 
Iron,  arsenic  and  cod-liver  oil,  with  change  of  air,  are  needed  in  con- 
valescence. Special  care  is  necessary  because  of  the  liability  to  dilatation  of 
.the  heart  and  inflammation  of  the  lungs. 


CHAPTER    LXV. 

TYPHOID  FEVER— PAEATYPHOID  FEVER. 

Typhoid  fever  is  a  general  blood  infection,  via  the  intestinal  mucosa 
•except  in  intra-uterine  life  when  the  infective  organism  is  conveyed  to  the 
foetus  by  the  umbilical  vein.  The  chief  characteristic  of  the  disease  in 
early  life  is  its  comparative  mildness,  though  at  times  it  is  just  as  severe 
as  in  adults.  On  account  of  this  peculiarity  it  is  probable  that  many  cases 
in  infants,  especially  in  hospital  practice,  are  overlooked.  Abortive  attacks 
are  frequent  and  the  intestinal  symptoms  not  severe.  Vomiting  and  head 
retraction  are  more  common,  haemorrhage  and  perforation  infrequent,  and 
diarrhoea  and  abdominal  distension  less  marked  than  in  later  life.  The 
babe  suffers  from  a  febrile  attack  and  diarrhoea,  is  supposed  to  have 
enteritis  or  entero-colitis,  and  gets  well.  Typhoid  fever  may  not  even  be 
suspected  and,  if  it  is,  the  difficulty  of  diagnosis  is  great.  In  older  children 
the  attack  is  often  of  the  ambulatory  type.  It  is  more  common  in  boys 
than  girls,  probably  by  reason  of  their  habits  at  games,  such  as  marbles, 
whip  top,  etc.,  rendering  them  more  liable  to  infection,  if  playing  in  the 
vicinity  of  ash-pits.  It  is  uncommon  before  the  fifth  year  of  life.  In 
breast-fed  infants  the  infection  is  conveyed  by  water  used  in  bathing, 
•directly  from  the  mother,  or  through  the  agency  of  flies. 

Congenital  Typhoid. — Typhoid  fever  in  the  mother  leads  to  abortion 
in  about  two-thirds,  generally  in  the  fifth  month  of  pregnancy.  In  10  out 
of  21  cases  collected  by  Hicks  and  French  (1905)  the  bacillus  was  trans- 
mitted to  the  foetus,  delivery  usually  taking  place  in  late  stages  of  the 
fever  and  the  child  sometimes  being  born  alive.  In  these  cases  bacilli  were 
generally  present  in  the  foetus,  whereas  in  cases  of  abortion  early  in  the 
course  of  the  fever  bacilli  were  not  found.  This  is  an  important  point  for 
it  suggests  the  advisability  of  inducing  labour  early  in  the  fever,  if  the 
child  is  viable,  in  order  to  prevent  intra-uterine  infection.  Though  the 
•child  may  be  born  alive  in  late  stages  of  the  fever,  it  almost  always 
succumbs.  Newborns  and  very  young  infants  of  women  with  typhoid 
may  exhibit  Widal's  reaction  but  no  symptoms  of  the  disease.  Such 
babes  have  had  the  fever  in  utero  or  have  acquired  the  agglutinating 
principle  from  the  maternal  blood  or  milk.  On  the  other  hand  the  serum 
reaction  is  often  absent  in  the  foetus.  Like  other  fevers,  typhoid  in  the 
mother  may  cause  malnutrition  or  pathological  metabolic  and  organic 
changes  in  the  foetus  through  the  transmission  of  toxins.  Such  infants 
may  be  physically  or  intellectually  defective. 


912 


Chapter  LXV. 


Symptoms. — Diarrhoea,  fever  and  splenic  enlargement  are  the  most 
frequent  signs  in  those  born  alive.  Occasional  symptoms  are  rose  spots, 
slight  jaundice,  haemorrhage,  tympanites,  vomiting,  constipation,  con- 
vulsions, cough  and  purpura.  Haemorrhages  may  take  place  into  the 
skin,  liver  and  kidneys.  The  mesenteric  glands  are  a  little  enlarged. 
Intestinal  lesions  may  be  absent  or  resemble  those  of  ileo-colitis.  Definite 
ulceration  of  Peyer's  glands  has  been  noted.  According  to  Helwig  Peyer's 
glands  are  fully  developed  by  the  sixth  month  of  foetal  life.  In  Blumer's 
case  (1900),  a  full-time  child  died  from  kaemorrhagic  disease,  the  mother 
having  had  typhoid  fever  4  months  before  confinement,  and  the  specific 
organism  was  found. 

Infantile  Typhoid. — The  symptoms  during  the  first  30  months  of  life 
are  well  shown  in  a  summary  based  on  nearly  400  cases  collected  by 
J.  P.  Crozer  Griffith  and  M.  Ostheirner  (1902). 


First 
Year. 

Second 
Year. 

Age  24-30 
months. 

Number  of  Cases 

139 

187 

68 

Fever 

46 

50 

42 

Diarrhoea 

42 

40 

24 

Rash 

26 

27 

23 

Spleen 

26 

26 

13 

Tympanites 
Vomiting 

18 
11 

18 
9 

12 

8 

Constipation 
Haemorrhage 

1 
1 

6 
1 

3 
1 

Perforation 

0 

2 

0 

Cough 

1 

20 

6 

Fits 

4 

6 

2 

Other  symptoms  in  the  first  year  were  collapse  3,  jaundice  3,  and  otitis,, 
albuminuria  and  noma  1  each  ;  in  the  second  year,  collapse  1,  epistaxis  4, 
laryngeal  obstruction  2,  otitis,  meningeal  signs,  aphasia,  parotitis  and 
desquamation  1  each,  and  relapses  6  ;  in  the  third  period,  collapse  2,. 
epistaxis  1,  meningeal  signs  3,  pneumonia  3,  otitis  1,  phlegmasia  alba 
dolens  1,  and  relapses  3. 

In  comparison  with  adult  typhoid  it  is  noticeable  that  diarrhoea  is. 
almost  invariably  present,  though  occasionally  constipation  may  be  intense 
throughout ;  vomiting  is  more  frequent ;  tympanites  is  rarely  severe  and 
sometimes  the  abdomen  is  retracted  ;  and  epistaxis  in  early  stages  is 
infrequent.  Many  cases  present  the  symptoms  of  enteritis,  viz.  green  and 
watery  stools,  slight  or  absent  tympanites,  irregular  fever,  cerebral  irritation, 
rapid  emaciation,  prostration,  albuminuria  and  weak  heart  sounds.  The 
duration  is  1-8  weeks ;  more  than  two-thirds  of  the  cases  lasting  1-3  weeks,., 
and  a  few  less  than  1  week. 


Typhoid  Fever — Paratyphoid  Fever.  913 

In  Older  Children. — Both  in  infants  and  children  the  onset  is  generally 
indefinite.  Feebleness  and  somnolence  may  mark  a  prodromal  stage  of 
2-14  days' duration.  It  is  sometimes  ushered  in  with  vomiting  and  severe 
abdominal  pains  ;  or  with  vomiting  and  high  fever,  up  to  104°  F.  in 
48  hours,  rarely  a  rigor ;  and  may  simulate  meningitis.  In  children  the 
common  early  symptoms  are  anorexia  and  perhaps  restlessness,  headache, 
drowsiness  at  unusual  times,  moderate  vomiting  and  constipation.  The 
onset  is  generally  more  rapid  and  less  insidious  than  in  adults.  Epistaxis 
is  present  in  less  than  half  the  cases. 

The  fever  rises  by  steps  to  its  maximum  in  3-5  days  and  is  high  but  well 
tolerated.  It  may  last  for  several  days  and  the  child  scarcely  feel  ill.  Its 
average  duration  is  2-3  weeks.  In  one  case  under  my  notice  the  tempera- 
ture chart  was  characteristic  but  the  fever  only  lasted  for  10  days.  The 
girl,  10  years  old,  had  no  definite  symptoms.  She  was  treated  for  typhoid 
during  the  fever  and  a  period  of  10  days  apyrexia.  A  typical  relapse  then 
occurred,  with  a  copious  rash  on  the  thirtieth  day  of  the  illness.  The 
fever  persisted  for  8  months  and  terminated  in  death  from  marasmus, 
though  there  were  no  definite  symptoms  throughout. 

In  several  other  children  the  fever  only  lasted  10  days.  Usually 
it  lasts  2-3  weeks  and  falls  by  lysis  during  a  period  of  7-10  days, 
sometimes  more  quickly,  and  occasionally  by  crisis.  The  pulse  rate 
corresponds  with  the  height  of  the  fever  or  is  lower.     It  is  seldom  dicrotic. 

Rash  is  common,  at  times  abundant,  and  may  appear  early,  generally 
in  7-10  days.  The  number  of  spots  is  no  measure  of  the  severity  of 
the  disease  but  duskiness  is  a  grave  sign. 

Anorexia  is  marked.  The  tongue  may  remain  almost  clean.  Usually 
it  presents  a  thick  white  coating,  dark  border  and  clean  tip,  forming  the 
"  typhoid  triangle."  It  is  dry,  brown  or  black,  and  cracked  in  severe  cases. 
Sordes  on  the  teeth,  rhagades  and  foul  breath  are  then  noted.  Vomiting 
is  not  infrequent  at  the  onset,  throughout  the  course,  and  as  a  terminal 
symptom.  Tenderness  and  pain  in  the  abdomen  may  be  present. 
Diarrhoea  is  about  as  frequent  as  constipation.  It  may  appear  late,  is 
rarely  severe,  but  is  sometimes  grave.  Tympanites  is  fairly  common 
after  the  first  week  unless  the  diet  is  very  carefully  regulated.  Intestinal 
haemorrhage  and  perforation  are  uncommon  in  the  very  young  because  of 
the  infrequency  of  severe  ulceration. 

The  spleen  is  almost  invariably  enlarged,  often  very  early  in  the 
disease.  In  a  10-year  old  boy,  taken  acutely  ill  with  no  definite  symptoms, 
it  was  so  large  and  hard  that  a  diagnosis  of  malarial  fever  had  been  given. 

The  nervous  symptoms  sometimes  predominate  over  the  intestinal 
ones,  but  are  rarely  severe,  especially  in  the  younger  children.  They  take 
the  form  of  restlessness,  insomnia,  fatuous  stupidity,  extreme  nervousness 
and  fear,  paroxysms  of  terror,  or  intermittent  and  perhaps  violent  delirium. 

3  x 


914  Chapter  LX  V. 

Headache,    drowsiness,    dulness    and    apathy    are    quite    frequent.     The 
typhoid  state  is  rare. 

Blood  Examination  shows  no  initial  leucocytosis.  Leueopenia  is 
progressive  after  the  first  and  up  to  the  fifth  week.  The  percentage  of 
haemoglobin  and  eosinophiles  is  reduced.  The  bacillus  is  often  present, 
even  in  early  stages,  and  may  be  found  in  film  preparations.  It  gets  into 
the  blood,  via  the  lymph  glands  and  spleen,  and  it  is  doubtful  whether  it 
multiplies  in  the  blood.  The  disease  is  a  true  septicaemia.  W.  Coleman 
and  R.  H.  Buxton  found  the  organism  in  the  blood  in  75  per  cent,  of  123 
cases.  Ten  c.c.  of  blood  were  taken  and  ox  gall,  peptone  and  peptone 
glycerine  were  used  as  culture  media.  The  usual  method  of  culture  is  to 
receive  5  c.c.  of  blood  into  300  c.c.  broth  and  incubate  it.  This  is  hardly 
practicable,  and  rarely  necessary,  in  private  practice  among  children.  The 
bacillus  has  been  found  in  the  blood  during  the  incubation  period  (Conradi), 
and  after  6  weeks'  freedom  from  fever  (Gennari  and  Lesieur). 

WidaVs  Test. — The  agglutinating  power  of  the  serum  is  weaker  in 
children  than  adults,  appears  earlier,  and  does  not  persist  as  long.  It  can 
be  transmitted  through  the  placenta  and  maternal  milk  but  is  then  of 
comparatively  short  duration.  The  reaction  may  persist  for  10  years, 
usually  less  than  5  years,  after  recovery.  It  is,  therefore,  sometimes 
present  in  cases  which  are  not  typhoid.  Complete  clumping  should  occur  within 
half  an  hour  with  a  dilution  of  1  in  200.  Negative  results  suggest  a  wrong 
diagnosis,  though  there  are  genuine  cases  in  which  the  reaction  is  absent. 
It  may  not  appear  until  late  in  the  disease  or  not  until  convalescence.  It 
is  generally  present  in  the  second  week,  rarely  as  soon  as  the  fifth  day,  and 
may  be  absent  throughout.  On  the  whole  it  is  a  valuable  confirmatory 
sign  and  perhaps  the  first  positive  one.  Thursfield  (1901)  obtained  the 
Teaction  in  42  out  of  100  sick  children  who  presented  symptoms  more  like 
typhoid  than  anything  else. 

The  urine  often  contains  albumin,  sometimes  casts  and  renal 
epithelium,  and  is  occasionally  nephritic  in  type  (renal  typhoid).  Ehrlich's 
diazo-reaction,  due  to  the  presence  of  some  aromatic  body,  is  almost  always 
present  in  the  second  week  and  before  the  Widal  test  is  positive. 

Morbid  Anatomy. — The  anatomical  lesions  are  much  less  marked  than 
in  adults.  There  is  a  catarrhal  ileo-colitis  or  enteritis,  with  infiltration  of 
Peyer's  patches  and  the  solitary  follicles,  enlargement  of  the  mesenteric 
glands,  and  a  large,  soft  spleen.  Ulceration  is  uncommon  in  the  first  year 
of  life.  In  older  children  it  may  be  very  extensive  and  involve  the  caecum 
and  large  intestine.  Swelling  of  the  agminated  and  solitary  glands  in 
children  is  not  distinctive  of  typhoid,  for  it  is  also  found  in  the  status  lym- 
phaticus  and  may  be  produced  by  various  toxic  processes.  On  the  other 
hand  absence  of  such  swelling  is  not  conclusively  negative,  for  some  such 
cases  give  Widal' s  reaction  and  run  the  course  of  typhoid.     Degeneration 


Typhoid  Fever — Paratyphoid  Fever.  915 

of  the  heart,  liver  and  kidneys,  bronchitis  and  broncho-pneumonia,  and 
hyperemia  of  the  meninges  and  brain  may  be  present. 

Complications  and  Sequels  are  comparatively  infrequent.  Haemor- 
rhage occurs  in  1-5  per  cent.  It  is  more  common  than  perforation  but  is 
rare  under  5  years  of  age.  Sometimes  there  is  little  constitutional  dis- 
turbance. Serious  bleeding  causes  sudden  fall  in  temperature  and  rise  in 
pulse  rate  ;  perhaps  collapse,  pallor,  pinched  nose,  cold  sweat  and  cold 
extremities.     Blood  is  passed  per  anum  in  a  few  hours  or  next  day. 

Perforation  is  found  after  death  in  many  cases  in  which  it  was  not 
suspected  during  life.  It  is  more  frequent  in  girls  than  boys,  but  rare  in 
children,  e.g.  4  out  of  210  (W.  J.  Butler,  1905),  9  out  of  375  (Kissel,  1904), 
0  out  of  277  (Wolberg).  It  is  most  frequent  in  the  third  week,  sometimes 
as  early  as  the  tenth  day,  or  not  until  the  fifth  week  and  later,  or  during  a 
relapse.  It  occurs  in  both  mild  and  severe  attacks.  The  site  is  in  the 
ileum  80-85,  large  intestine  10-15,  and  appendix  5  per  cent.,  occasionally 
in  the  jejunum  or  a  Meckel's  diverticulum.  Its  onset  is  gradual  or  sudden, 
and  the  symptoms  often  obscure,  latent  or  absent.  Attention  should  be 
paid  to  the  state  of  the  abdomen,  pain,  pulse-rate,  condition  of  the  patient 
;and  the  blood  count. 

Warning  symptoms  are  abdominal  pain  and  tenderness,  local  or 
general ;  rising  leucocytosis  ;  local  muscular  rigidity  and  tenderness  ;  and 
^haemorrhage.  Some  cases  are  ushered  in  with  rigor,  pain  and  rise  of  tempera- 
ture ;  others  with  severe  vomiting  and  hiccough.  The  pain  is  sudden,  intense 
and  paroxysmal ;  diffuse  or  localised  ;  in  any  locality,  especially  the  right 
iliac  fossa  ;  and  may  radiate  to  the  pubes  or  penis.  It  may  pass  off  in  a 
few  minutes,  last  for  days,  be  associated  with  vomiting,  or  be  absent 
altogether.     Local  tenderness  is  usually  present. 

The  abdomen  is  flat  or  distended,  rigid,  moves  on  respiration  or  is 
perhaps  fixed,  and  is  tender.  Liver  dulness  is  abolished.  Tympanites  is 
due  to  peritonitis  and  often  associated  with  vomiting.  The  temperature 
falls  suddenly  from  collapse  or  peritonitis  ;  it  may  rise.  The  pulse  and 
breathing  suddenly  increase  in  frequency,  and  respiration  is  shallow  and 
-costal.  Hiccough,  vomiting,  sweating  and  shivering  are  sometimes 
present.  The  child  is  restless,  looks  ill  and  anxious,  and  exhibits  symptoms 
of  collapse.  Secondary  signs  of  peritonitis  develop.  Leucocytosis  is 
usually  present  early.  Sudden  abdominal  pain  and  tenderness,  with 
leucocytosis,  warrant  operation.  Leucocytosis  is  not  positive  proof,  and 
may  not  be  marked  until  peritonitis  and  collapse  have  supervened. 
Moreover,  the  signs  of  perforation  and  leucocytosis  may  be  present,  although 
the  gut  is  intact.     There  may  be  leucopenia. 

The  diagnosis  is  difficult  and  the  prognosis  bad.  Abdominal  pain  in 
"the  course  of  typhoid  fever  is  due  to  other  causes,  viz.  gastritis,  colic, 
constipation,   fsecal  impaction,   ileo-colitis,   diarrhoea,   distended  bladder, 


916  Chapter  LX  V. 

intestinal  strangulation,  rupture  of  an  infected  mesenteric  gland  ;  peri- 
tonitis, appendicitis,  cholecystitis,  iliac  phlebitis  ;  pleurisy  or  pneumonia  ; 
and  haemorrhage  or,  indeed,  no  definite  cause.  The  prognosis  is  most 
favourable  if  the  perforation  is  in  the  appendix.  About  90  per  cent.  die,, 
one-half  within  2  days,  unless  treated  surgically.  No  opium  is  permissible 
until  a  diagnosis  has  been  made  and  the  question  of  operation  decided. 
Exploration  can  be  done  under  local  anaesthesia  if  necessary.  A  general 
anaesthetic  is  preferable.  Many  cases  can  be  saved  by  early  and  rapid 
operation,  30-40  per  cent,  according  to  Osier.  The  first  operation  was  done- 
by  Kussmaul  in  1887.  Finney  (1889)  collected  112  cases  and  Keen  added 
38  a  few  months  later.  Out  of  111  no  less  than  27  recovered  ;  6  out  of  12' 
under  15  years  of  age.  A  girl  under  my  care  recovered  but  was  left  with  a 
faecal  fistula  which  slowly  healed.  Operation  for  secondary  peritonitis- 
almost  invariably  fails  to  effect  a  cure. 

The  nervous  symptoms  are  numerous.  Sometimes  there  are  signs  of 
meningeal  irritation  (meningismus)  though  nothing  abnormal  is  found 
after  death  ;  or  serous  meningitis,  with  bacilli  in  the  cerebrospinal  fluid,, 
and  oedema  and  round-celled  infiltration  about  the  blood  vessels  ;  or  a. 
purulent  meningitis.  The  clinical  signs  are  of  varied  type  (Rocaz  and 
Carles,  1907)  : — (1)  Intense  headache,  frequent  vomiting,  constipation,, 
irregular  pulse  and  breathing,  hyperesthesia,  vasomotor  disturbance  and 
head  retraction.  (2)  Signs  like  those  of  cerebrospinal  meningitis,  viz.. 
Kernig's  sign,  rigidity  of  neck,  spine  and  limbs,  and  symptoms  as  in  the- 
first  type.  (3)  Convulsions,  rapidly  fatal,  in  infants.  (4)  Clinically  like 
tuberculous  meningitis.  The  fluid  obtained  by  lumbar  puncture  contains 
in  the  first  type  pus  and  typhoid  bacilli  in  pure  or  mixed  culture  ;  in  the 
second,  turbid  or  transparent  fluid  with  typhoid  or  other  organisms  ;  in  the- 
third,  normal  fluid  under  high  pressure  ;  and  in  the  fourth,  clear  fluid  and 
abundant  lymphocytes.  The  last  2  varieties  are  apparently  the  result  of 
the  action  of  toxin  on  the  meninges.  Lumbar  puncture  is  essential  for 
diagnosis,  for  the  removal  of  organisms  and  toxins,  and  for  the  reduction  of 
pressure. 

Ocular  palsy,  aphasia,  spastic  hemiplegia,  Jacksonian  epilepsy,  tetany 
and  mild  peripheral  neuritis  have  occurred.  The  psychical  changes  are- 
mania,  dementia  and  melancholia  in  order  of  frequency,  or  a  more  or 
less  confusional  state.  Marked  dementia  is  the  most  grave.  Most  of* 
these  patients  get  well. 

Other  complications  and  sequels  are  bed-sores,  due  to  emaciation  and' 
mal-assimilation,  and  not  always  preventable  ;  boils,  abscess,  hemorrhagic 
bullae,  purpura ;  pneumonia,  pleurisy,  empyema,  gangrene  of  lung ; 
perichondritis  of  the  thyroid  cartilage,  in  a  12-year  old  boy,  which  neces- 
sitated tracheotomy  ;  stenosis  of  the  larynx,  secondary  to  perichondritis  ; 
necrosis  of  the  jaw;  myositis  of  the  rectus  abdominis;  cholecystitis, 
perforation  of  the  gall  bladder  ;    general  septic  peritonitis,  without  per- 


Typhoid  Fever — Paratyphoid  Fever.  917 

foration ;  arteritis,  with  or  without  thrombosis,  and  perhaps  gangrene  ; 
otitis  media,  secondary  parotitis,  noma,  recto-vagina]  fistula,  purulent 
arthritis,  and  necrosis  of  bone.  Myocardial  degeneration  is  dangerous 
and  apt  to  be  overlooked.  It  is  more  chronic  than  in  diphtheria,  but  may 
be  acute  and  severe.     In  one  girl  tuberculosis  developed  during  the  fever. 

Course  and  Prognosis. — The  disease  is  milder  and  more  variable  than 
in  adults.  Some  cases  are  abortive,  afebrile,  ambulatory,  or  mild  and 
lasting  only  8-10  days.  Others  are  as  severe  as  in  adults.  In  renal 
typhoid  pyrexia  and  hsematuria  are  the  only  symptoms,  but  the  bacilli 
are  found  in  the  urine  and  Widal's  test  is  positive.  A  pneumonic  type, 
like  broncho-pneumonia  at  the  onset,  is  rare.  Anorexia,  fever,  diarrhoea 
and  restlessness  may  lead  to  profound  emaciation.  The  hair  may  fall  out, 
and  the  nails  show  transverse  furrows  or  drop  off.  The  temperature  is 
variable  and  may  fall  by  crisis.  Branny  desquamation  is  not  uncommon, 
and  even  large  flakes  may  be  cast  off.  It  begins  at  the  end  of  the  febrile 
period,  in  10-15  days,  in  the  axilla  and  spreads  to  the  trunk  and  limbs  but 
not  to  the  hands  or  feet.  Bad  signs  are  severe  meteorism,  weak  cardiac 
first  sound  at  the  apex,  thready  pulse,  severe  diarrhoea,  picking  at  the  bed- 
clothes, waking  delirium,  foul  mouth  and  insensibility.  Sudden  death  is 
due  to  toxic  action  on  the  vagus,  reflex  abdominal  irritation,  perforation, 
collapse,  or  myocardial  degeneration.  It  usually  results  from  syncope  in 
the  third  week  and  has  occurred  in  latent  and  unsuspected  cases.  The 
mortality  is  small,  about  3-5  per  cent.,  and  lower  during  the  first  than  the 
second  5  years  of  life.  Green  vomiting  and  diarrhoea  are  very  unfavourable. 
A  high  pulse  rate  and  low  temperature  may  indicate  haemorrhage.  Anaemia 
and  debility  may  persist  for  months,  and  there  is  frequently  a  tendency  to 
obesity  in  convalescence. 

Relapses. — Eelapses  develop  in  about  15  per  cent.  The  younger  the 
■child,  the  more  likely  are  they  to  occur,  and  there  may  be  more  than  one. 
Persistent  splenic  enlargement  is  presumptive  evidence  in  favour  of 
relapse.  The  temperature  may  rise  by  steps.  More  frequently  it  rises 
rapidly,  keeps  high  for  a  time,  and  falls  quickly.  Mild  abdominal  symptoms 
are  present  in  about  half,  and  a  rash  in  three-fourths  of  the  cases.  Com- 
plications are  mild  and  infrequent.  A  relapse  lasts  1-2  weeks,  possibly 
5  weeks,  and  is  rarely  fatal.  Succeeding  relapses  are  milder.  In  excep- 
tional cases  intercurrent  relapses  occur,  the  temperature  rising  again  before 
the  fever  of  the  preceding  relapse  has  subsided.  These  are  occasionally 
serious  and  prolonged  cases,  and  likely  to  prove  fatal  from  asthenia. 

Diagnosis. — Green  stools,  tympanites,  listlessness  and  mild  pyrexia 
cannot  be  distinguished  from  enteritis  except  by  Widal's  test,  the  diazo- 
reaction,  and  the  blood  count.  Gaertner  infection  is  diagnosed  by  agglu- 
tination tests  and  the  recovery  of  the  bacillus  from  the  stools.  The 
diagnosis  of  paratyphoid  depends  on  the  serum  reactions.  At  the  onset  the 
disease  is  liable  to  be  mistaken  for  enteritis,  appendicitis,  peritonitis,  lobar 


918  Chapter  L  X  V. 

pneumonia  with  delayed  physical  signs,  malaria,  meningitis  and  miliary 
tuberculosis.  Much  stress  can  be  laid  on  the  character  of  the  temperature 
chart  in  the  first  few  days  and  on  splenic  enlargement,  constipation  and 
rose  spots. 

Treatment. — Prevention  of  the  spread  of  the  disease  consists  in  anti- 
typhoid inoculation  of  those  exposed  to  infection,  and  disinfection  of  the 
excreta  of  those  infected.  Inoculation  is  practically  never  required  for 
children.  All  clothing  and  bedding  should  be  disinfected  by  live  steam  if 
available,  or  by  immediate  soaking  in  carbolic  acid  solution  and  subsequent 
boiling.  The  buttocks  must  be  washed  with  bichloride  of  mercury,  1  in  1000.. 
The  stools  contain  the  bacillus  at  the  beginning  of  the  second  week.  Add 
to  each  two  volumes  of  carbolic  acid,  5  per  cent,  solution,  and  let  them 
stand  for  several  hours.  The  Local  Government  Board  recommends 
corrosive  sublimate  oz.  \,  crude  hydrochloric  acid  oz.  1,  anilin  blue  gr.  2, 
water  3  gallons  ( =  1  in  1000)  ;  it  is  poisonous  and  not  deodorant.  Izal  or 
cyllin  2-5  per  cent.,  and  formaldehyde  4-5  per  cent,  strength  are  also  used- 
Fresh  chlorinated  lime,  1  part  to  2  of  water,  is  satisfactory.  The  dejecta- 
must  be  covered  with  it.  Air-slaked  lime  is  valueless.  It  should  fce= 
freshly  burnt  and  mixed  with  water.  Use  freshly  made  milk  of  lime  in 
the  proportion  of  3  volumes  to  1  of  faeces.  Add  60  parts  of  water  slowly 
to  100  of  lime.  Milk  of  lime  is  made  from  this  by  mixing  1  part  by  weight 
with  8  of  water.  It  is  mixed  thoroughly  with  the  faeces  by  stirring  and 
allowed  to  stand  for  24  hours.  The  urine  contains  the  bacillus  in  20-35  per 
cent.  It  is  turbid  and  shimmers.  It  can  be  disinfected  in  \-\  hour  by 
formalin  10  per  cent.,  1  part  to  10  ;  carbolic  acid  5  per  cent.,  3  parts  to  10  ; 
or  bichloride  of  mercury  1  in  1000,  1  part  to  40  of  urine.  A  jar  containing 
750  c.c.  carbolic  acid  or  100  c.c.  mercury  solution  is  enough  for  1500  c.c. 
urine.  The  urine  should  be  poured  in  and  the  j  ar  emptied  daily.  The  urinal 
must  be  kept  in  a  separate  jar  of  the  disinfectant.  Chlorinated  lime  and 
liquid  chlorine  are  also  good  disinfectants. 

Specific  treatment  is  at  present  only  on  trial.  Chantemesse's  serum  is 
sometimes  used. 

Diet. — Impress  on  the  parents  that  the  child  cannot  digest  much 
food  and  will  emaciate,  but  will  regain  weight  afterwards.  In  very  acute 
and  severe  stages  it  may  be  advisable  to  give  water  only  for  12-24  hours  ; 
especially  if  there  is  abdominal  distension,  toxaemia,  and  the  passage  of 
undigested  stools.  Weak  cold  tea  is  harmless,  stimulating  and  checks 
vomiting.  The  diet  must  be  such  as  is  suitable  for  any  ulcerative,  intestinal 
condition.  It  should  be  easily  digestible  and  assimilable,  non-fermentative,, 
leave  no  solid  residue,  and  contain  sufficient  nutriment,  salts  and  water- 
Feed  infants  on  human  milk  or  whey.  If  the  child  is  hungry  and  can 
digest  more,  give  peptonised  milk,  malted  milk,  diluted  milk,  koumiss,, 
butter-milk,  dextrinised  gruels,  meat  juice,  chicken  or  veal  tea,  various- 
broths,  Mellin's  or  Benger's  food,  liquid  custard,  beaten  up  egg,  custard 


Typhoid   Fever — Paratyphoid  Fever.  919 

pudding,  junket  and  similar  articles.  Liquid  custard  is  made  of  5  yolks  of 
egg  to  milk  1  pint,  sugar  and  flavouring  agents.  Food  should  be  liquid  or 
merely  thickened,  and  must  depend  in  quality  and  quantity  on  the 
character  of  the  stools  which  require  careful  examination  for  curds,  fseculent 
debris,  blood  and  sloughs.  If  there  are  curds  the  milk  must  be  peptonised, 
diluted  or  omitted.  The  caloric  value  of  various  foods  should  be  taken  into 
account,  e.g.  a  pint  of  milk  =  450  calories,  an  ounce  of  maltine  —  240 
calories.  Other  suitable  additions  to  the  diet  are  fruit  juice,  lime  juice, 
glucose  dr.  1  in  beef  tea  -|  pint,  maltose,  lactose,  treacle,  honey,  biscuit 
powder,  bread  jelly,  bread  crumbs,  cocoa,  scraped  meat  or  raw  meat  pulp. 

It  is  unnecessary  to  keep  the  child  on  a  minimum  diet,  if  more  can  be 
digested.  In  fact  it  is  probable  that  starvation  and  malnutrition  predis- 
pose to  extensive  ulceration,  haemorrhage  and  perforation.  The  appetite, 
the  state  of  the  tongue  and  abdomen,  and  the  character  of  the  stools  are 
the  best  guides  to  the  amount  of  food  permissible.  Although  in  many  cases 
a  liberal  diet  is  beneficial,  even  during  the  febrile  stage,  it  is  important  that 
it  be  given  in  a  fluid  or  semi-solid  form.  Irritant  particles  of  food  are  apt 
to  be  injurious  and  much  too  little  regard  is  often  paid  to  the  effects  of  milk 
curds.     Milk  alone  may  cause  diarrhoea. 

During  convalescence  the  diet  is  augmented  by  increasing  the  quantity 
and  variety  of  the  articles  mentioned.  At  the  end  of  a  week  of  apyrexia 
junket,  bread  sauce  and  baked  custard  are  suitable  additions  to  a  more 
rigidly  liquid  diet.  In  another  3  days  a  lightly  boiled  egg  and  bread  and 
butter  are  given.  After  a  further  24-48  hours  the  diet  can  be  rapidly 
increased  to  full  diet  at  the  end  of  14  days  freedom  from  fever.  Hunger 
is  often  great  during  the  convalescent  stages  and  over-eating  must  be 
guarded  against. 

For  vomiting  rely  on  diet,  bismuth,  sod.  bicarb,  or  hydrochloric  acid. 
For  tympanites  give  water  freely  and  omit  food  temporarily  ;  prescribe 
salol,  chlorine  water,  calomel,  or  sod.  sulphat.  in  hot  water  until  the  bowels 
act.  An  ice  bag  to  the  abdomen  may  be  used  with  discretion.  For  con- 
stipation regulate  the  diet  by  diluting  milk,  and  adding  meat  preparations, 
maltose  and  malted  foods,  and  give  enemata  or  small  frequent  doses  of 
calomel  or  sod.  sulph.  For  diarrhoea  regulate  the  diet,  and  give  ol.  ricini 
in  small  doses,  bismuth,  tr.  ferri  perchlor.,  tannigen,  tannalbin,  and 
enemata  of  starch  with  or  without  opium.  For  hcemorrhage  starve  the  child 
and  give  gelatine,  salines  sub  cutem,  and  codeia  or  codeine  phosphate  ; 
for  perforation,  operate  or  rely  on  starvation  and  opium. 

Antipyretic  measures  need  rarely  be  energetic.  Cold  baths,  10°  F. 
below  the  temperature  of  the  patient,  are  unsuitable  for  profuse  haemorrhage, 
perforation,  and  for  young  children.  Rely  on  an  ice  cap,  cold  or  tepid 
sponging,  cold  compresses  and  cold  packs.  Measures  which  are  disliked,  or 
cause  excitement  and  collapse,  are  apt  to  do  more  harm  than  good.  Cold 
is  beneficial  as  an  antipyretic.     It  relieves  bronchitis,  delirium  and  coma  ; 


920  Chapter  LXV. 

reduces  the  pulse  rate  and  temperature  ;  but  does  not  avert  haemorrhage 
and  perforation,  or  shorten  the  disease.  The  feet  must  be  kept  warm. 
A  bath  at  95-100°  F.,  with  cold  to  the  head,  is  useful  for  restlessness  and 
delirium.    Quinine  is  the  most  suitable  drug. 

Intestinal  antiseptics  are  unreliable  in  action  and  irrational  measures 
in  practice.  Calomel  is  the  best  for  it  reaches  the  lower  part  of  the  small 
intestine  before  being  converted  into  perchloride  (P.  W.  Latham).  Give 
it  in  doses  of  gr.  §•-£  every  4  hours.  It  is  liable  to  cause  stomatitis,  ulcera- 
tion of  the  gums  and  diarrhoea.  Benzo-naphthol  is  harmless.  Syr. 
Cyllini  may  be  given,  and  other  drugs  already  described  (p.  300).  Liq. 
hyd.  perchlor.  and  tr.  fer.  perchlor.  are  sometimes  given  in  combination  for 
diarrhoea.  The  latter  drug  readily  parts  with  its  chlorine.  Other  appro- 
priate drugs  are  quinine  and  nascent  chlorine  ;  sulphurous  acid  with  syr. 
limon.  and  aq.  chlorof.  ;  ol.  terebinth,  in  small  frequent  doses  ;  essential 
oil  of  cinnamon,  small  frequent  doses  in  gelatine  capsules  or  emulsion  ; 
and  urotropin  for  bacilluria.  As  a  general  rule  the  simpler  the  treatment,  the 
better  the  results  in  children.  Some  of  the  above  remedies  are  unpleasant 
to  take  and  apt  to  upset  the  digestion.  An  effervescent  mixture  of  quinine 
in  highly  febrile  cases,  with  calomel  in  small  doses  if  there  is  constipation, 
gives  good  results.  Opium  is  rarely  needed.  A  drop  or  two  of  the  tincture 
may  be  given,  if  the  nervous  symptoms  are  prominent  and  mental  rest 
requisite.  It  is  often  inadvisable,  for  the  symptoms  depend  on  toxaemia 
and  elimination  is  of  most  importance. 

Alcohol  is  frequently  required.  It  must  be  given  if  the  first  sound  of 
the  heart  fails  and  is  useful  in  high  fever.  Brandy  is  the  best  stimulant. 
For  cardiac  failure  give  also  digitalis,  strychnia,  nux  vomica,  caffeine  and 
sal  volatile  ;  for  toxaemia,  high  enemata  of  saline  solution  to  stimulate  renal 
excretion  ;  for  collapse,  camphorated  oil  sub  cutem,  or  tr.  capsici  m.  5-15  in 
oil  or  water  per  rectum  (Ager,  1906),  repeated  every  10-15  minutes  for 
2  hours  if  necessary,  in  addition  to  other  remedies  ;  and  for  headache, 
restlessness  and  fever  rely  on  hydrotherapy.  An  occasional  small  dose  of 
phenacetin  and  caffeine  is  permissible. 


PARATYPHOID    FEVER. 

There  are  many  organisms  intermediate  between  the  colon  and  typhoid 
bacillus.  Apparently  b.  coli,  paracolon  bacillus,  paratyphoid  a,  para- 
typhoid R,  and  the  typhoid  bacillus  represent  a  series  of  a  group,  to  which 
also  belong  b.  enteritidis  of  Gartner  and  b.  psittacosus.  The  paratyphoid  a 
is  culturally  like  the  paracolon  bacillus.  The  paratyphoid  j3  organism  is 
culturally  unlike  the  paracolon  and  resembles  the  typhoid  bacillus,  but 
produces  a  primary  acidity  and  terminal  alkalinity  in  milk.  It  does  not 
coagulate  milk,  nor  produce  indol  in  broth.     It  ferments  glucose,  but  not 


Typhoid  Fever — Paratyphoid  Fever.  921 

lactose.  The  typhoid  organism  does  not  ferment  glucose,  nor  produce 
terminal  alkalinity  in  milk.  Both  the  a  and  ft  organisms,  especially  the 
latter,  produce  typhoid-like  symptoms,  and  thus  differ  from  paracolon  and 
colon  infections. 

Over  100  cases  are  on  record,  a  few  under  12  years  of  age.  The  disease 
is  probably  by  no  means  rare,  even  in  the  young.  Possibly  5  per  cent,  of 
cases  clinically  typhoid  are  of  this  nature.  Its  geographical  distribution 
is  "widespread.  It  occurs  sporadically,  in  house  epidemics  and  in  general 
epidemic  form.  Sometimes  there  is  a  mixed  infection  with  typhoid  and 
paratyphoid  organisms.  The  seasonal  incidence,  age  and  sex  of  the 
patients  are  those  of  typhoid. 

Symptoms. — It  begins  with  anorexia,  headache,  pain  in  the  back  and 
limbs,  and  irregular  fever ;  sometimes  vomiting  and  abdominal  pain  ; 
rarely  an  initial  chill.  The  tongue  is  more  or  less  furred,  labial  herpes 
-sometimes  present,  and  there  are  the  usual  signs  of  malaise.  Constipation 
is  more  common  than  diarrhoea.  Abdominal  distension  is  infrequent  and 
due  to  unsuitable  food.  Rose  spots  come  out  in  50  per  cent.  The  spleen 
is  palpable  in  only  half  the  cases  though  the  splenic  dulness  is  generally 
increased.  Bronchitis  is  common  ;  epistaxis,  albuminuria  and  vomiting 
•occasional.  The  urine  may  contain  indican  and  give  the  diazo-reaction. 
Leucopenia  is  slight  or  absent.  The  pulse  varies  with  the  fever,  usually 
90-100  per  min.,  and  is  sometimes  slow  and  irregular,  sometimes  dicrotic. 
The  fever  resembles  that  of  typhoid  in  its  course,  but  is  more  intermittent 
and  more  apt  to  end  by  crisis.  There  is  less  ansemia  and  wasting  than  in 
typhoid,  no  delirium  except  in  severe  cases,  and  occasionally  somnolence 
and  apathy.  The  course  is  that  of  mild  typhoid.  Some  cases  are  severe  and 
a  few  are  fatal.  The  duration  is  3-5  weeks,  perhaps  only  10  days  or  as 
long  as  9  weeks.     Relapses  are  not  uncommon. 

The  complications  are  hasmorrhage  in  about  5  per  cent.,  rarely  severe, 
pleurisy,  broncho-pneumonia,  endocarditis,  phlebitis,  meningitis,  peri- 
tonitis, cholecystitis,  pyelonephritis,  cystitis,  orchitis,  suppurative 
arthritis,  furunculosis  and  myositis. 

The  diagnosis  is  based  on  the  agglutinating  properties  of  the  blood 
serum,  the  course  of  the  disease,  and  the  recovery  of  the  specific  bacillus 
from  the  blood  or  faeces.  No  case  can  be  accepted  as  scientifically  proved 
unless  the  organism  is  cultivated,  the  serum  reactions  obtained,  and  the 
absence  of  Eberth's  bacillus  certain.  The  serum  does  not  agglutinate  the 
typhoid  organism.  In  2  cases  (Allen,  Pratt)  the  (3  bacillus  was  recovered 
from  the  gall  bladder ;  and  in  one  of  Pratt's  cases  from  a  suppurating 
testis  after  supposed  typhoid.  The  general  blood  infection  by  the  j3 
organism  is  like  that  due  to  the  typhoid  bacillus  in  its  symptoms,  course  and 
•complications.  So  alike  is  it,  that  many  physicians  refuse  to  recognise 
paratyphoid  fever  as  a  specific  disease,  preferring  to  regard  it  as  a  mild 
-variety  of  typhoid. 


922  Chapter  LXV. 

The  anatomical  changes  in  fatal  cases  are  those  of  a  general  blood 
infection.  Typical  ulceration  of  Peyer's  patches  is  lacking.  In  Van 
Ingen's  case  the  spleen  was  not  enlarged,  and  several  ulcers  were  found  just 
above  the  ileo-caecal  valve,  with  "  deep  punched-out  appearance,  extending 
in  some  cases  to  the  peritoneal  coat,"  but  Peyer's  glands  seemed  normal. 
In  Wills  and  Scott's  case  extensive,  superficial,  ragged  ulceration,  without 
infiltration,  was  found  a  short  distance  above  the  ileo-csecal  valve.  Typhoid 
fever  can  occur  without  changes  in  the  agminated  glands.  Lazarus-Barlow 
states  that  not  more  than  20  cases  of  this  type  are  on  record  and  only  6  of 
them  scientifically  proved  ;  possibly  some  were  paratyphoid  fever.  In 
private  practice  the  difficulty  of  diagnosis  is  great.  Neither  the  parents 
nor  doctor  regard  the  child  as  sufficiently  ill  to  warrant  blood  examination 
and  cultures.  The  organism  can  be  recovered  from  the  stools.  The 
treatment  is  essentially  the  same  as  that  of  typhoid  but  the  diet  may  be 
somewhat  more  generous. 


CHAPTER    LXVI. 

SPECIFIC    FEVERS. 

Infection  and   Disinfection — Scarlet  Fever. 

The  infective  disorders,  so  far  described,  are  those  in  which  definite- 
causal  organisms  have  been  discovered.  Of  these  diseases  diphtheria  and 
influenza  are  distinctly  contagious,  while  syphilis,  tuberculosis,  typhoid  and 
paratyphoid  fever  are  communicable.  Malaria,  due  to  a  protozoon,  might 
also  be  included. 

The  specific  fevers  are  those  which  run  a  definite  course,  uninfluenced  by 
treatment,  after  a  recognised  incubation  period.  So  far  bacteriologists  have 
been  unable  to  prove  that  any  one  of  the  various  organisms  isolated  by  them 
is  the  true  causative  agent.  The  factors  necessary  for  infection  are  a 
susceptible  subject,  and  an  infective  agent  in  a  sufficiently  large  dose.  The 
external  conditions  must  be  suitable  for  its  life  and  growth,  and  there 
must  be  a  vehicle  for  its  conveyance. 

Susceptibility  varies  in  different  races,  families  and  individuals,  in  the 
same  individual  at  different  times,  in  different  diseases,  and  according  to 
the  mode  of  infection.  Children  are  more  liable  than  adults,  the  latter 
being  frequently  protected  by  a  previous  attack.  Measles  is  the  most 
infectious  fever.  The  virulence  of  the  virus  varies  in  different  epidemics 
and  in  the  course  of  the  same  epidemic,  becoming  milder  toward  the  end. 
It  is  modified  by  season  and  locality. 

The  virus  is  conveyed  directly  by  the  air  currents  or  by  direct  contact, 
as  in  kissing  or  from  infected  hands,  etc.  Or  it  may  be  conveyed  more 
indirectly  by  (1)  doctors,  nurses,  attendants  and  animals  ;  (2)  infected 
milk,  water  or  food  ;  (3)  by  fomites,  e.g.  in  various  articles  handled  by  the 
sick  or  contaminated  in  the  sick-room,  viz.  toys,  books,  articles  of  clothing, 
wall  papers,  etc.  During  epidemics  there  are  individuals  whose  suscep- 
tibility is  so  slight  that  the  resulting  illness  may  be  trivial  and  entirely 
disregarded.  These  ambulatory,  mild  and  unsuspected  cases  are  often 
the  source  of  outbreaks  of  diphtheria,  influenza,  typhoid  fever  and  any  of 
the  true  specific  fevers.  A  further  cause  is  the  persistence  of  infectivity 
in  the  apparently  cured.  The  diphtheria  bacillus  is  found  in  healthy 
throats  and  often  for  a  long  time  after  an  attack.  Epidemics  of  typhoid 
have  been  traced  to  typhoid  "  carriers,"  patients  whose  urine  or  faeces  still 
contain  the  organism. 


•924  Chapter  LX  VI. 

Prevention  of  Spread  of  Infection. — The  suppression  of  contact  is  the 
primary  essential.  Expired  air,  except  on  coughing  and  spluttering,  is 
sterile.  Hence  the  dangerous  aerial  zone  round  a  patient  is  very  small. 
The  child  is  isolated  at  home  or  in  a  hospital. 

For  home  isolation  choose  a  medium  sized  room,  without  carpets  or 
•curtains  and  containing  a  minimum  amount  of  furniture,  at  the  top  of  the 
house  and  facing  west,  south-west  or  south.  The  bed  must  be  narrow  and 
of  iron.  A  flat  of  2-3  rooms,  with  lavatory  attached,  is  the  most  suitable 
•accommodation,  for  the  nurse  must  be  isolated  as  well.  An  open  fireplaec 
and  open  window  afford  the  best  ventilation.  Keep  down  dust  by  dusting 
with  a  cloth  damped  with  izal  or  other  disinfectant,  and  clean  the  floor 
in  a  similar  manner.  A  paraffined  parquet  floor  and  painted  walls,  washed 
twice  a  week,  are  ideal  conditions. 

Home  isolation  is  superior  to  hospital  treatment,  if  it  can  be  carried  out 
efficiently.  Fewer  secondary  cases  occur.  Frequently  it  is  defective  or 
ineffective.  There  is  a  slight  risk  of  the  infection  being  conveyed  by 
members  of  the  household.    Susceptible  ones  should  be  removed. 

In  hospitals  all  cases,  whether  mild  or  severe,  are  aggregated  in  wards. 
Occasionally  there  is  segregation  in  single  rooms  or  cubicles,  but  it  is 
expensive  in  structural  and  nursing  arrangements,  and  more  trying  for  the 
patient.  There  is  always  the  risk  of  a  mild  case  becoming  severe,  from 
further  infection ;  that,  if  an  erroneous  diagnosis  has  been  made,  the 
disease  may  be  acquired  in  the  ward  ;  that  secondary  infection  of  the 
naso-pharynx  may  take  place  and  increase  the  duration  of  infectivity  ;  and 
that  relapses  or  second  attacks  are  more  apt  to  occur  from  re-infection. 
Hospital  isolation  has  not  proved  successful  in  limiting  the  prevalence  of 
scarlet  fever. 

In  order  to  prevent  return  cases  do  not  encourage  the  child  to  mix 
■or  sleep  with  others  on  going  home.  Guard  against  chills,  for  catarrh  of 
the  mucous  membranes  is  conducive  to  the  growth  of  stray  infective 
organisms.  Disinfect  the  mucosa  and  provide  separate  towels  and 
utensils. 

The  physician  should  visit  his  infectious  cases  last  on  his  rounds,  put 
on  a  long  white  overall  before  entering  the  room,  avoid  personal  contact 
as  much  as  practicable,  and  take  special  care  against  being  infected  by 
discharges  when  examining  the  throat,  nose,  skin,  etc.  On  leaving  the 
room  he  must  disinfect  his  instruments  and  hands,  washing  with  soap  and 
a  nail-brush,  and  using  a  lotion  of  lysol,  or  1  in  1000  sublimate.  The  nurse 
must  take  every  precaution  against  conveying  the  virus.  She  should  use 
a  nasal  spray  and  an  antiseptic  gargle  when  nursing  cases  of  diphtheria 
and  scarlatina  anginosa. 

Disinfection. — The  room  is  disinfected  by  free  ventilation  and  washing 
with  izal  or  cyllin  2  per  cent.  Sublimate  lotion  is  poisonous  and  spoils 
metallic  substances,  permanganate  stains,  and  phenol  has  an  unpleasant 


Scarlet  Fever.  925- 

smell.  Food  utensils  arc  put  in  a  pan  of  water  and  boiled  for  an  hour. 
Linen,  towels  etc.  are  placed  for  24  hours  in  a  wooden  tub  of  water  con- 
taining in  each  gallon  1  dr.  of  hyd.  perchlor.  1,  common  HCL  2  parts,, 
and  then  sent  to  the  wash.  Longer  soaking  and  stronger  solutions  destroy 
the  fabric.  Or  soak  them  in  a  solution  of  zn.  sulphate,  oz.  4,  sod.  chlorid. 
oz.  2,  water  1  gallon,  and  boil  for  2  hours.  Saturated  steam  at  115°  C.  is 
the  most  satisfactory  means  of  disinfecting  articles  not  spoilt  by  moisture. 
Disinfectants  have  been  standardised  in  relationship  to  carbolic  acid.. 
Thus  for  (3  typhosus  perchloride  of  mercury  has  a  co-efficient  20,  i.e.  is. 
20  times  as  strong,  while  the  co-efficients  of  other  disinfectants  are  cyllin  15, 
creolin  2-5,  lysol  2-5,  formalin  0*3,  lysoform  0-1,  sanitas  0-02.  The  price 
is  a  great  consideration.  Carbolic  acid  is  Is.,  cyllin  4s.  per  gallon.  For  the- 
disinfection  of  excreta  see  typhoid  fever  (p.  918). 

The  room  is  finally  disinfected  by  sheets  soaked  in  formalin,  500  c.c. 
per  1000  cub.  feet  air  space,  to  evolve  gas  ;  fumigation  or  spraying  with 
formic  aldehyde  2  per  cent.  It  can  be  fumigated  with  powdered  sulphur, 
put  in  a  pan  with  red  hot  coal  and  stood  on  bricks  over  water,  the  room 
being  moistened  by  steam  and  closed  for  24  hours.  Autan,  a  mixture  of 
barium  chloride  and  paraformaldehyde,  is  useful  and  merely  requires  the 
addition  of  water  for  evolution  of  steam  and  gas.  The  formalin-per- 
manganate method,  dependent  on  mixing  pot.  permang.  1  and  formalin 
2  parts,  is  dangerous  for  explosion  may  result.  After  disinfection  the  room 
should  be  papered  and  painted. 

The  Coincidence  and  Interaction  of  Diseases. — Two  acute  diseases 
may  run  their  course  without  influencing  each  other  to  a  recognisable 
extent.  The  total  effect  is  generally  one  of  increased  malaise.  Measles 
and  diphtheria  in  the  very  young  are  almost  invariably  fatal.  Measles 
may  be  coincident  with  scarlet  fever  or  varicella  ;  scarlet  fever  with 
varicella,  variola,  pertussis,  diphtheria,  typhoid  or  erysipelas  ;  typhoid 
with  paratyphoid  or  diphtheria,  etc.  In  one  child  diphtheritic  palsy  and 
poliomyelitis  were  associated ;  in  another,  suffering  with  tuberculous 
meningitis,  the  meningococcus  was  isolated  on  lumbar  puncture.  A  more 
common  coincidence  is  an  acute  illness  in  the  course  of  a  chronic  one.  The 
beneficial  influence  of  erysipelas  on  new  growths,  lupus,  chronic  eczema  and 
chronic  ulcers,  has  often  attracted  attention.  Vaccination  with  calf  lymph 
has  been  noted  to  modify  pertussis  and  render  it  comparatively  harmless,, 
and  sometimes  has  a  good  influence  on  eczema  and  chronic  skin  affections. 
Possiblv  in  many  cases  the  effect  is  merelv  one  of  coincidence. 


SCARLET    FEVER. 

Scarlatina  is  an  affection  of  the  skin  and  throat,  with  many  complica- 
tions. The  disease  is  mild,  apart  from  streptococcal  infection.  Com- 
plications and  fatal  cases  are  due  to  such  infection  and  septicceinia. 


926  Chapter  LX  VI. 

It  is  doubtful  whether  there  is  a  special  family  liability  to  infection, 
•severity  or  immunity.  Negroes  are  less  susceptible  than  Caucasians. 
Epidemics  may  follow  the  re-assembling  of  schools  after  holidays.  Both 
sexes  are  equally  liable.  The  disease  is  infrequent  in  infancy.  Suscep- 
tibility increases  up  to  the  sixth  year  and  then  slowly  diminishes.  About 
1  per  cent,  of  the  cases  are  under  1  year  of  age,  50  per  cent,  under  6,  and 
90  per  cent,  under  10  years.  It  has  been  reported  in  the  third  week  of  life. 
Malnutrition,  uncleanliness  and  bad  teeth  predispose  to  a  severe  attack 
of  the  anginal  type. 

Bacteriology. — Edington  (1886)  isolated  a  diplococcus,  streptococcus 
mbigenosus,  and  a  bacillus.  Class  of  Chicago  (1899)  cultivated  a  large 
Gram-negative  diplococcus  or  tetracoccus  from  300  consecutive  cases,  and 
from  surgical  scarlet  fever.  It  was  found  by  Schamberg  and  Gildersleeve 
(1904)  in  only  15  out  of  100  cases.  Curtois  (1899)  found  an  organism, 
allied  to  the  S.  pyogenes  and  S.  erysipelatosus,  in  the  urine  of  42  out  of 
97  cases  and  in  the  heart  blood  after  death.  Klein  (1887)  has  also  isolated 
from  the  blood  a  micrococcus  or  streptoccocus  very  like  Eding ton's  organism. 
An  outbreak  of  scarlet  fever  at  Hendon  in  1885  was  traced  to  cows  with  a 
specific,  contagious  and  infectious  disease  apparently  due  to  a  similar 
organism.  There  is  no  positive  proof  that  cows  get  scarlet  fever.  An 
epidemic  of  400  cases  in  London  and  Surrey  (1909)  was  traced  to  cow's 
milk.  Human  infection  of  the  milk  could  not  be  proved  and  apparently  the 
infective  agent  was  derived  from  a  newly  calved  cow.  This  was  suggested 
as  a  cause  by  Sir  W.  Power  (1882).  Palmirsky  and  Zebrowski  regard  the 
S.  conglomeratus  as  the  specific  organism,  but  up  to  the  present  there  is 
no  reliable  proof  in  favour  of  any  one  germ.  Many  of  the  organisms  found 
are  due  to  secondary  infection.  In  a  mild  epidemic  Hektoen  found 
streptococci  in  the  blood  in  12  out  of  100  non-fatal  cases.  In  a  severe 
epidemic  Jochmann  found  them  in  25  out  of  161  cases,  and  all  died. 
Baginsky  and  Sommerfeld  noted  a  general  streptococcal  infection  in  82  fatal 
cases,  and  indeed  it  may  be  regarded  as  the  constant  cause  of  a  fatal  issue, 
though  sometimes  absent  in  fulminating  cases.  This  organism  (S.  pyogenes) 
is  constantly  present  in  the  throat.  It  is  absent  from  the  blood  in  a  large 
number  of  cases. 

Mode  of  Infection. — The  virus  is  not  transferable  to  animal?.  It  can 
be  transmitted  a  short  distance  through  the  air  by  coughing  and  sneezing. 
Contact  infection,  direct  or  indirect,  is  the  chief  mode  of  transmission.  The 
virus  is  destroyed  by  the  usual  methods  of  disinfection.  In  the  absence 
of  sunlight  and  air  it  can  remain  alive  outside  the  body  for  months,  and  can 
probably  multiply  if  moisture  is  present.  The  contagium  is  present  in  the 
pharyngeal  and  faucial  mucus  ;  in  the  discharges  from  the  throat  and  nose, 
and  from  the  ears  if  infected  ;  and  possibly  in  the  desquamation,  urine  and 
faeces.  Mild  cases  and  contacts  distribute  infection  as  readily  as  severe 
ones.     Healthy  persons  have  been  known  to  act  as  carriers.     Epidemics 


Scarlet   Fever.  927 

have  been  traced  to  milk  from  infected  farms  and  even  to  milk  kept  in  a 
kitchen  to  which  scarlet  fever  patients  had  access. 

The  throat  contains  the  contagium  in  the  early  stages.  The  disease 
is  infective  in  the  pre-emptive  stage,  as  soon  as  the  throat  is  affected. 
J.  W.  Stickler  (1899)  mixed  some  mucus  with  weak  carbolic  acid  and 
injected  it  sub  cutem  into  10  children,  setting  up  scarlet  fever  in  all.  The 
contagium  may  remain  latent  in  the  mucosa  of  the  throat,  nose  and  naso- 
pharynx for  a  long  time.  Rhinitis  is  often  present  and  intractable,  though 
not  necessarily  infectious.  Otorrhcea  may  be  the  supposed  source  of 
infection  but,  seeing  that  it  is  so  often  associated  with  rhinitis,  the  infective 
agent  may  be  in  the  nose.  Infection  has  alio  been  ascribed  to  eczematous 
conditions  of  the  nose,  mouth,  ears  and  anus,  and  to  various  complications 
such  as  empyema  and  suppurating  glands. 

Desquamation  has  been  regarded  as  the  main  source  of  infection,  but 
during  recent  years  considerable  doubt  has  been  thrown  upon  it.  The 
rash  is  an  erythema,  probably  due  to  toxaemia,  and  the  evidence  that  the 
squamae  contain  infective  germs  is  unreliable.  There  is  no  distinct  evidence 
that  the  virus  is  present  in  the  skin.  Infectivity  begins  before  desquamation 
and  may  continue  long  after  it  is  completed.  It  is  proved  by  the  so-called 
"  return  cases  "  that  a  child  who  has  been  sent  home  from  a  fever  hospital, 
after  complete  desquamation,  may  spread  the  disease.  Many  of  these 
have  been  traced  to  uncured  complications  of  the  throat,  nose  and  ear. 
Turner  (Metropolitan  Asylums  Board  Report,  1906)  in  an  analysis  of  1000 
successive  cases,  found  that  return  cases  occurred  in  3*27  per  cent,  of  397 
without  complications  ;  2-62  per  cent,  of  347  cases  with  rhinorrhcea  ; 
1-54  per  cent,  of  256  cases  with  other  complications.  Of  those  with  nasal 
discharge  180  were  kept  over  10  weeks  in  hospital.  The  general  conclusion 
is  that  return  cases  are  not  due  to  coincidence ;  that  they  are  often  due  to 
rhinorrhcea  ;  and  that  late  desquamation  is  little  or  not  at  all  infective. 

Apparently  genuine  cases  have  mixed  with  other  children  while  still 
desquamating,  even  in  the  fourth  week,  without  conveying  the  disease. 
Lauder  of  Southampton  (1904)  reported  that  204  cases  discharged  while 
peeling  gave  rise  to  only  2  return  cases.  At  Leicester  120  desquamating 
cases  were  discharged  from  hospital  without  any  secondary  cases  developing. 
On  the  other  hand  infection  has  been  traced  apparently  to  the  squamae 
conveyed  by  letters,  books,  etc.,  but  they  may  have  possibly  been  con- 
taminated by  mucus  from  the  mouth.  According  to  Fowler  of  Pottsville, 
Texas  (1903),  casts  from  cases  occurring  in  the  spring  of  1900  were  preserved 
by  the  mother  in  a  cardboard  box  and  exhibited  in  February,  1901,  to  2 
parents  and  a  boy  aged  3  years.  The  child  developed  malignant  scarlet 
fever  on  the  fourth  day  and  spread  the  infection  to  6  other  persons,  of  whom 
2  were  adults,  and  all  died.  There  was  no  scarlet  fever  in  the  district. 
Here,  too,  the  possibility  of  contamination  with  pharyngeal  mucus  cannot 
be  excluded.     At  present  it  is  advisable  to  regard  the  primary  desqua- 


928  Chapter  LXVL 

mation  as  infectious  and  the  later,  or  secondary  desquamation,  of  the 
hands  and  feet  as  harmless. 

The  contagium  is  deposited  on  the  mucous  membrane,  probably  of  the 
throat,  and  there  develops  and  makes  its  way  into  the  blood.  In  surgical 
or  inoculation  scarlet  fever,  the  poison  is  deposited  on  the  raw  surface  and 
passes  directly  into  the  blood.  Some  children  are  susceptible  to  this  mode 
of  infection,  though  apparently  immune  to  infection  through  the  mucous 
membranes. 

Duration  of  Infectivity. — Infectivity  exists  from  the  onset  to  the  end  of 
the  primary  desquamation.  It  is  slight  within  the  first  24  hours,  most 
active  during  the  period  of  sore-throat  and  the  height  of  the  fever,  and  is 
prolonged  by  catarrhal  conditions  or  complications.  It  is  not  improbable 
that  nasal  or  faucial  catarrh,  due  to  the  disinfecting  hot  bath  and  trans- 
ference from  the  hospital,  leads  to  the  development  of  latent  infection 
hidden  in  the  folds  of  mucous  membrane  ;  just  as  in  diphtheria  the  specific 
organism  can  sometimes  be  recovered  for  many  months  from  the  throat. 
As  a  rule  infectivity  does  not  last  for  more  than  6  weeks.  But  absolute  safety 
can  never  be  determined.  Nasal  discharges  must  be  viewed  with  suspicion. 
The  infectivity  of  mucoid  and  purulent  discharges  may  last  for  months.  The 
contagium  may  remain  in  clothing,  books,  furniture,  etc.,  for  long  periods 
of  time,  and  can  be  shut  up  in  wall  papers  by  pasting  a  new  one  over  the 
old.    It  appears  to  require  moisture  for  its  development. 

Quarantine. — The  child  should  not  be  allowed  to  mix  with  others 
for  6  weeks  from  the  onset,  2  weeks  after  terminal  disinfection,  or  longer  if 
there  is  a  persisting  otorrhcea,  nasal  catarrh,  or  pharyngeal  trouble.  Some- 
times the  period  is  shortened  to  4  weeks.  In  view  of  the  uncertainty  of 
the  infectivity  of  squamae,  it  is  not  advisable  to  permit  a  child  to  return 
to  school  until  desquamation  is  complete.  Previously  he  should  have 
several  soap  and  water  baths,  followed  by  sponging  with  carbolic  acid 
1  in  50  or  bichloride  of  mercury  1  in  5000.  The  hair  should  be  cut  short  and 
disinfected.  R.  Milne  (1908)  maintains  that  the  spread  of  the  disease  can 
be  entirely  prevented  by  complete  inunction  with  carbolic  oil,  10  per  cent., 
or  eucalyptus  oil,  twice  a  day  for  4  days,  and  once  daily  until  the  tenth  day. 
The  throat  is  swabbed  with  the  carbolic  oil  every  2  hours  for  the  first  day. 
It  would  be  rash  at  present  to  rely  on  such  treatment. 

Children  exposed  to  infection  should  be  quarantined  for  a  week,  unless 
they  have  only  been  in  contact  for  a  few  hours  with  a  very  early  case. 
Those  living  in  the  same  house  as  a  patient  should  not  be  allowed  to  mix 
with  others,  for  they  may  act  as  carriers  even  without  having  a  mild  and 
unrecognised  attack.  They  should  use  antiseptic  gargles  of  Condy's 
fluid  or  lysol,  1  in  1000.  A  case  in  a  hospital  ward  must  be  at  once  sent 
out,  and  the  ward  closed  if  the  infection  spreads. 

The  Incubation  Period  varies  from  1-9  days.  It  is  rarely  more  than 
a  week,  commonly  2-4  days,  and  occasionally  only  a  few  hours.    If  of  longer 


Scarlet  Fever.  929 

duration,  it  is  probable  that  the  source  of  infection  has  been  overlooked  or 
that  the  germ  has  remained  latent  in  some  fold  of  mucous  membrane. 
It  depends  partly  on  the  point  of  entrance,  the  virulence  of  the  poison,  and 
the  susceptibility  of  the  patient.  Generally  speaking  a  short  incubation 
period  indicates  a  severe  attack.  This  does  not  apply  to  inoculation  or 
surgical  cases,  in  which  the  germ  enters  the  blood  stream  directly  and  the 
incubation  period  may  be  only  6  hours. 

Symptoms. — The  onset  is  almost  invariably  abrupt  and  in  severity  is 
proportionate  to  the  severity  of  the  attack.  In  the  adult  the  sequence  of 
invasion  is  sore-throat,  headache,  fever  and  vomiting  ;  in  the  child  vomiting 
or  convulsions,  fever,  and  sore-throat.  Vomiting  is  the  first  and  most 
characteristic  sign.  It  occurs  once  or  twice  ;  and  may  be  very  frequent  and 
severe,  even  in  mild  cases.  It  is  associated  with  sore-throat,  shivering, 
headache,  rapid  rise  of  temperature,  and  general  malaise  in  proportion  to  the 
severity  of  the  attack.  Some  cases  are  so  mild  that  there  are  no  particular 
symptoms.  Others  are  so  severe  that  the  patient  dies  before  the  charac- 
teristic rash  or  sore-throat  develops.  Mild  cases  with  insidious  onset, 
slight  malaise  and  little  fever,  may  be  followed  by  severe  nephritis.  The 
face  is  flushed  and  perhaps  swollen.  The  sore-throat  precedes  the  rash. 
The  rash  may  be  the  only  sign,  or  it  may  be  so  faint  or  transitory  as  to 
escape  notice.  A  delayed  rash  is  often  associated  with  marked  angina. 
The  child  may  only  vomit  once  or  twice,  or  the  vomiting  may  be  severe 
and  persistent  for  even  24  hours.  Occasionally  epistaxis,  diarrhoea  and 
pains  in  the  limbs  are  present  at  the  onset. 

With  rare  exceptions  the  temperature  remains  up  until  the  rash  is  out. 
It  reaches  its  maximum  on  the  first  to  the  fifth  day,  generally  the  second 
or  third  day,  remains  up  for  a  variable  period,  and  subsides  by  lysis,  or 
perhaps  by  crisis  in  2  or  3  days.  It  usually  persists  for  about  a  week. 
Occasionally  it  does  not  rise  until  the  rash  has  come  out.  Subsequent  fever 
indicates  complications. 

The  rash  generally  appears  on  the  second  day,  almost  invariably 
12-36  hours  from  the  onset,  and  is  rarely  delayed  beyond  the  third  day. 
The  symptoms  increase  as  the  rash  develops  and  usually  subside  as  it  fades. 
It  is  a  punctate  erythema  ;  minute,  brightish  or  dusky  red  spots  on  a 
general  erythema,  as  if  the  skin  had  been  sprinkled  with  cayenne  pepper, 
giving  it  a  lobster-coloured  appearance.  The  erythema  may  appear  first, 
but  more  usually  is  simultaneous  with  the  punctse  ;  and  the  relative  pro- 
portions vary  in  different  cases.  The  rash  comes  out  first  on  the  neck 
at  its  junction  with  the  sternum  and  spreads  peripherally  in  all  directions, 
especially  on  the  inner  aspect  of  the  limbs.  It  sometimes  begins  behind  the 
ears  or  as  erythema  of  the  forehead  and  cheeks,  avoiding  the  regions  round 
the  mouth  and  thus  producing  the  "  circumoral  pallor."  It  is  most  marked 
on  the  parts  protected  from  exposure,  notably  the  groins  and  axillae.  It 
spreads  very  rapidly,  and  is  usually  fully  developed  and  reaches  the  hands 

3  o 


930  Chapter  LXVI. 

and  feet  in  24  hours  or  less  ;  but  it  may  be  delayed  or  driven  in  again  by 
exposure  to  cold,  and  brought  out  by  heat  or  a  hot  bath.  A  case,  diagnosed 
as  diphtheria  in  a  hospital  out-patient  department  on  account  of  the 
condition  of  the  throat,  may  be  typically  scarlet  fever  as  a  result  of  the 
warmth  of  the  ward.  The  rash  may  become  distinctly  papular  ;  chiefly 
on  the  fore-arms  and  legs.  If  so,  these  papules  persist  for  some  time  after 
the  erythema  fades,  are  of  diagnostic  value,  and  disappear  gradually.  The 
skin  is  hot  and  burning,  and  perhaps  itches.  A  certain  amount  of  swelling, 
chiefly  of  the  face  and  hands,  is  seen  in  bad  cases.  On  pressure  the  rash 
leaves  a  yellowish  discoloration  ;  later  on,  a  palish  brown.  It  remains 
at  its  maximum  until  the  third  day  of  the  illness  ;  and  lasts  for  3-7  days, 
occasionally  1 1  days,  but  very  rarely  a  longer  or  shorter  time.  It  disappears 
in  the  same  order  as  that  of  its  development. 

Atypical  rashes  may  be  limited  to  the  groins  and  inner  aspect  of  the 
arms  and  thighs.  The  rash  is  rarely  completely  absent,  a  little  is  probably 
present  in  the  axillae  and  groins.  Sometimes  it  closely  resembles  the  rash  of 
rotheln,  occasionally  it  is  like  true  measles,  and  in  malignant  cases  it  may  be 
dusky,  vesicular  or  hsernorrhagic.  Milk-white  patches,  due  to  vaso-con- 
striction,  may  be  noted. 

Desquamation  is  branny.  It  commences  as  minute  points  and  causes 
a  pin-hole  or  worm-eaten  appearance  of  the  skin.  Then  it  becomes  flaky, 
in  the  form  of  fine,  scales  on  the  neck  and  chest,  and  occasionally  between 
the  fingers.  It  begins  on  the  fourth  to  sixteenth  day,  generally  the  seventh 
to  tenth,  as  soon  as  the  rash  has  faded.  It  bears  no  absolute  relative 
proportion  to  the  rash,  but  as  a  rule  is  most  marked  if  a  characteristic  vivid 
•eruption  is  noted.  It  is  most  extensive  on  the  palms  and  soles  where  the 
rash  is  least  visible  and  the  epidermis  thickest.  It  does  not  occur  in  every 
case.  Desquamation  is  completed  on  the  trunk  in  3-5  weeks  from  the 
onset,  but  on  the  hands  and  feet  may  take  8-18  weeks.  Large  portions, 
like  the  fingers  of  a  glove,  may  be  cast  off.  The  new  epidermis  is  thin  and 
gives  the  skin  a  pinkish  colour.  This  is  most  marked  at  the  tips  of  the 
fingers,  which  peel  first,  and  affords  a  characteristic  contrast  with  the 
thick  grey  patches  in  course  of  separation.  The  peeling  alone  may  afford 
a  reliable  means  of  diagnosis  in  the  absence  of  a  history  of  an  attack. 

Varieties. — The  disease  varies  greatly  in  severity.  For  convenience  of 
description  cases  may  be  divided  into  groups,  although  there  is  no  strict 
line  of  demarcation  between  them. 

1.  Scarlatina  Simplex  is  of  mild,  medium  or  great  severity.  In  the 
mild  cases  there  is  no  complaint  of  sore-throat,  a  slight  and  indefinite  rash, 
and  a  temperature  little  or  not  at  all  raised.  Thus  two  children  in  succession 
had  a  slight  rash  somewhat  like  that  of  mild  rotheln,  T.  99°  F.  for  a  few 
hours,  and  no  vomiting  or  constitutional  symptoms.  Another  child 
developed  severe  S.  anginosa  and  a  nurse  typical  scarlet  fever.  Some 
mild  cases  are  characterised  by  slight  fever,  rash  and  a  little  redness  or 


Scarlet  Fever.  931 

the  throat,  with  or  without  subsequent  desquamation  ;  in  others  the 
rash  is  absent ;  and  in  a  few  desquamation  is  alone  noted.  In  cases  of 
medium  severity  the  attack  is  ushered  in  by  vomiting,  T.  101-103°  F. 
moderate  sore-throat  and  typical  rash.  The  fever  lasts  for  about  a  week. 
In  the  severe  type  the  onset  is  more  acute,  vomiting  may  be  frequent, 
possibly  convulsions  occur,  and  the  temperature  rises  to  103-105°  F.  The 
rash  is  intense  and  comes  out  early,  delirium  and  restlessness  are  present, 
and  the  fever  is  more  prolonged. 

2.  Scarlatina  Anginosa  vel  Septica  is  a  variety  in  which  the  throat 
symptoms  are  predominant  and  severe.  It  is  most  common  in  hospital 
cases,  the  ill-nourished  and  the  uncleanly.  It  often  begins  mildly,  but  on 
the  third  to  the  fifth  day  the  throat  signs  become  exaggerated,  the 
temperature  rises  higher,  and  the  cervical  glands  enlarge.  The  rash  becomes 
petechial  or  haemorrhagic,  especially  on  the  knees  and  elbows,  and  is,  there- 
fore, of  a  septic  type.     Diarrhoea  is  not  infrequent. 

The  throat  in  mild  cases  shows  nothing  but  a  little  redness  and  con- 
gestion of  the  fauces  ;  possibly  a  punctate  or  erythematous  rash  on  the 
soft  and  hard  palate  ;  or  a  ring  of  bright  redness  of  the  edges  of  the  palate 
and  pillars  of  the  fauces.  In  more  severe  ones  there  is  a  vivid,  carmine- 
like redness,  intense  and  dusky,  of  the  whole  of  the  fauces,  palate  and  buccal 
mucosa,  with  considerable  swelling  and  pain  on  swallowing.  The  tonsils 
swell,  perhaps  meet  in  the  middle  line,  and  are  more  or  less  covered  with 
■dirty  yellow  secretion,  somewhat  like  that  of  follicular  tonsillitis  at  first. 
The  pharynx  becomes  full  of  muco-pus,  the  glands  enlarge,  the  nose  dis- 
charges, and  the  tonsils  ulcerate  in  a  few  hours.  Thus  the  3  stages  are 
those  of  swelling,  exudation,  and  ulceration.  In  S.  anginosa  there  is 
great  swelling,  and  ulceration  of  the  tonsils  and  palate  is  rapid  and 
extensive,  sometimes  gangrenous.  The  tonsils,  uvula  and  fauces  become 
covered  with  a  soft,  white,  pultaceous,  easily  detachable  deposit,  sometimes 
pseudo-membranous.  The  whole  buccal  cavity  may  be  involved  and  the 
mischief  may  extend  to  the  pharynx,  nose  and  ears,  which  become  filled 
with  foul  secretion.  The  ulceration  may  be  deep  and  cause  severe  haemor- 
rhage. Occasionally  the  throat  at  the  onset  shows  extensive  swelling  like 
that  of  erysipelatous  inflammation,  without  any  sloughing  or  ulceration. 
Sometimes  it  presents  all  the  appearances  of  diphtheria  within  1 2  hours. 

Secondary  to  the  throat  symptoms  is  the  rapid  development  of  cervical 
■adenitis  and  infiltration  of  the  cellular  tissue,  forming  the  anginous  collar  or 
"  bull-neck."  The  breathing  is  interfered  with  by  the  pressure  and  the 
head  is  thrown  back.  These  glands  frequently  suppurate  and  occasionally 
there  is  extensive  sloughing. 

The  general  symptoms  of  the  anginal  form  are  those  of  septicaemia  of 
iaucial  origin.  The  breath  is  offensive  ;  the  mouth  intensely  congested, 
perhaps  ulcerated  and  the  discharge  offensive  ;  and  the  nose  is  similarly 
■affected.     Food  is  taken  with  'difficulty  because  of  anorexia,  local  con- 


932  Chapter  LXVL 

ditions  and  apathy.  The  temperature  is  high  and  prolonged,  delirium 
common,  and  a  typhoidal  condition  may  supervene.  Death  takes  place 
from  septicaemia,  pyaemia,  or  some  septic  complication,  in  7-14  days  or  less, 
or  perhaps  not  for  weeks.  Streptococci  are  found  in  abundance  in  the- 
fauces,  glands,  blood  and  tissues. 

3.  Scarlatina  Maligna  or  Toxic  Scarlet  Fever  is  the  most  fatal  of  all 
varieties.  It  is  due  to  a  large  dose  of  a  virulent  poison,  or  extreme 
susceptibility.  Its  frequency  varies  in  different  countries  and  different 
epidemics.  The  symptoms  are  those  of  toxaemia,  mainly  cerebral.  It  is 
generally  ushered  in  acutely  with  convulsions,  vomiting,  and  the  rapid 
development  of  cyanosis,  stupor  or  coma,  muttering  delirium,  tremor, 
prostration  and  hyperpyrexia.  Prostration  and  vomiting  may  be  marked 
and  persistent  from  the  onset.  The  pulse  is  feeble  and  frequent.  The- 
temperature  may  reach  106-108°  F.  in  a  few  hours  and  the  patient  die 
comatose  within  24  hours,  before  the  rash  appears.  The  frequency  of 
respiration  and  cyanosis  suggest  pneumonia.  Pyrexial  changes  only  are 
found  post  mortem.  In  a  less  severe  type  life  is  prolonged  for  a  few  days.. 
The  throat  is  red,  cedematous  and  covered  with  dry  sticky  mucus  ;  the 
submaxillary  glands  are  a  little  enlarged  ;  the  rash  vivid  and  sometimes 
blotchy.  Occasionally  cases  pass  into  the  septic  type  and  develop  green 
foetid  diarrhoea.     Quite  three-fourths  of  these  malignant  cases  die. 

4.  Scarlatina  Hemorrhagica  is  a  sub-variety  of  the  last  type.  The 
epidemic  malignant  purpura  of  the  older  writers  was  scarlatina.  Haemor- 
rhages take  place  into  the  skin  and  kidneys,  and  from  the  mucous  mem- 
branes. Similar  haemorrhages  may  occur  in  cases  of  medium  severity,  and 
be  indicative  of  secondary  toxaemia. 

5.  Surgical  or  Inoculation  Scarlatina. — Apparently  individuals  during 
the  puerpurium  and  those  with  open  wounds,  abrasions,  sores,  burns,  etc.,. 
are  peculiarly  susceptible  to  this  disease.  It  may  be  acquired  in  the 
ordinary  way  by  such  a  patient,  or  be  due  to  direct  inoculation  through  the 
raw  surface.  Care  must  be  taken  to  exclude  the  vasomotor  and  toxic- 
erythematous  rashes,  due  to  serum  disease,  intestinal  toxaemia  or  soap  and 
water  enemata  ;  and  the  septic  rashes  liable  to  follow  burns,  vaccination,, 
surgical  operations  and  other  injuries.  If  the  scarlatina  is  merely  coin- 
cident and  of  the  acquired  type,  it  differs  in  no  way  from  the  ordinary 
attacks.  Only  inoculation  scarlatina  should  be  regarded  as  genuinely 
surgical.  It  has  followed  the  simplest  operations,  the  scratching  of  pimples- 
and  vaccination.  According  to  Henoch  the  incubation  is  4-7  days  in 
operation  cases.  It  may  be  only  a  few  hours.  A  membranous  exudate 
appears  on  the  edges  of  the  wound,  with  secondary  swelling  and  redness  of 
the  surrounding  skin  and  adenitis.  The  rash  spreads  to  the  rest  of  the 
body,  but  it  does  not  always  begin  locally.  The  wound  improves  after  the- 
rash  reaches  its  maximum,  and  desquamation  begins  round  it.  The  throat 
symptoms  are  slight.    There  is  no  sore-throat  in  the  cases  of  septic  rash. 


Scarlet  Fever.  933 

General  Symptoms. — The  patient  is  flushed,  noticeably  so  on  the 
•cheeks  in  comparison  with  the  circumoral  pallor.  The  skin  is  burning  and 
■dry.  The  lips  are  dry  and  in  bad  cases  covered  with  sordes.  The  mouth  is 
partly  open  if  there  is  much  angina.  The  breath  is  said  to  have  a  peculiar, 
sweet,  almost  aromatic,  acetone-like  odour  in  the  early  stages.  In  the 
presence  of  angina  and  ulceration  it  is  offensive,  f  oetid,  and  even  gangrenous. 

The  tongue  is  characteristic  at  certain  stages.  The  early  "  strawberry 
tongue,"  is  swollen  and  covered  with  thick,  moist,  creamy  white  fur 
through  which  the  fungiform  papillae  stand  out  prominently.  It  looks 
somewhat  like  an  unripe  strawberry.  It  begins  to  peel  on  the  second  or 
third  day,  perhaps  not  till  the  fourth,  and  in  another  2  days  it  has  a  bright, 
•raw,  red,  clean  appearance  with  red  prominent  papillae  like  that  of  a  ripe 
strawberry  or  raspberry.  The  peeling  begins  at  the  tip  and  edges,  spreads 
backward  until  the  tongue  is  entirely  denuded  of  epithelium,  and  is  generally 
■complete  on  the  fourth  day.    The  tongue  becomes  normal  in  about  7-10  days. 

The  pulse  rate  is  a  valuable  diagnostic  point.  It  is  often  remarkably 
frequent,  unduly  so  in  proportion  to  the  temperature,  and  even  120-180  or 
more  per  minute  in  comparatively  slight  fever.  Infrequency  and 
irregularity  are  common  in  convalescence.  The  breathing  is  increased  in 
proportion  to  the  fever.  The  temperature  is  high  in  proportion  to  the  rash 
and  hyperpyrexia  may  occur.  Recovery  has  followed  a  temperature  of 
107-6°  F.     The  condition  of  the  glands  depends  on  the  throat. 

The  blood  shows  leucocytosis  of  polymorphs,  and  20  per  cent,  reduction 
in  haemoglobin  and  the  number  of  red  cells  (Mackie,  1901).  The  leucocytosis 
is  present  in  the  mildest  cases  ;  is  most  marked  after  full  eruption,  and 
persists  for  a  few  days  after  the  fall  of  temperature  ;  and  does  not  depend 
•on  the  height  of  the  fever.  It  is  increased  in  severe  rash,  bad  angina,  and 
sepsis.  Its  absence  in  severe  cases  is  a  bad  sign.  From  5-15  per  cent,  of 
■eosinophiles  are  present,  probably  due  to  the  skin  being  involved. 

Complications. — The  post-scarlatinal  infections  rarely  begin  before 
"the  fourteenth  day  or  later  than  the  twenty-eighth  day,  but  no  patient  is 
safe  until  the  seventh  week.  They  are  ushered  in  by  a  rise  of  temperature 
which  lasts  for  a  variable  period  and  drops  by  lysis.  Such  a  rise  of 
temperature  may  occur  without  signs  or  symptoms.  The  complications 
arc  due  to  general  infection,  or  direct  extension  from  the  throat.  The 
•common  throat  complication  is  the  streptococcal  infection,  already  referred 
to,  in  which  the  exudation  resembles  follicular  secretion  or  false  membrane 
even  within  12  hours  of  the  onset.  A  diphtheritic  looking  throat  during  the 
first  week  of  the  disease  is  almost  invariably  streptococcal.  It  extends 
to  the  posterior  nares  and  causes  adenitis.  It  rarely  spreads  to  the  larynx 
and  is  not  followed  by  paralysis.  Later  on,  say  after  the  disappearance 
of  the  rash,  such  a  throat  is  probably  true  diphtheria,  liable  to  involve 
the  larynx  and  to  produce  the  usual  effects  of  diphtheria.  It  is  not  an 
uncommon  complication,  and  patients  seem  very  susceptible  to  it  during 


934  Chapter  LXVI. 

convalescence.  Epidemics  of  post-scarlatinal  diphtheria  and  of  diphtheria- 
in  scarlet  fever  wards  are  not  infrequent.  Some  of  these  cases  yield  both 
streptococci  and  diphtheria  bacilli  on  culture.  Ulceration,  necrosis  and 
gangrene  are  not  uncommon.  The  tonsils  become  greyish  black  masses  of 
necrotic  tissue,  sloughing  and  giving  rise  to  foetid  odour  and  discharge. 
The  cellular  tissues  in  the  neck  are  involved,  severe  and  fatal  haemorrhage 
may  occur,  or  there  is  asthenia  and  profound  cachexia.  Gangrene  of  the 
tonsils  and  fauces  may  occur  in  the  cachetic  and  is  invariably  fatal. 

Perforation  of  the  soft  palate  is  a  rare  terminal  stage  of  ulcerative 
angina  and  is  due  to  cellular  necrosis.  It  is  usually  bilateral,  appears  in 
a  few  hours  in  the  severest  cases,  and  is  very  resistant  to  treatment. 

A  slight  initial  adenitis  is  nearly  always  present.  The  epitrochlear 
glands  are  enlarged,  even  in  the  mildest  cases,  and  the  inguinal  glands  in 
80  per  cent.  (Baum,  1907). 

Secondary  adenitis  is  due  to  infection  from  the  mouth  and  throat. 
It  may  be  extreme  and  set  up  a  diffuse,  brawny,  cedematous  cellulitis 
of  the  neck.  When  a  single  gland  only  is  affected,  it  is  much  more  likely 
to  suppurate  and  break  down.  The  pus  may  make  its  way  into  the 
mediastinum  and  cause  purulent  pericarditis,  empyema  and  pyaemia.  Post- 
scarlatinal adenitis  generally  affects  the  submaxillary  lymph  nodes,  and  is 
usually  limited  to  one  gland  on  one  side  only.  It  is  ushered  in  with  high 
fever  for  a  short  time,  24  hours  or  less,  and  the  swelling  subsides  in  2-6  days. 
It  is  rarely  as  marked  as  in  the  primary  stages  of  the  disease  and  is  less, 
likely  to  suppurate.     It  is  often  associated  with  albuminuria. 

Rhinitis  occurs  in  5-10  per  cent.,  is  easily  recognised  by  the  discharge, 
and  may  persist  for  months.  Necrosis  of  the  nasal  cartilage  is  rare. 
Otitis  media  (p.  994)  occurs  in  15-20  per  cent. 

Albuminuria  is  present  in  15  per  cent,  of  all  cases,  but  in  less  than 
5  is  there  an  acute  nephritis.  It  is  due  to  the  cloudy  swelling  from  the 
fever,  or  a  mild  and  transient  catarrhal  nephritis  in  the  first  week.  A 
small  amount  of  albumin  and  a  few  hyaline  casts,  and  occasionally  renal 
epithelium,  granular  casts  and  a  few  red  and  white  cells  are  found  in  the 
urine.     True  scarlatinal  nephritis  is  glomerular  in  type  (p.  576). 

Hemorrhagic  purpura  is  sometimes  associated  with  acute  nephritis 
or  grave  fatty  degeneration,  but  albuminuria  is  not  always  present.  It 
may  occur  during  convalescence,  and  is  probably  toxic  in  origin,  a  sequel 
of  severe  angina  and  pyrexia.  The  bleeding  takes  place  subcutaneously 
and  from  the  mucous  membrane.     It  is  very  fatal,  even  within  24  hours. 

The  cardiac  muscle  may  be  soft  and  friable  as  early  as  the  fourth  day, 
and  sometimes  there  is  acute  diffuse  myocarditis.  Dilatation  is  due 
to  cloudy  swelling,  anaemia,  myocarditis,  and  the  increased  blood  pressure 
in  nephritis.  It  may  be  acute  and  cause  sudden  death.  Endocarditis 
and  pericarditis  are  rare.  They  are  due  to  septic  conditions  or  scarlatinal 
rheumatism.    Endocarditis  may  occur  in  mild  cases  and  produce  permanent 


Scarlet  Fever.  935 

damage.  The  functional  murmur  of  dilatation  must  not  be  ascribed  to 
endocarditis.  Embolism,  and  its  effects,  and  malignant  endocarditis  are 
not  unknown. 

The  pulse  usually  drops  to  or  below  normal  when  the  temperature 
comes  down.  It  may  fall  quite  suddenly  and  before  the  fever,  or  may 
remain  high  though  the  fever  has  subsided.  A  later  acceleration,  with 
irregularity,  apical  murmur  and  accentuated  pulmonary  second  sound, 
suggests  a  cardiac  affection. 

Gangrene  of  the  extremities  is  rare,  and  due  to  thrombosis  or  endar- 
teritis. It  may  come  on  as  early  as  the  sixth  day.  It  is  "  dry,"  and 
usually,  but  not  always,  symmetrical  and  bilateral.  If  limited  to  a  limb, 
it  may  terminate  favourably  after  amputation.  Both  legs  were  amputated 
above  the  knees  in  a  boy,  aged  4  years  (Pearson  and  Littlewood,  1897). 
The  buttocks  and  thighs  are  sometimes  affected  simultaneously  or 
successively  and  the  process  ends  fatally. 

Laryngeal  affections  are  rare  except  in  diphtheritic  complications. 
Broncho-pneumonia,  pneumonia  and  empyema  may  occur  in  the  septic 
type,  and  serous  pleurisy  and  oedema  of  the  lung  in  nephritis. 

Obstructive  jaundice  is  due  to  intercurrent  disease  or,  exceptionally, 
is  septic  in  origin  and  fatal.  Diffuse  inflammation  may  extend  from  the 
pharynx  to  the  oesophagus  and  cause  ulceration  and  stenosis.  Vomiting- 
after  the  onset  is  frequently  uraemic.  Diarrhoea  occurs  in  uraemia  and 
sepsis.  Peritonitis  is  very  rare  and  is  part  of  a  general  streptococcal 
infection  late  in  the  disease.  It  is  purulent  and  diffuse,  but  not  always 
fatal. 

Convulsions  may  occur  at  the  onset.  In  the  course  of  the  disease  they 
are  generally  uraemic  or  meningeal  in  origin,  e.g.  meningitis,  haemorrhage, 
thrombosis  or  embolism.  Aphasia,  hemiplegia,  encephalitis,  peripheral 
neuritis,  and  epilepsy  are  exceptional. 

The  joint  affections  are  rheumatic  or  pyaemic.  Scarlatinal  rheumatism, 
or  synovitis,  is  uncommon  under  5  years  of  age.  It  comes  on  at  the  end  of 
the  first  or  beginning  of  the  second  week  ;  affects  the  upper  rather  than 
the  lower  extremities,  the  wrists  and  hands  chiefly  ;  and  may  involve 
the  elbows  and  knees,  and  even  all  the  joints.  There  is  moderate  swelling, 
pain  and  redness,  and  slight  fever.  It  runs  a  mild  course  of  a  few  days' 
duration,  and  rarely  suppurates.  It  differs  from  rheumatism  in  the  absence 
of  acid  sweats,  in  not  responding  to  salicylates,  and  in  not  jumping  about 
from  joint  to  joint.  It  varies  in  frequency  in  different  epidemics,  has  little 
or  no  tendency  to  relapse,  infrequent  heart  complications  and  no  special 
predilection  for  rheumatic  patients.  Chorea  is  extremely  rare.  Probably 
it  is  due  to  toxaemia,  though  true  rheumatism  may  occur  during  convales- 
cence. Pyaemic  arthritis  is  often  multiple  and  associated  with  pyaemia. 
It  may  start  as  an  epiphysitis.     The  large  joints  are  affected  and  suppurate. 


936  Chapter  LXVI. 

Four  or  five  weeks  after  the  onset  a  transverse  linear  groove  or  slight 
ridge  may  appear  at  the  root  of  the  nails,  being  most  marked  on  the  thumb. 
It  travels  up  the  nail  as  it  grows,  reaching  the  free  edge  in  about  6  months. 
It  is  more  marked  in  adults  than  in  children,  after  a  severe  than  a  slight 
rash,  is  due  to  nutritional  disturbance,  and  may  occur  in  other  febrile  states. 
In  rare  instances  the  nails  are  shed.  Sometimes  the  skin  shows  atrophic 
striae,  similar  to  the  "striae  patellares"  occasionally  seen  after  typhoid  fever. 

Diagnosis. — Typical  cases  are  easily  recognised,  but  those  which  are 
very  mild,  extremely  malignant,  or  atypical  in  character  and  course  may 
be  impossible  of  diagnosis.  The  occurrence  of  desquamation,  or  of 
secondary  cases,  may  be  the  only  positive  indication,  and  even  these  are 
not  absolutely  reliable.  The  desquamation  may  be  uncharacteristic, 
may  be  absent,  and  can  occur  in  other  affections.  Secondary  cases  may 
be  due  to  other  modes  of  infection.  Considerable  importance  should  be 
attached  to  undue  frequency  of  the  pulse  in  mild  and  apyrexial  cases, 
provided  it  is  not  due  to  nervousness  ;  and  to  the  condition  of  the  tongue 
in  relation  to  the  rash  and  the  duration  of  the  illness.  Frequent  vomiting 
during  the  first  24  hours  may  be  the  only  sign  that  a  sore-throat  is 
scarlatinal.  If  the  patient  dies  before  the  rash  or  sore-throat  develops, 
the  diagnosis  is  impossible.  The  nervous  and  toxeemic  symptoms  may 
suggest  pneumococcal  infection,  cerebrospinal  meningitis  or  some  severe 
•cerebral  disease. 

Ordinarily  the  diagnosis  is  based  on  the  acute  onset  with  vomiting, 
the  rapid  rise  of  temperature,  the  appearance  of  the  throat,  the  unduly 
frequent  pulse,  the  characters  of  the  rash  on  the  second  day,  and  later  on, 
the  tongue,  course,  complications  and  peeling.  The  "  throat "  may  be 
mistaken  for  simple  catarrh,  acute  tonsillitis,  follicular  tonsillitis  or 
diphtheria.  Scarlatiniform  rashes  may  occur  in  these  affections,  but  the 
date  of  appearance  and  the  distribution  are  often  distinctive.  A  diagnosis 
must  never  be  based  on  the  rash  alone.  There  is  especial  difficulty  under 
the  age  of  one  year  for  the  skin  is  so  easily  reddened.  The  erythema  must 
not  be  mistaken  for  that  due  to  fever,  liniments,  poultices,  scalds,  burns  and 
sunburn.  The  erythema  of  influenza  may  be  associated  with  faucial  catarrh, 
enlarged  and  painful  cervical  glands,  fever  and  aching  pains.  It  comes  out 
on  the  second  or  third  day,  and  may  be  followed  by  branny  desquamation, 
though  it  does  not  appear  to  be  ushered  in  by  vomiting.  The  cases  closely 
resemble  mild  scarlatina.  Erythematous  rashes  may  occur  in  the  prodromal 
stages  of  measles,  variola  and  varicella  ;  in  diphtheria,  serum  disease  and 
typhoid  fever ;  after  soap  and  water  enemata  ;  from  drugs  such  as  bella- 
donna, antipyrin  and  quinine  ;  and  in  urticaria,  and  various  forms  of  sepsis 
and  toxaemia.  In  mild  cases  it  is  diagnosed  with  extreme  difficulty  from 
the  rash  of  rotheln,  aberrant  types  of  measles  and  erythema  infectiosum. 
Rhinitis,  otitis  and  adenitis  are  strong  evidence  of  a  recent  attack  of  scar- 
latina.    Peeling,  albuminuria  and  changes  in  the  nails  may  be  present. 


Scarlet  Fever.  937 

Fourth  Disease.— Filatow  (1885)  described  under  the  name  of  "  rubeola 
scarlatinosa,"  and  Dukes  (1900)  under  the  name  of  "fourth  disease," 
an  affection  intermediate  in  character  between  scarlet  fever  and  rotheln. 
Like  the  latter  disease  its  incubation  period  is  9-21  days,  and  there  are 
often  no  symptoms  though  the  rash  is  copious.  It  may  be  ushered  in  with 
slight  sore-throat,  and  occasionally  malaise  for  some  hours,  headache, 
anorexia,  drowsiness,  chilliness  and  backache,  but  no  vomiting.  According 
to  Dnkes  the  rash  is  bright  rosy-red,  somewhat  raised,  and  diffused  over 
the  whole  body  in  a  few  hours.  The  amount  of  desquamation  is  variable, 
and  has  no  relation  to  the  severity  of  the  rash,  and  it  takes  place  in  the 
form  of  small  scales  rather  than  flakes,  for  a  week  or  two.  The  temperature 
is  not  raised  in  proportion  to  the  rash  ;  the  pulse  rate  is  not  unduly  increased ; 
and  the  characters  of  the  tongue,  conjunctivae,  throat  and  glands,  and  the 
course  of  the  disease  are  almost  identical  with  rotheln.  Klein  (1904) 
states  that  the  incubation  period  is  a  few  days  to  14  ;  and  the  onset  is 
sudden,  with  slight  signs  of  cold  in  nose  and  eyes,  deep  faucial  redness, 
and  submaxillary  adenitis.  The  tongue  on  the  third  day  is  like  that  of 
scarlet  fever.  The  rash  appears  on  the  face  first,  then  on  the  back  and 
abdomen,  seldom  on  the  extremities,  lasts  for  1-3  days,  and  is  not  followed 
by  desquamation.  These  descriptions  are  not  identical.  Dukes  maintains 
that  he  has  seen  scarlet  fever  both  before  and  after  this  disease.  The 
evidence  is  in  favour  of  some  epidemics  being  cases  of  mild  scarlet  fever. 
The  absence  of  definite  faucial  inflammation,  of  peeling  of  the  tongue,  and 
of  kidney  disease,  and  the  subsidence  of  the  fever  on  the  third  or  fourth 
day,  are  quite  frequent  in  scarlatina.  The  apparent  lack  of  infectivity 
after  the  third  week  is  not  of  much  assistance,  seeing-  that  it  has  been  noted 
in  scarlatinal  patients  even  while  desquamating. 

Course  and  Prognosis. — Both  depend  on  the  variety  and  severity  of  the 
disease,  and  the  prevailing  type  of  epidemic.  It  may  be  extremely  mild  or 
peculiarly  malignant.  After  a  series  of  epidemic  years,  its  virulence  declines 
until  it  becomes  a  very  mild  affection.  The  mortality  varies  from  4-40  per 
cent.  It  is  much  higher  under  2  years  of  age  than  at  any  other  period  of 
life,  and  still  very  high  up  to  the  end  of  the  fifth  year.  In  recent  years  the 
mortality  during  the  first  5  years  of  life  has  been  5-7  per  cent.,  in  the 
second  5  years  1-2,  and  in  the  third  5  years  under  1  per  cent.  Fatal 
cases  die  from  acute  toxaemia  in  the  malignant  or  toxic  type  ;  from  pyaemia 
or  septicaemia  in  the  severe  anginal  and  later  stages  of  the  toxic  variety  ; 
or  from  some  complication  of  a  severe  attack,  e.g.  pneumonia,  nephritis, 
or  throat  mischief  ;  or  from  nephritis  in  late  stages,  sometimes  even  after 
a  mild  attack. 

The  prognosis  must  be  guarded  as  to  severity  and  the  probability 
of  sequels,  which  are  impossible  to  prevent.  Many  depend  on  the  state  of 
the  mouth.  Wait  until  the  third  day  before  pronouncing  definitely  on  the 
■severity.    Cases  are  usually  regarded  as  milder  than  they  really  are.     The 


938  Chapter  LXVL 

amount  of  the  rash  varies  directly  as  the  severity  in  many  cases,  but  by  no- 
means  in  all.  The  temperature  is  not  a  reliable  guide,  though  as  a  general 
rule  the  severity  varies  with  the  height  of  the  fever.  It  may  be  moderate 
in  a  very  malignant  case,  and  up  to  105°  F.  in  comparatively  mild  attacks. 
A  fall  of  several  degrees  does  not  always  indicate  improvement.  The 
ordinary  mild  case  has  a  little  fever  for  a  few  days,  perhaps  only  1  day,  while 
a  more  severe  attack  may  have  fever  from  1-3  weeks,  the  temperature 
falling  by  lysis.  An  undue  rise  of  temperature  in  the  course  of  the  disease 
may  indicate  complication.  In  a  case  of  medium  severity  the  symptoms 
last  4-7  days. 

The  character  of  the  first  sound  of  the  heart  is  a  measure  of  the  severity 
of  the  toxaemia.  Cold  extremities  and  cyanosis  show  heart  weakness.  A 
very  high  temperature,  high  pulse  rate,  cardiac  debility,  gastro-intestinal 
and  nervous  symptoms,  and  great  angina  are  bad  signs.  Hyperpyrexia 
may  prove  fatal. 

Nephritis  may  occur  in  the  mildest  cases,  but  is  most  prevalent  if  there 
are  streptococcal  complications,  i.e.  many  such  cases  are  streptococcal 
nephritis.  With  increasing  age  the  mortality  from  scarlatinal  nephritis 
decreases  from  about  2  per  cent,  under  5  years  of  age  to  02  per  cent,  over 
15  years  (Turner),  and  four-fifths  of  all  cases  get  well.  Possibly  it  may  be 
a  cause  of  chronic  interstitial  nephritis  in  later  life. 

Relapses  and  Second  Attacks. — Eelapses  occurred  in  1-09  per  cent,  of 
14,143  cases  in  the  Metropolitan  Asylums  Board  Hospitals  (Sloan,  1903). 
Ordinarily  an  attack  confers  immunity  for  the  remainder  of  life  but  second 
attacks  are  not  rare,  and  some  patients  are  extremely  susceptible.  The 
liability  to  erroneous  diagnosis,  notably  rotheln,  must  not  be  forgotten 
before  accepting  a  case  as  one  of  relapse  or  recurrence.  The  first  attack 
should  present  a  characteristic  onset,  angina,  rash  and  strawberry  tongue. 
So-called  relapses  may  be  due  to  temporary  abeyance  of  the  rash  for  a  few 
days,  perhaps  on  account  of  exposure  to  cold  ;  to  sepsis,  especially  in 
anginal  cases  ;  or  to  food  poisoning,  an  enema  or  drug.  Apart  from  these 
causes  there  are  a  certain  number  of  cases  in  which  a  genuine  relapse  occurs, 
just  as  in  typhoid  fever.  It  is  ushered  in  by  vomiting,  sore-throat  and 
fever,  as  in  the  first  attack.  It  is  usually  mild  and  of  short  duration  ; 
sometimes  more  severe,  quite  as  liable  to  complications,  and  even  fatal. 
Eelapses  and  second  attacks  are  more  frequent  in  hospitals  than  in  private 
practice.  They  may  occur  in  mild  cases  after  admission  to  hospital,  gener- 
ally coming  on  in  1-3  weeks.  They  must  not  be  put  down  to  contraction 
of  the  disease  in  hospital  in  a  case  of  mistaken  diagnosis,  and  are  probably 
due  to  a  larger  dose  of  a  more  virulent  poison,  the  patient  being  insufficiently 
protected.  Such  relapses  have  occurred  at  intervals  of  14  days  to  6  weeks  i 
after  the  first  attack.  Eelapses  in  isolated  cases  have  been  ascribed  to 
auto-infection,  re-infection  from  profuse  growth  of  the  contagium  in  the 


Scarlet  Fever.  939 

throat  or  naso-pharynx,  but  it  is  difficult  to  understand  how  such  infection 
occurs,  or  why,  if  it  does  occur,  relapses  are  not  much  more  frequent. 

Treatment. — The  child  is  kept  in  bed  until  the  temperature  has  been 
normal  for  a  week,  or  for  3  weeks  from  the  onset  in  even  mild  cases.  The 
clothing  should  be  light ;  linen  during  fever  and  flannel  when  the  tempera- 
ture is  down.  The  diet  is  limited  to  milk  and  milk  foods  for  3  weeks  or 
until  there  is  no  fear  of  nephritis.  Some  physicians  insist  on  a  milk  diet 
for  4-6  weeks,  or  until  peeling  is  over,  giving  plenty  of  water  and  fruit 
juices  to  keep  the  urine  alkaline.  Others  allow  solid  diet  as  soon  as  the 
fever  has  subsided,  and  the  patient  can  swallow.  It  is  doubtful  whether 
meat  and  soups  are  injurious,  even  if  there  is  nephritis. 

The  bowels  must  be  kept  open  by  calomel  and  saline  cathartics  ;  an 
enema  being  given  at  once  if  the  temperature  is  high.  Warm  baths  reduce 
the  temperature  and  quiet  restlessness.  For  high  fever,  especially  if  there 
is  hyperpyrexia,  a  typhoid  state  or  cerebral  symptoms,  ice  to  the  head, 
sponging  and  cold  packs  are  necessary.  Tepid  sponging  and  bromides  are 
good  for  sleeplessness  ;  phenacetin  or  an  ice  bag  for  severe  headache. 

No  special  treatment  is  required  for  the  rash.  If  the  itching  is  severe 
inunction  with  5  per  cent,  ichthyol  ointment  is  of  value.  It  subdues  the 
swelling  of  the  skin,  relieves  the  itching,  reduces  the  nervous  irritability, 
usually  brings  down  the  fever  3-4°  F.  within  2  hours,  and  improves  the 
general  condition.  Tepid  sponging,  weak  carbolic  lotion,  warm  carbonate 
of  soda  lotion,  gr.  10  to  1  oz.  with  a  little  mucilage,  and  rice  powder  are  also 
useful.  Eucalyptus  oil  is  said  to  prevent  the  spread  of  infection,  if  rubbed 
in  universally.  As  soon  as  the  rash  and  fever  have  subsided,  peeling  should 
be  encouraged  by  means  of  a  warm  bath  daily  with  plenty  of  soap  and 
water,  followed  by  inunction  with  ichthyol  ointment  1-5  percent.,  carbolised 
vaseline  or  carbolised  oil  5  per  cent.,  salicylic  acid  ointment  1  per  cent., 
or  borated  vaseline  5  per  cent.  An  ointment  of  resorcin  1,  lanolin  6,  and 
ol.  sesami  2  parts,  and  a  5  per  cent,  resorcin-salicylic  superfatted  soap,  are 
recommended  by  Jameson  to  hasten  desquamation.  Carbolic  preparations 
must  be  used  with  caution  as  they  are  apt  to  irritate  the  skin. 

The  throat  and  nose  are  treated  by  ordinary  methods  (pp.  234,  373), 
especially  formamint  lozenges  and  swabbing.  Attention  to  these  parts 
may  prevent  otitis,  but  the  treatment  is  difficult  to  carry  out  in  many 
children.  Cold  compresses  to  the  neck  every  3  hours  relieve  throat  affections. 
The  mouth  must  be  kept  moist  and  free  from  mucus  by  frequent  drinks  of 
lemonade  ;  and  borated  vaseline  applied  to  the  lips  and  nose.  If  there  is 
extensive  ulceration,  hot  applications  externally  and  ice  to  suck,  or  sips  of 
hot  water,  afford  relief.     Tracheotomy  may  be  needed  for  great  oedema. 

Toxic  cases  are  treated  by  hydrotherapeutic  measures,  and  septic  cases 
by  Moser's  serum  or  Marmorek's  polyvalent  anti-streptococcal  serum. 
Moser's  serum  is  expensive,  difficult  to  obtain  and  of  doubtful  value,  though 
it  is  said  to  reduce  the  mortality  in  hospital  cases  from  15  to  9  per  cent. 


"940  Chapter  LXVI. 

One  dose  only  of  25-100  c.c.  is  given.  In  8-12  hours  the  temperature  falls 
rapidly  and  the  pulse  is  less  frequent,  the  rash  does  not  develop  or  fades 
more  quickly,  the  general  malaise  is  less,  and  restlessness,  delirium  and 
somnolence  usually  disappear.  Stimulants  can  be  used  freely  in  toxic  and 
septic  cases,  and  for  cardiac  weakness. 

For  otitis  instil  a  few  drops  of  warm  5  per  cent,  carbolised  glycerin 
2  or  3  times  daily,  and  apply  hot  or  cold  compresses.  Puncture  the 
■drum  if  there  is  much  pain  and  high  temperature.  For  otorrhcea  instil 
hydrogen  peroxide  3  volume  strength. 

Rheumatic  complications  are  mild,  transient,  and  require  no  special 
treatment.  The  prophylaxis  of  nephritis  consists  of  confinement  to  milk 
and  farinaceous  diet,  and  bed  for  3  weeks,  and  to  the  house  for  another 
2  weeks.  Give  plenty  of  diluents  and  encourage  excretion  by  the  kidneys. 
Encourage  desquamation.  Spray  the  throat  with  chlorine  water  or 
Listerine.  Give  alkalies  and  laxatives  internally.  Urotropine  is  of  no 
special  value.  Uraemia  is  treated  by  saline  injections,  high  rectal  irrigations 
and  venesection. 

Biniodide  of  mercury  gr.  -rJ-J  every  4  hours  ;  carbolic  acid  internally  ; 
bisulphite  of  soda  m.  3-10  of  the  saturated  solution,  two-hourly  ;  and  1  oz. 
•doses  hourly  of  decoction  of  cinnamon,  have  been  claimed  by  different 
practitioners  as  specifics.  There  is,  however,  no  special  drug  treatment, 
£,nd  reliance  must  be  placed  on  the  general  methods  adopted  in  fever. 
Expectant  treatment  gives  the  best  results.  Care  is  needed  during 
convalescence,  to  prevent  cardiac  dilatation  and  nephritis.  Undue  exertion 
and  chill  must  be  avoided.  Iron,  arsenic  and  cod-liver  oil  are  the  best 
tonics.  Persistent  otorrhcea  and  rhinitis  must  be  carefully  treated  as 
possible  sources  of  infection. 


CHAPTER    LXVIT. 

SPECIFIC  FEVEKS. 

German    Measles — Measles — Erythema    Injectiosum. 

German  Measles — Syn.  :  Rotheln — Rubella — Rose  Rash — Spring  Rash- 
—  Epidemic  Roseola — Hybrid  or  False  Measles. — Rotheln  is  a  mild  and 
feebly  infective  fever  which  occurs  in  epidemics,  simulating  true  measles  or 
scarlet  fever.  With  these  diseases  it  has  often  been  confounded.  It  was 
described  by  de  Berger  in  Germany  in  1752  ;  by  Maton  in  England  in 
1815  ;    and  clearly  differentiated  by  Wagner  in  1834. 

It  occurs  at  all  ages,  but  is  rather  more  frequent  in  the  later  half  of 
childhood  than  in  the  earlier  half.  Nurslings  are  rarely  affected,  but  cases 
have  occurred  within  the  first  3  weeks  of  life  and  intra-uterine  infection 
has  been  recorded.  After  the  age  of  10  years  it  is  more  frequent  than 
measles.  It  is  most  frequent  from  March  to  June  and  at  its  maximum  in 
May.     Epidemics  sometimes  occur  in  the  autumn. 

The  incubation  period  is  usually  14-17  days.  Most  cases  begin  on  the- 
fifteenth  or  sixteenth  day,  a  few  as  early  as  the  twelfth  or  as  late  as  the 
twenty-second.  Contacts  must  therefore  be  quarantined  for  23  days- 
The  infection  is  usually  direct.  It  may  be  conveyed  by  intermediaries,, 
objects  or  persons.  It  is  concentrated  in  closed  rooms,  schools,  etc.  The 
disease  is  mainly  infectious  in  its  early  stages,  especially  at  the  height  of 
the  rash,  feebly  so  and  for  a  short  time  only. 

Symptoms. — Its  symptomatology  is  much  the  same  as  that  of  varicella,, 
excepting  as  regards  the  rash.  The  prodromal  period  is  often  absent  and 
rarely  lasts  for  more  than  24  hours.  Sometimes  there  is  a  slight  degree  of 
fever,  up  to  101°  F.,  malaise  in  proportion  to  the  fever,  headache,  suffusion 
of  the  eyes,  sore-throat,  cough,  and  some  catarrh.  Occasionally  the  neck 
is  stiff,  and  the  cervical  and  occipital  lymph  nodes  enlarged.  The  catarrhal' 
symptoms  are  present  in  30-50  per  cent.,  the  conjunctiva  being  injected, 
and  the  naso-pharynx  involved.  A  few  attacks  are  ushered  in  by  shivering, 
giddiness,  coryza,  and  pain  in  the  back  ;  and  exceptionally  by  anorexia,, 
nausea  and  vomiting,  headache,  drowsiness,  convulsions,  delirium  and 
rigors,  or  epistaxis. 

The  temperature  is  normal  in  half  the  cases  ;  or  may  rise  to  100-102°  F.,. 
rarely  to  104-106°  F.  High  fever  is  accompanied  by  restlessness,  sleep- 
lessness and  delirium.     The  fever  is  highest  as  the  rash  reaches  its  maximum. 


942  Chapter  LXV1I. 

and  falls  as  the  rash  fades,  being  proportionate  to  its  severity.  Its  duration 
varies  from  a  few  hours  to  4  or  5  days.  It  may  fall  abruptly  as  soon  as  the 
rash  appears,  but  generally  subsides  gradually  with  its  disappearance.  The 
degree  of  malaise  depends  on  the  fever. 

The  rash  is  out  of  proportion  to  the  general  symptoms.  It  comes  out 
on  the  first  day,  within  a  few  hours  of  the  onset,  and  may  be  the  first  sign 
of  illness.  It  appears  first  and  chiefly  on  the  face  and  scalp,  at  the  junction 
of  the  scalp  and  forehead,  on  the  region  round  the  mouth  and  invading  the 
circumoral  region  right  up  to  the  lips,  on  the  cheeks  or  behind  the  ears. 
It  spreads  rapidly  over  the  body,  especially  the  chest  and  back,  and  attains 
full  development  within  24  hours.  It  may  cause  slight  facial  oedema, 
especially  about  the  eyelids.  It  may  appear  on  the  palms  and  soles.  It 
often  disappears  from  the  face,  as  it  comes  out  on  the  trunk  and  there 
coalesces  into  a  scarlatiniform  rash.  It  may  appear  on  the  chest  first,  or 
simultaneously  over  the  whole  of  the  body  with  a  special  predilection  for 
the  cheeks,  neck  and  under  the  chin,  the  buttocks  and  external  aspect 
of  the  thighs.  Usually  the  extremities  are  the  last  parts  affected.  It 
appears  on  the  roof  of  the  mouth  which  looks  dry,  mottled  and  dusky  red. 

The  most  common  type  is  a  morbilliform  or  maculo-papular  rash.  The 
spots  are  rather  larger  than  the  punctate  spots  of  scarlet  fever,  and  smaller 
than  the  papular  ones  of  measles.  They  are  often  minute  at  first,  increase 
in  size,  and  may  coalesce.  They  vary  in  size,  are  discrete,  and  pale  pink 
or  rose-red  in  colour,  sometimes  resembling  spots  of  red  ink  on  blotting 
paper.  Coalescence  produces  raised  blotchy  patches  on  the  face  and  a 
little  swelling  of  the  features.     This    rash  often  itches. 

A  much  less  common  type  is  the  scarlatiniform  rash.  There  is  a  diffused 
redness  which  suggests  scarlet  fever,  but  some  of  the  maculo-papules  can 
be  found  on  the  extremities  and  perhaps  on  the  forehead.  It  may  itch. 
Urticarial  patches  may  be  present  in  both  varieties. 

Many  intermediate  types  are  seen.  Occasionally  a  temporary  or 
abortive  rash  is  followed  in  2  or  3  days  by  a  typical  one.  The  morbilliform 
rash  is  sometimes  dark  red,  and  rarely  hemorrhagic.  It  is  less  dusky  than 
measles  and  does  not  coalesce  into  crescents.  It  lasts  1-4  or  even  8  clays, 
usually  2  or  3,  and  fades  gradually  in  the  order  of  eruption.  It  fades  much 
more  rapidly  than  that  of  measles  ;  and  frequently  causes  slight  mealy 
or  branny  desquamation  for  a  few  days,  and  a  little  temporary  pigmentation 
or  discoloration  of  the  skin.  The  desquamation  may  be  profuse. 
Secondary  rashes,  probably  relapses,  occasionally  occur. 

The  tongue,  is  clean,  or  a  little  furred  in  proportion  to  the  fever.  It  has 
been  known  to  peel.  The  pulse  rate  depends  on  the  temperature.  Slight 
catarrhal  symptoms  of  the  throat,  nose  and  conjunctiva  are  frequent, 
with  itching,  smarting,  lachrymation  and  even  photophobia.  A  secondary 
sore-throat  may  appear  about  the  fifth  day. 


Measles.  943 

The  glands  behind  the  ears  and  posterior  border  of  the  sterno-mastoids 
are  almost  always  enlarged,  perhaps  before  the  eruption.  Occasionally 
the  axillary,  and  more  often  the  inguinal  glands,  are  also  affected.  They 
are  movable,  tender,  hard  and  shotty,  like  peas  or  equal  to  horse-beans  in 
size,  and  do  not  suppurate. 

Complications  are  practically  unknown.  Acute  laryngitis  is  the  most 
severe  and  fatal  one.  Death  has  occurred  from  pneumonia,  and  from 
mild  arthritis  with  sudden  heart  failure.  The  catarrh  may  spread  to  the 
bronchial  tubes  and  produce  lobular  pneumonia.  Rare  complications  are 
albuminuria,  diarrhoea,  acute  enteritis,  otitis,  joint  pains  and  arthritis. 
Some  of  these  may  have  been  of  scarlatinal  origin.  The  disease  is  almost 
invariably  harmless. 

Diagnosis. — Many  cases  are  wrongly  described  under  this  name.  It 
is  most  likely  to  be  confounded  with  mild  or  abortive  measles.  It  is 
doubtful  whether  cases  need  ever  be  mistaken  for  scarlet  fever,  but  the 
converse  error  in  diagnosis  is  excusable.  The  difficulties  may  be  insu- 
perable. I  have  known  three  physicians  pronounce  a  septic  rash  to  be 
scarlet  fever,  measles,  and  German  measles.  From  measles  it  is  differen- 
tiated by  its  mild  catarrhal  symptoms,  post-auricular  and  post-cervical 
adenitis,  the  mild  invasion,  early  appearance  of  the  rash,  absence  of  buccal 
spots  and  of  diazo-reaction,  and  the  presence  of  extensive  rash  with  slight 
constitutional  disturbance.  Similar  points  must  be  borne  in  mind  in 
diagnosing  it  from  scarlet  fever.  Throat  signs  may  be  of  little  diagnostic 
value.  In  rotheln  importance  must  be  attached  to  the  appearance  of 
rash  on  the  cheeks  and  circumoral  area,  the  presence  of  distinct  maculo- 
papules  on  the  extremities  and  on  the  palms  and  soles,  clean  tongue, 
absence  of  vomiting,  and  a  pulse-rate  only  increased  in  proportion  to 
the  fever.  Mild  cases,  in  which  there  is  little  or  no  rash,  are  apt  to  be 
regarded  as  due  to  pharyngeal  catarrh  with  secondary  adenitis.  Isolated 
cases  should  be  treated  as  aberrant  scarlet  fever  or  measles,  for  the  sake 
of  precaution. 

Treatment. — Generally  speaking  the  child  should  be  kept  in  bed  5  days, 
indoors  3  days,  sent  out  in  the  fresh  air  for  6  days,  and  then  disinfected. 
The  duration  of  infection  must  be  regarded  as  possibly  14  days,  though  it  h 
probably  only  a  week  in  mild  cases.     The  treatment  is  purely  symptomatic. 

MEASLES. 

Syn.  :    Morbilli — Rubeola. 

Measles  is  a  very  fatal  disease  and  highly  infectious  in  early  stages. 
It  plays  havoc  with  school  attendance.  It  may  occur  from  intra-uterine 
infection  and  is  then  mild.  Infants  are  more  or  less  immune,  possibly  from 
transmission  of  immunity  from  the  mother.  It  is  mild  during  the  first 
>6  months  and  very  severe  during  the  second  year  of  life. 


944  Chapter  LXVII. 

The  disease  is  spread  by  direct  infection  ;  through  the  medium  of 
doctors,  attendants,  etc.  ;  or  by  animals,  such  as  cats.  The  virus  is 
short-lived  outside  the  body.  It  is  most  infective  during  the  invasion 
period  and  while  the  rash  is  out,  especially  if  there  is  much  catarrh. 
Catarrhal  states  and  the  aggregation  of  children  in  schools  are  potent 
factors  in  its  spread.  Borini  (1905)  cultivated  a  small  bacillus  from  the 
blood.     Les.age  has  isolated  a  micrococcus. 

The  incubation  period  is  8-14  days,  commonly  9-12  days.  Balme  (1904) 
gives  a  wider  limit  of  6-18  days.  It  is  often  associated  with  a  notable  loss 
of  weight,  beginning  on  the  third  to  fifth  day  (Meunicr's  sign),  although  the 
child  appears  in  perfect  health.  Another  early  sign  is  a  polynuclear  leucocv- 
tosis  which  reaches  its  maximum  about  the  sixth  day  before  the  rash  appears. 
It  then  falls  so  much  that  during  the  eruption  in  uncomplicated  cases 
leucopenia  is  present.  Malaise,  sneezing  and  vomiting  have  been  occasion- 
ally noted. 

Symptoms. — It  assumes  anomalous  forms  less  frequently  than  other 
acute  exanthemata.  Cases  may  be  very  mild,  with  short  and  slight 
fever  and  no  complications  ;  of  medium  severity  ;  or  severe,  with  high 
fever,  long  duration,  and  bad  complications.  The  typical  course  is  an 
incubation  period  of  10-11  days,  an  invasion  of  2-4  days,  rash  for  3-5  days,. 
and  convalescence  7  days  ;  in  all  a  total  of  3-4  weeks.  In  the  weak  and 
delicate  the  invasion  period  may  be  prolonged  to  8  or  9  days. 

The  attack  is  ushered  in  with  fever,  malaise,  cough,  and  catarrh  of 
the  nose,  pharynx,  larynx,  bronchi  and  conjunctiva?.  The  discharge  from 
the  nose  is  usually  serous,  and  may  become  purulent.  Epistaxis  may  occur 
in  severe  cases,  and  is  common  in  the  malignant  ones.  Coryza  may  be 
absent,  but  the  absence  of  all  prodromata  is  rare.  Running  from  the  nose, 
sneezing,  swelling  of  the  eyelids,  lachrymation  and  photophobia  are 
frequently  present.  Vomiting  may  occur  on  the  first  day,  on  the  appear- 
ance of  the  rash,  or  in  the  intervening  period.  After  the  first  day  it  is  due 
to  the  catarrh  of  the  fauces  or  an  enanthem  in  the  bronchial  tubes. 
Diarrhoea  is  fairly  common  and,  if  associated  with  abdominal  pain,  is  a  sign 
that  the  attack  is  severe.  The  cough  is  short,  dry,  even  paroxysmal,  and 
sometimes  barking.  It  is  due  to  irritation  of  the  fauces,  larynx  or  bronchi. 
An  atypical  onset  may  be  characterised  by  fever  and  cough,  alone  or  with 
some  submaxillary  adenitis.  The  temperature  may  then  fall  but  the 
cough  and  catarrh  persist,  and  gradually  the  fever  returns.  Catarrh  ot 
the  nose  and  eyes  may  not  begin  until  the  fourth  day.  In  some  cases  the 
disease  is  ushered  in  by  acute  laryngitis  so  severe  to  necessitate  tracheotomy. 
Laryngitis  generally  indicates  severity,  though  it  may  occur  in  mild  cases. 
Usually  it  is  slight  and  disappears  as  soon  as  the  rash  comes  out.  The 
cough  is  hoarse  and  croupy,  and  the  voice  hoarse.  The  signs  are  those  oi 
croup  and  may  be  mistaken  for  diphtheria.     Headache,  nocturnal  delirium 


Measles.  945 

and  convulsions,  in  the  order  named  arc  symptoms  of  increased  severity  of 
the  disease. 

Prodromal  rashes  are  quite  common  in  children  on  the  first  or  second 
day,  rarely  after  the  onset  of  catarrh,  and  often  before  the  appearance 
of  buccal  spots.  They  either  disappear  or  merge  into  the  true  rash. 
Goodall  (1907)  states  that  the  most  common  one  is  a  punctate  erythema, 
general  or  patchy,  limited  to  the  trunk.  In  other  cases  it  takes  the  form 
of  discrete  papules,  with  blotches  and  irregular  patches  of  confluent  papules  ; 
of  isolated  macules  or  papules  ;  urticaria  ;  or  ill-defined  erythematous 
mottling.  The  rash  is  sometimes  polymorphic,  has  no  special  distribu- 
tion, but  is  most  apt  to  appear  on  the  trunk  and  behind  the  ears,  and 
does  not  itch.     It  has  no  prognostic  value. 

Buccal  s'pots  were  described  by  Flindt  in  1884,  by  Filatow  in  1895, 
and  Koplik  in  1896.  They  are  almost  always  present  1-3  days  before  the 
rash  appears.  Usually  they  appear  on  the  first  or  second  day,  and  if  later 
the  rash  is  often  delayed.  They  are  situated  on  the  buccal  mucosa, 
opposite  the  lower  molar  teeth  ;  and  may  be  found  on  the  labial  mucosa, 
palate,  uvula  and  fauces,  and  even  on  the  gums  and  under  the  tongue. 
They  are  seen  best  in  good  daylight,  concentrated  by  lens  or  reflected  by  a 
short  focus  mirror,  and  may  be  overlooked  in  artificial  light.  Koplik 
described  them  as  "  irregular,  stellate  or  round,  rose-coloured  spots,  with  a 
bluish-white  speck  in  the  middle.  The  rose  spots  become  confluent,  but 
the  specks  rarely  or  never  coalesce.  They  are  raised  and  firmly  adherent, 
and  they  disappear  at  the  height  of  the  rash."  The  specks  somewhat 
resemble  miliary  tubercles  as  seen  in  the  meninges.  At  first  they  appear 
as  tiny  hyperaemic  areas.  The  typical  specks,  much  smaller  than  a  pin's 
head,  appear  in  the  centre  in  a  short  time.  This  reddened  base  or  areola 
is  not  always  present.  Occasionally  the  spots  are  quite  large.  They  may  be 
very  few  or  numerous,  and  may  become  confluent.  The  number  does  not 
vary  with  the  severity  of  the  attack  or  the  extent  of  the  rash.  Their 
duration  is  2-4  days,  and  they  often  disappear  with  great  rapidity.  The 
central  speck  is  the  pathognomonic  feature  and  is  formed  of  the  puffy 
apex  of  a  papilla. 

Buccal  spots  may  simulate  thrush  and  aphthous  stomatitis,  but  the 
patches  in  these  affections  are  larger,  more  coalescent,  more  irregularly 
distributed,  opaquely  white,  and  have  no  red  areolae.  The  orifices  of  buccal 
glands,  bubbles  of  air,  or  tiny  particles  of  milk,  food  and  inspissated  mucus, 
may  cause  confusion.  In  infants,  under  6  months,  the  spots  are  seldom 
present  until  the  rash  comes  out.  If  they  are  absent  or  few  in  number,  the 
attack  is  usually  mild.     They  are  not  found  in  other  conditions. 

The  folate  generally  shows  a  blotchy  discoloration  ;    dark  or  purple 

-    patches,  triangular  or  oval  in  shape  and  best  seen  on  the  hard  palate.     They 

usually  come  out  a  day  before  the  rash  and  are  least  marked,  or  absent,  in 

mild   cases.     This    is    called  the  "  morbillary  enantlwm."     An  cryihcma(o- 

3  p 


946  Chapter  LXVII. 

pultaceous  stomatitis  (Combe)  may  precede,  by  2  days,  or  accompany  the 
rash.  The  mucous  membrane  of  the  cheeks  and  gums  is  swollen  and  red, 
at  times  violet.  The  gums  are  covered  with  an  opalescent  or  whitish 
epithelial  coating,  thin  and  easily  detachable,  but  they  do  not  bleed  or 
f ungate.  The  fauces  and  soft  palate  are  injected.  Petechial  haemor- 
rhages in  the  mouth  at  an  early  stage  indicate  severity.  They  may  develop, 
with  ulceration  of  the  mucosa,  in  the  course  of  the  disease. 

The  post-cervical  and,  more  frequently,  the  submaxillary  glands  are 
often  enlarged  before  the  rash  appears.  Occasionally  there  is  found  a 
general  glandular  enlargement  and  splenic  hyperplasia.  Troublesome 
cough,  dyspnoea,  and  dry  bronchitic  rales  may  also  be  present,  and  subside 
a3  the  rash  comes  out. 

The  invasion  period  is  terminated  by  the  eruption  of  the  rash  on  the 
fourth  day,  or  any  day  from  the  second  to  the  ninth.  If  the  incubation 
period  is  shortened,  the  invasion  is  often  prolonged,  and  vice  versa.  The 
rash  generally  appears  on  the  fourteenth  day  after  exposure,  and  is 
associated  with  a  maximum  degree  of  catarrh.  Delay  in  its  appearance  is 
usually  a  sign  of  severity.  The  symptoms  increase  in  severity  with  the 
appearance  and  extent  of  the  rash  and  include  anorexia,  thirst,  swelling 
of  the  face,  dulness,  drowsiness,  delirium,  convulsions,  and  all  those  due 
to  catarrh.  A  systolic  murmur  and  slight  cardiac  dilatation  are  frequently 
present  during  the  acme  of  the  rash.  Albumin  is  present  for  a  short 
time,  and  the  urine  gives  the  diazo-reaction,  even  24-48  hours  before  the 
eruption. 

The  rash  appears  first  on  the  forehead,  at  the  margin  of  the  scalp,  and 
behind  the  ears.  Not  infrequently  it  comes  out  primarily  on  the  buttocks 
and  round  the  anus.  Spreading  from  the  forehead  it  affects  the  temples, 
chin  and  face,  neck,  upper  arms,  trunk,  forearms  and  hands,  thighs,  legs  and 
feet.  It  disappears  in  the  same  order.  It  varies  between  a  type  like  that 
of  German  measles  or  scarlet  fever,  and  one  like  urticaria.  In  colour 
it  varies  from  pale  to  bright  red  ;  pale  in  mild  cases,  and  livid  in  severe 
ones  or  if  there  are  heart  or  lung  complications.  It  is  composed  of  maculo- 
papules  of  variable  size,  never  quite  circular,  and  usually  with  ill-defined 
edges.  The  spots  may  coalesce  into  somewhat  crescentic  patches,  leaving 
intervening  areas  of  healthy  skin  and  causing  a  mottled  appearance.  It 
attains  its  full  development  in  3-5  days.  Subsequent  desquamation  is 
slight  or  absent.  When  present,  it  is  branny  or  of  small  flakes,  and  most 
marked  on  the  trunk,  while  the  hands  and  feet  remain  free.  Pigmentation 
may  be  visible  for  2  weeks. 

The  temperature  rises  as  the  rash  comes  out.  Frequently  it  reaches 
104°  F.  at  the  onset,  and  falls  to  normal  the  next  day,  remaining  down  for 
1-3  days.  It  then  gradually  rises  and  reaches  its  maximum  with  full, 
development  of  the  rash,  after  which  it  rapidly  falls  by  crisis.  Thus  the 
temperature  chart  shows  2  marked  pinnacles  with  an  intervening  period  or 


Measles.  947 

remission.  Frequently  the  early  signs  of  measles  and  fever  are  present 
for  12-24  hours  ;  then,  in  another  24  hours,  the  temperature  falls  and  the 
symptoms  disappear,  and  the  child  seems  quite  well.  Such  remissions  last 
for  12  hours  to  4  days  ;  sometimes  there  are  more  than  one  but  they  are 
then  shorter.  The  signs  recur  as  the  rash  comes  out.  In  some  cases 
there  is  no  initial  rise  ;  while  in  others  the  disease  runs  an  afebrile  course, 
notably  so  in  breast-fed  babies. 

Varieties. — Apyrexial  measles  is  a  mild  attack.  Abortive  measles 
(morbilli  sine  morbillis),  or  measles  without  eruption,  is  occasionally  seen 
during  epidemics.  It  is  characterised  by  prodromal  symptoms,  prodromal 
rash  and  buccal  spots.  In  many  supposed  cases  the  rash  is  present, 
though  trivial  and  overlooked,  but  in  some  the  most  careful  examination 
fails  to  reveal  any  sign  of  it.  Fever,  coryza,  conjunctivitis,  etc.  may  be 
present.  Such  cases  are  usually  mild  but  have  proved  fatal.  Rubeola 
sine  catarrho  of  Willan  occasionally  occurs  and  is  characterised  by  rash 
without  catarrh,  conjunctivitis  or  fever.  In  black  measles  the  rash  is 
purpuric,  either  in  consequence  of  malignancy,  or  of  heart  or  lung 
complications. 

The  gastro-intestinal  type  is  one  in  which  the  predominant  symptoms 
are  diarrhoea  and,  less  often,  bilious  vomiting.  These  symptoms  come  on 
about  the  second  or  third  day  of  the  rash,  sometimes  later,  and  occasionally 
in  the  invasion  period.  There  is  often  a  slight  fall  of  temperature.  The 
stools  are  frequent,  green  and  foetid  ;  and  rarely  muco-purulent  and 
hemorrhagic  from  necrotic  or  gangrenous  ulceration  of  the  colon.  It  may 
terminate  fatally  in  the  typhoid  state  or  from  broncho-pneumonia. 

In  septic  measles  there  is  marked  prostration  and  high  fever.  It  is  due 
to  secondary  streptococcal  infection  of  the  blood  and  is  often  fatal  in  a  few 
days.  Pulmonary  measles  usually  occurs  in  the  first  year  of  life,  and  is 
generally  fatal.  The  rash  is  more  or  less  livid  and  fades  quickly.  There 
is  generally  cyanosis  with  dyspnoea,  restlessness  and  collapse.  Acute 
necrosis  of  the  lung  occurs.  In  hcemorrhagic  measles  the  rash  is  brownish 
livid  in  colour,  the  temperature  is  high  and  the  constitutional  symptoms 
are  severe. 

Diagnosis. — The  most  important  differential  features  are  the  prodromal 
Tashes,  remission  of  temperature,  buccal  spots,  conjunctivitis  and  early 
laryngitis,  and  the  diazo-reaction.  The  urine  gives  this  reaction  in  measles, 
but  not  in  German  measles.  Conjunctivitis  begins  and  is  most  marked 
over  the  bulbar  conjunctiva,  at  the  usual  site  of  phlyctenules.  This 
early  distribution  and  limitation  may  distinguish  it  from  simple  conjunc- 
tivitis. The  leucocytosis  during  incubation,  and  subsequent  leucopenia, 
may  be  of  some  assistance.  In  the  early  stages  the  illness  is  apt  to  be 
•mistaken  for  acute  coryza  ;  and,  later  on,  the  skin  eruption  may  simulate 
that  of  German  measles,  serum  disease,  and  various  skin  rashes.  In  rare 
instances  the  disease  has  been  coincident  with  scarlet  fever  (p.  925). 


948  Chapter  LXVII. 

Complications. — The  pulmonary  complications  are  the  chief  important 
ones,  and  of  these  bronchitis  and  broncho-pneumonia  are  the  most  frequent, 
occurring  in  10-25  per  cent.  Laryngitis  tardive,  the  form  secondary  to- 
eruption,  is  more  serious  than  the  primary  variety  and  begins  on  the  third 
or  fourth  day  of  the  rash.  It  may  be  complicated  by  microbial  infections 
such  as  diphtheria,  but  the  diphtheria  bacillus  is  not  always  found  in  the 
membrane.  It  gives  rise  to  obstruction  and  glottic  spasm,  and  may 
produce  subsequent  ulceration  of  the  vocal  cords  and  arytenoids  and 
perichondritis.  Broncho-pneumonia  is  due  to  a  mixed  infection,  to 
virulent  streptococci  of  septic  type,  or  to  staphylococcal  infection  and 
general  pysemia.  It  may  be  followed  by  acute  necrotic  pneumonia  or 
bronchiectasis.  Sometimes  the  pneumonia  is  lobar  in  type,  because  of  its 
extent.  Atelectasis  occurs  in  babies.  Empyema  is  an  occasional  sequel. 
Circulatory  complications  are  mainly  dilatation  and  sometimes  myocarditis  ; 
or  bradycardia  with  oedema,  albuminuria  and  syncopal  attacks. 

Stomatitis  is  present  in  15  per  cent.  ;  diarrhoea  in  10  per  cent,  and  often 
associated  with  severe  abdominal  pain  and  vomiting.  Ulcerative  stomatitis., 
cancrum  oris,  tonsillitis,  and  parotitis  occasionally  occur. 

The  skin  may  exhibit  impetigo,  ecthyma,  diaper  rash,  eczema,  milaria 
and  herpes.  Noma  vulvse  is  an  occasional  sequel,  and  dry  gangrene  of  the 
prepuce  has  been  reported.  The  eyes  may  show  chronic  conjunctivitis, 
blepharitis,  hordeolum,  palpebral  abscess,  phlyctenules,  or  haziness  and 
sometimes  ulceration  of  the  cornea.  Otorrhcea  and  otitis  (p.  995)  are 
common,  if  adenoids  are  present,  and  may  terminate  in  mastoiditis,  sinus 
thrombosis,  and  meningitis.  Excoriations  of  the  nose  and  lips,  rhinorrhcea 
and  epistaxis  occur. 

The  nervous  complications  are  hyperpyrexia  ;  convulsions  ;  cerebral 
symptoms,  such  as  restlessness  and  irritability,  perhaps  following  a  fit : 
and  encephalitis.  Cases  of  acute  encephalitis  of  various  parts  of  the 
cerebrum  and  cerebellum  ;  false  disseminated  sclerosis,  perhaps  a  sequel 
of  encephalitis ;  acute  disseminated  myelitis ;  ascending  paralysis, 
resembling  diphtheritic  palsy  ;  paralysis  of  the  soft  palate,  independent  of 
diphtheria ;  paralysis  of  the  external  rectus  muscle  of  the  eye ;  and 
peroneal  neuritis  and  atrophy,  have  all  been  reported.  Other  rare 
complications  are  severe  pains  in  the  joints,  purulent  arthritis,  acute 
nephritis,  parotitis,  and  empyema  of  the  frontal  sinus.  The  submaxillary 
and  cervical  glands  are  frequently  enlarged.  Sometimes  all  the  glands  are 
affected  on  account  of  the  skin  changes  and  toxa?mia,  and  there  may  be  aj 
general  tendency  to  lymphatic  hyperplasia.  The  bronchial  glands  seem 
particularly  prone  to  enlargement  and  secondary  tuberculous  infection. 

Course  and  Prognosis. — Recovery  rapidly  takes  place  after  the  fal 
of  temperature.  Prolonged  cases  may  show  intermittent,  remittent,  o 
continuous  fever.  The  general  indications  of  severity  are  a  short  incubatioi 
period,  laryngitis  at  the  onset,  vomiting  during  the  course,  diarrhoea  anc 


Measles.  949 

abdominal  pain,  epistaxis,  livid  rash  and  cerebral  symptoms.  The  outlook 
is  more  favourable  when  the  rash  develops  rapidly,  and  if  it  is  large  and 
blotchy.  A  fine  rash  or  one  that  fades  rapidly  may  be  a  bad  sign.  If  there 
are  many  buccal  spots  there  is  usually  much  rash.  Severe  nervous 
symptoms  are  usually  temporary,  but  a  prolonged  high  temperature  or  a 
further  rise  indicates  complications.  Debility,  rickets,  and  broncho- 
pneumonia increase  the  gravity  of  the  case. 

The  mortality  is  small,  except  in  infants  from  6  months  to  2  years  old, 
and  greatly  depends  upon  the  treatment  adopted.  The  disease  is  seldom 
fatal  within  a  week.  Apparently  it  is  mild  under  6  months  of  age,  and 
especially  severe  in  the  second  year.  In  the  first  3  years  of  life  the  mortality 
is  about  10  per  cent.,  possibly  as  much  as  20  per  cent.  In  the  next  2  years 
it  falls  to  5  per  cent.,  and  from  5-10  years  of  age  it  is  only  1  per  cent.  Over 
that  age  it  is  practically  never  fatal. 

Sometimes  a  relapse  or  second  rash  develops  in  12-14  days,  with  sickness 
and  fever.  The  rash  is  uniformly  distributed  and  typically  morbilliform. 
If  the  temperature  does  not  come  down  to  normal,  the  case  should 
be  rather  regarded  as  one  of  recrudescence.  Second  attacks  are  rare  and 
iisually  mild.  There  may  be  no  rash,  except  buccal  spots,  or  merely  a 
fleeting  eruption.  The  accuracy  of  the  diagnosis  is  confirmed  by  the 
infection  of  other  children.  Many  such  cases  are  due  to  error  in  diagnosis 
of  the  first  or  second  outbreak. 

Children  who  have  recently  had  measles  are  more  liable  to  whooping 
cough,  influenza,  diphtheritic  infection  of  the  skin  and  mucous  membranes, 
and  tuberculosis. 

Treatment. — The  child  must  be  kept  in  bed  until  the  temperature  has 
been  down  for  at  least  3  days,  and  indoors  for  3  weeks  unless  it  is  warm 
weather.  The  ordinary  nursing  precautions  and  treatment  for  fever  must 
be  adopted.  Keep  the  room  at  60°  F.  and  well  ventilated.  On  account 
of  the  eye  irritation  it  should  be  darkened,  or  the  cot  screened  from  light 
and  draughts.  Use  boric  acid  lotion,  2  per  cent.,  for  the  eyes  and  borated 
vaseline  for  the  nose.  The  mouth  and  nostrils  must  be  kept  clean,  the 
face  and  hands  washed  daily,  and  the  body  sponged  between  warm  blankets. 
Hot  drinks  and  a  hot  bath  bring  out  the  rash.  The  diet  must  consist  of 
suitably  diluted  milk  and  carbohydrate  foods,  and  no  fruit  should  be 
allowed  until  the  risk  of  diarrhoea  is  over.  The  pulmonary  catarrh  is  treated 
on  the  ordinary  lines  of  bronchitis,  if  it  is  severe.  Other  treatment  is 
symptomatic  and  directed  to  the  relief  of  nervous  symptoms,  cardiac 
weakness  and  severe  dyspnoea.  Dyspnoea  generally  depends  on  dilatation 
of  the  right  side  of  the  heart.  During  desquamation  a  warm  bath  is  given 
daily  and  the  skin  oiled  with  eucalyptol  or  carbolic  oil,  1  in  40.  Good  food, 
cod-liver  oil  and  iron,  and  general  care  are  very  important  during 
■convalescence. 


950  Chapter  LXVIL 

The  Prevention  of  Measles. — Children  should  be  excluded  from  schools 
until  5  years  of  age.  Over  this  age  75  per  cent,  of  London  school  children 
are  protected,  and  the  mortality  is  small  among  those  who  contract  tin- 
disease.  Prompt  notification  is  of  value,  provided  that  a  class  is  closed  for 
16  days  as  soon  as  the  first  case  appears.  If  an  epidemic  is  prevalent,  every 
school  child  with  cough,  sneezing  or  redness  of  the  eyes,  should  be  sent 
home.  All  the  children  should  be  examined  daily  for  buccal  spots.  Contacts 
should  be  quarantined  for  16  days,  and  kept  from  school  for  21  days. 

Cases  must  be  well  isolated  and  put  under  medical  care.  Other 
children  must  be  excluded  from  the  house.  No  child  should  be  allowed  to 
mix  with  others  for  a  month  after  the  onset  of  the  disease. 

Erythema  Infectiosum. — Syn.  :  Fifth  Disease — E.  infectiosum  mor- 
billiforme — E.  simplex  marginatum — Megalerythemaepidemicum. — EschericL 
claimed  this  as  a  new  exanthem  in  1896.  It  is  a  feebly  contagious  disease 
with  slight  subjective  symptoms  and  a  maculo-papular,  rose-red  rash,  most 
marked  on  the  cheeks,  legs  and  outer  surface  of  the  arms.  Epidemics  occur 
in  families  and  schools,  most  often  in  spring  or  summer.  The  common  age 
is  4-14  years.  The  incubation  period  is  6-14  days.  The  rash  is  usually 
the  first  sign.  It  may  be  preceded  by  slight  malaise,  sore-throat  and 
debility.  It  only  affects  the  skin,  and  comes  out  first  and  characteristically 
on  the  face. 

The  cheeks  present  a  symmetrical,  confluent,  rose-red  efflorescence,  with 
defined,  slightly  raised  edges  or  shading  off  into  normal  skin,  rather  sharply 
limited  by  the  naso-labial  folds  and  the  temples,  and  extending  to  the 
angles  of  the  jaw.  The  skin  is  hot  and  swollen,  and  does  not  itch.  Its 
colour  suggests  erysipelas  and  disappears  on  pressure.  Discrete  spots  are 
often  seen  on  the  forehead,  chin,  and  about  the  ears.  On  the  second  day 
the  rash  appears  on  the  body,  chiefly  the  extensor  surface  of  the  limbs  and 
spreading  peripherally,  the  trunk  being  almost  free.  On  the  limbs  it  is 
more  morbilliform  and  less  rose-red.  In  many  cases  it  has  a  lace-work 
aspect.  About  the  elbows  it  becomes  confluent.  On  the  buttocks  it  is 
marked.  It  is  more  macular  than  papular,  and  shows  little  elevation 
except  on  the  face.  It  disappears  from  the  face  hi  4-5  days  and  from 
elsewhere  in  6-12  days.  The  colour  fades  from  the  centre  first  and  leaves 
red  irregular  rings  visible  for  a  time,  the  skin  assuming  a  "  geographical 
map  "  or  "  marbled  "  aspect  (cutis  marmorata).  Subjective  symptoms 
and  complications  are  rare.  Perhaps  there  is  slight  fever  for  24  hours, 
and  a  tongue  furred  but  never  like  that  of  scarlatina.  There  is  no  coryza, 
cough,  conjunctivitis,  glandular  enlargement,  desquamation  or  pigmentation. 

It  is  apparently  perfectly  harmless,  but  leads  to  unnecessary  isolation 
of  the  child  and  expense  to  the  parents  if  mistaken  for  scarlet  fever  or 
measles.  The  child  should  be  kept  in  bed  while  feverish  and  isolated 
until  the  rash  has  gone. 


CHAPTER    LXVIII. 

SPECIFIC    FEVERS. 

Varicella —  Vaccinia —  Variola. 

VARICELLA. — Syn.  :  Chicken  pox — Glass  pox. — This  is  an  infectious 
disease  characterised  by  the  eruption  of  a  papulo-vesicular  rash  and  slight 
constitutional  disturbance.  It  is  sometimes  so  severe,  especially  in  adults, 
as  to  simulate  small  pox.  One  attack  produces  almost  complete  immunity. 
It  may  occur  at  any  age  and  has  been  transmitted  to  the  foetus  in  utero. 
It  is  infectious  from  the  onset  of  the  rash  and  while  it  is  out.  Epidemics 
are  sometimes  extensive.  The  contagium  has  not  been  isolated 
although  it  is  present  in  the  pocks,  for  the  disease  has  been  inoculated  from 
them  with  difficulty.  Probably  it  is  conveyed  aerially  and  at  times  by 
intermediaries.     The  virus  is  easily  destroyed  under  favourable  conditions. 

The  incubation  period  is  from  14-17  days.  Most  cases  begin  on  the 
fifteenth  day  ;   a  few  on  the  thirteenth  or  not  until  the  nineteenth  day. 

Symptoms. — Prodromal  symptoms  are  slight  or  absent.  Occasionally 
there  is  a  scarlatiniform,  purpuric  or  morbilliform  rash  which  fades  soon 
after  the  pocks  appear  ;  sometimes  a  little  fever,  headache  and  general 
malaise;  epistaxis  not  infrequently  ;  and  perhaps  colic,  vomiting,  and  pain 
in  the  joints  and  back.  Often  the  rash  is  the  first  sign.  The  temperature 
rises  to  101-102°  F.,  rarely  to  104-105°  F.  It  is  synchronous  with  the 
rash,  highest  as  the  rash  reaches  its  maximum,  proportionate  to  its  severity. 
and  falls  as  it  fades.  Its  duration  varies  from  a  few  hours  to  5  days,  or  it 
may  be  prolonged  by  sepsis.  The  constitutional  symptoms  depend  on 
the  degree  of  fever.  Delirium  is  exceptional.  Epistaxis  may  be  due  to 
vesicles  in  the  nose. 

The  rash  is  superficial  and  comes  out  on  the  first  day,  within  24  hours 
of  the  onset.  It  appears  first  on,  and  may  be  limited  to,  the  trunk. 
Occasionally  it  begins  on  the  face  and  spreads  to  the  trunk  and  extremities  : 
or  on  the  scalp,  face  and  trunk  simultaneously.  It  is  generally  most  profuse 
on  the  hairy  parts  and  those  covered  up.  It  is  marked  on  the  trunk,  notably 
the  back,  and  usually  spares  the  hands  and  forearms.  On  the  extremities 
it  may  be  limited  to  a  few  shotty  papules.  Occasionally  it  is  vesicular  from 
the  onset,  looking  like  drops  of  clear  water  on  the  skin,  without  any  evidence 
of  local  inflammation.  Most  commonly  it  starts  as  discrete,  small  macules 
or  papules  with  a  surrounding  red  areola.  Some  papules  abort  or  persist, 
while  most  of  them  become  vesicular,   forming  clear  vesicles  on  a  red 


952  Chapter  LXVIII. 

base  which,  is  never  papular.  The  vesicles  are  very  thin-walled,  and  vary 
in  size  from  a  pin  head  to  £-  in.  or  more  in  diameter.  They  are  formed  within 
a  few  hours  and  attain  their  full  development  in  6-24  hours,  being  then  as 
large  as  those  of  variola  at  the  end  of  4-5  days.  They  are  generally  uni- 
locular and  easily  evacuated,  but  evacuation  is  not  a  reliable  diagnostic 
feature.  They  are  circular  on  the  scalp  and  limbs,  irregularly  round  on  the 
face,  and  elliptical,  oval  or  circular  on  the  trunk.  At  first  their  contents  are 
translucent,  then  somewhat  sero-purulent.  In  2  days  they  dry  up  in  the 
centre,  becoming  somewhat  umbilicated,  and  form  scabs.  Both  primary  and 
secondary  umbilication  may  occur.  The  scabs  dry  up  and  fall  off  in 
1-3  weeks,  leaving  an  occasional  scar. 

The  rash  comes  out  in  successive  crops,  every  3  or  4  days,  and  is 
therefore  found  in  all  stages.  In  number  the  pocks  vary  from  1  or  2  to  a 
copious  rash  all  over  the  body.  In  marked  cases  they  are  present  on  the 
scalp,  the  mucous  membrane  of  the  mouth,  and  even  the  conjunctival  and 
vulvar  mucosa.  The  degree  of  pustulation  depends  on  the  severity  of  the 
infection,  the  constitutional  state,  scratching  and  local  infection.  Sometimes 
it  is  as  severe  as  in  variola,  and  the  rash  may  become  confluent.  Irritation 
may  be  intense,  especially  under  clothing  exerting  local  pressure. 

V.  sine  varicellis  can  occur,  a  prodromal  rash  alone  being  present. 

V.  bullosa. — In  a  few  days  large  bullae  form,  even  3-4  ins.  diameter.  It  is 
not  serious.  V.  hcemorrhagica  is  rare.  The  vesicles  may  be  few,  or 
multiple  and  confluent.  The  bleeding  takes  place  into  the  tissues  at  the 
base  of  the  pocks,  into  the  skin,  and  perhaps  from  the  mucous  membrane 
of  the  eyes,  mouth  or  alimentary  tract.     Fever  and  toxaemia  are  present. 

V.  gangrenosa  or  gangrenous  dermatitis. — These  two  conditions  are 
not  identical  but  v.  gangrenosa  is  essentially  a  gangrenous  dermatitis.  In 
unhealthy  infants,  exceptionally  in  those  apparently  strong  and  healthy, 
the  vesicles  become  pustules,  the  suppuration  extends  deeply,  superficial 
scabs  form  and  separate,  and  leave  cleanly  cut,  punched  out  ulcers  with 
black  gangrenous  sloughs  at  the  bottom.  Occasionally  hremorrhage  occurs 
into  the  vesicles  and  the  base  is  much  inflamed.  These  ulcers  and  gan- 
grenous spots  may  coalesce,  involve  a  large  area,  extend  to  the  fascia  and 
muscles,  give  rise  to  secondary  adenitis  and  abscess,  and  usually  end 
fatally.  The  process  may  be  limited  to  a  few  spots.  A  similar  affection 
may  follow  vaccination,  echthyma  and  pemphigus.  In  varicella  these 
ulcers  are  most  common  on  the  chest,  in  vaccinia  on  the  arms,  and  in 
echthyma  or  the  buttocks. 

Complications  and  Sequels. — Scarring  is  generally  trivial.  A  few  scars 
are  left  by  an  attack  of  medium  severity,  usually  on  the  face  after  a  severe 
pustular  rash.  Other  complications  depend  on  the  rash  and  secondary 
infection,  viz.,  slowly  healing  sores,  furuncles,  abscess,  osteomyelitis, 
pyseinia,  suppurative  phlebitis,  pericarditis,  pleurisy,  otitis,  gangrene  of 
the  legs,  and  erysipelas  ;    retention  of  urine,  due  to  a  pock  in  the  urethra 


Vaccinia.  953 

aind  swelling  of  the  prepuce  (Coombs,  1905)  ;  laryngitis  and  tracheitis 
<(varicellar  croup),  broncho-pneumonia  ;  stomatitis,  tonsillitis,  conjunc- 
tivitis and  vulvitis,  and  secondary  infections  of  these  regions  ;  encephalitis 
.and  its  sequels ;  serous  or  suppurative  arthritis ;  and  even  cerebral 
hcemorrhage,  ascribed  to  a  pyoemic  embolus  in  a  boy  13  years  old  (Maitland 
Thompson,  1898).  Keratitis,  perforation  of  the  soft  palate,  and  Raynaud's 
<lisease  have  been  recorded  as  sequels.  Nephritis,  latent,  slight  or  severe, 
is  sometimes  a  late  complication,  coming  on  in  15-21  days. 

Diagnosis. — The  age  of  the  patient,  presence  of  vaccination  scars, 
successive  crops  of  rash,  characteristic  vesicles  and  surrounding  areola?, 
and  the  rash  on  the  scalp  and  mucous  membranes  are  the  chief  diagnostic 
features.  From  variola  it  is  distinguished  by  the  mild  or  absent  prodromal 
period,  mild  character,  the  distribution,  early  appearance  and  rapid  vesicu- 
lation  of  the  rash,  unilocular  vesicles,  absence  of  umbilication  except 
during  crusting,  and  polymorphism,  several  stages  of  the  rash  being  present 
•on  a  limited  area  of  skin.  A  severe  attack  may  be  more  like  variola  than 
modified  small  pox  is.  In  urticaria  there  may  be  transparent  vesicles,  the 
prurigo  varicelli  forme  of  Hutchinson,  but  they  are  situated  on  a  papular 
base,  there  is  no  fever,  and  the  itching  is  intense.  Pemphigoid  bulla?  are 
much  larger  and  sero-sanguineous.  Varicella  may  assume  a  pemphigoid 
form  in  the  newborn.  The  vesicular  rash  of  congenital  syphilis  is  associated 
with  squama?  and  other  signs.  The  scarlatiniform  prodromal  rash  is 
unaccompanied  by  sore-throat  and  vomiting  of  scarlatina.  These  diseases 
may  be  coincident,  but  are  very  unlikely  to  be  simultaneous  in  onset. 

Prognosis  is  excellent.  The  disease  is  often  so  mild  as  not  to  require 
treatment.  Fatal  cases  without  complications  have  been  reported  in  a 
healthy  girl,  8  months  old,  from  severe  and  extensive  rash  (Nisbet,  1894), 
and  in  a  child  (Furbringer,  1896).  A  purpuric  prodromal  rash,  with 
hemorrhages  from  the  mucous  membranes,  is  likely  to  prove  fatal. 

Treatment. — Keep  the  nails  short  to  prevent  scratching.  For  its  relief 
•order  lukewarm  baths,  vinegar  and  water,  dusting  powder,  carbolised  oil  or 
vaseline,  or  ichthyol  1  in  50  of  vaseline.  Use  iodoform  for  gangrenous  cases. 
Attend  to  the  mouth  and  genitals.  Adopt  the  usual  measures  in  the 
treatment  of  fever  and  isolate  the  child  until  the  crusts  have  dropped  off. 


VACCINIA. 

Sijn.  :      Vaccination — Cow-pox. 

The  inoculation  of  cow-pox,  attenuated  small-pox,  produces  fever, 
general  malaise  and  a  local  eruption  of  pocks,  an  affection  known  as 
vaccinia.     "Vaccination"    is  the  process  of  inoculation.     Vaccinia  is  not 


954  Chapter  LXVIII. 

infectious  but  is  directly  communicable  by  inoculation.  A  mother  or 
nurse  may  develop  a  vaccine  pock  on  the  lip,  chin,  cheek,  occipital 
region  of  scalp,  hand,  mamma?,  etc.,  through  direct  infection  by  the 
contents  of  a  vaccine  pustule  or  from  infected  towels,  etc.  Accidental 
vaccination  almost  invariably  produces  a  single  pock,  "which  may  be 
mistaken  for  a  chancre  or  malignant  pustule.  It  causes  adenitis  and 
leaves  a  scar. 

Vaccination  protects  absolutely  from  variola  for  a  period  of  time  vary- 
ing with  the  extent  of  the  vaccination  and  the  degree  of  immunity  produced. 
It  is  essential  in  all  countries  where  small-pox  exists.  Efficient  vaccina- 
tion in  infancy,  combined  with  re-vaccination  about  puberty  and  10  years 
later,  will  completely  protect  most  individuals  throughout  life.  On 
exposure  to  infection,  as  in  the  case  of  doctors  and  nurses,  re-vaccination  is 
advisable  if  5  years  have  elapsed  since  the  last  efficient  vaccination.  In 
countries  where  vaccination  and  re-vaccination  are  strictly  enforced, 
small-pox  is  practically  non-existent.  In  countries,  where  sentimental 
objections  to  inoculation  and  so-called  interference  with  the  rights  of  the 
subject  are  allowed  undue  weight,  as  in  Great  Britain,  outbreaks  of  the 
disease  are  not  infrequent.  The  risks  are  those  incidental  to  any  scratch, 
together  with  those  special  to  the  lymph  which  may  perchance  be 
contaminated. 

Vaccine  is  lymph  prepared  from  healthy  calves  under  strict  pre- 
cautions to  prevent  contamination.  It  is  supplied  in  tubes  or  on  ivory 
points,  and  is  glycerinated  to  inhibit  and  eliminate  non-spore-bearinst 
organisms.  The  use  of  calf  lymph  obviates  the  trivial  risk  of  conveying 
congenital  syphilis,  when  using  human  lymph.  Erysipelas  and  other 
pyogenic  infections  were  said  to  be  spread  by  human  lymph.  Unfortunately 
some  of  these  risks  are  still  present.  The  fear  of  tuberculosis  can  be 
disregarded,  for  the  calf  is  killed  to  see  that  it  is  healthy.  Yet  calf  lymph 
has  been  known  to  spread  tetanus,  and  cannot  be  guaranteed  free  from 
pus-producing  organisms.  Considerable  pustulation  is  often  produced, 
perhaps  due  to  the  presence  of  staphylococci  in  the  lymph,  the  skin,  or  on 
unclean  instruments,  etc.  Further,  it  is  impossible  to  estimate  accurately 
the  strength  of  the  vaccine,  as  it  cannot  be  standardised,  and  the  same 
vaccine  produces  different  effects  on  different  individuals. 

Age  for  Vaccination. — It  must  be  done  before  the  age  of  6  months, 
unless  a  medical  certificate,  of  postponement  or  an  exemption  order  is 
obtained.  In  Germany  the  limit  is  2  years.  The  objection  to  a  late  age 
limit  for  compulsory  vaccination  is  the  difficulty  in  tracing  the  children. 
The  earlier  the  operation  is  done,  the  fewer  are  the  constitutional  symptoms 
and  the  less  the  discomfort  of  the  baby.  In  the  first  week  of  life  it  is 
borne  best  of  all.  During  the  first  2  months  there  is  little  upset.  After  • 
6  months  the  disturbance  is  more  marked  and  the  fever  often  considerable. 
The  drawback  to  early  vaccination  is  that  every  subsequent  rash  is  ascribed 


Vaccinia.  955 

to  it.  The  rashes  of  congenital  syphilis,  intertrigo  and  eczema  etc.  are  apt 
to  develop  about  3-6  weeks  of  age.  Moreover,  malnutrition  from  bad 
feeding  becomes  evident  about  the  third  or  fourth  month  of  life.  Hence, 
if  a  baby  is  delicate  or  ill-nourished,  if  the  skin  suggests  a  liability  to  disease, 
or  if  there  is  a  suspicion  of  congenital  syphilis,  it  is  advisable  to  postpone  the 
operation.  As  a  rule,  it  should  be  done  about  the  end  of  the  first  month, 
provided  the  child  is  well  and  gaining  weight  satisfactorily.  If  postponed,  it 
should  be  done  when  the  weather  is  reasonably  cool  and  when  the  child 
is  not  teething. 

Mode  of  Operation. — Choose  the  left  arm  at  the  level  of  the  insertion 
of  the  deltoid  muscle,  or  the  left  leg  about  the  middle  of  the  outer  half  of 
the  calf.  There  is  no  objection  to  the  latter  site  in  infants,  if  it  is  protected 
from  becoming  soiled  by  excreta.  Wash  the  skin  thoroughly  with  soap  and 
water,  and  dry  by  rubbing  vigorously  with  a  clean  towel.  Expel  the 
vaccine  gently  on  to  the  skin,  using  an  india-rubber  bulb  attachment  to  the 
tube  in  preference  to  the  mouth,  and  insert  it  by  scratching  obliquely  with 
a  clean  needle.  For  each  insertion  make  a  few  downward  and  transverse 
scratches,  sufficiently  deep  to  cause  the  appearance  of  blood,  while  keeping 
the  skin  stretched  by  means  of  the  hand  which  holds  the  arm.  A  total 
area  of  about  half  a  square  inch  should  be  inoculated.  Three  insertions 
are  enough,  if  of  suitable  size.  A  great  deal  of  trouble  arises  from  inefficient 
vaccination.  Public  vaccinators  make  3-5  insertions,  and  competing  general 
practitioners  tempt  the  public  by  offering  "  one-mark "  vaccination. 
To  this  there  is  no  objection  if  it  is  done  thoroughly,  but,  if  only  a  small 
area  of  skin  is  inoculated,  the  protection  afforded  is  insufficient  and 
vaccination  as  a  protective  measure  is  brought  into  disrepute.  It  is  best 
to  make  3  or  4  insertions,  each  about  as  big  as  a  3d.  piece,  rather  than 
one  large  one.  Large  areas  produce  large  pustules  and  large  sores,  if  the 
scabs  get  rubbed  off  or  infected.  A  similar  result  ensues  from  the  coales- 
cence of  smaller  areas  too  close  together.  The  size  of  the  scar  is  not  a 
reliable  measure  of  the  degree  of  protection,  for  it  may  depend  on 
suppuration. 

During  the  operation  the  child  cries  from  the  restraint  of  movement, 
rather  than  from  actual  pain.  As  soon  as  the  lymph  is  dry,  a  pad  of 
protective  antiseptic  gauze  is  strapped  on.  This  is  not  essential  if  the 
babe  is  properly  nursed  and  looked  after,  but  it  is  a  safeguard  against 
infection.  Clean  linen  is  a  cool  and  satisfactory  dressing  ;  wet,  greasy  and 
adherent  dressings  favour  rupture  of  the  pustules.  The  drawback  to 
protective  dressings  is  that  considerable  suppuration  niav  take  place 
underneath  without  attracting  attention.  The  skin  must  not  be  washed 
for  12  hours  after  vaccination. 

Course  and  Symptoms.— The  scratch  heals  quickly.  On  the  third  to 
hfth  day  the  site  become  red  and  swollen.  One  or  more  vesicles  appear, 
coalesce,  are  fullv  formed  bv  the  seventh  to  ninth  day,  and  have  a  swollen 


'956  Chapter  LXVIII. 

red  areola.  The  areolae  of  neighbouring  pocks  often  coalesce  and  the 
umbilicated  vesicles  stand  out  on  a  swollen  red  base.  The  main  vesicles 
•are  sometimes  surrounded  by  smaller  ones.  The  corresponding  lymph 
nodes  are  enlarged  and  tender.  In  2-3  more  days  the  inflammatory  process 
subsides  and  the  vesicles  gradually  dry  up  into  scabs,  or  burst  and  discharge 
a  sero-purulent  fluid.  The  swelling  subsides,  scabs  form  and  drop  off 
in  1-3  weeks  (3-4  weeks  from  the  onset),  and  reddish  scars  are  left  which 
become  bluish-white,  white,  and  finally  foveated  or  honeycombed  and 
depressed. 

In  severe  cases  the  swelling  is  extensive,  perhaps  down  to  the  elbow 
or  involving  the  whole  limb,  and  there  is  much  pain  and  constitutional 
disturbance,  viz.  fever,  restlessness,  sleeplessness,  anorexia  and  malaise. 
The  pustule  rapidly  enlarges  and  the  local  inflammation  spreads  deeply 
into  the  subcutaneous  tissues,  forming  an  ulcer  of  variable  depth  which 
takes  several  weeks  to  heal.  All  the  ulcers  may  coalesce  or  black  sloughs 
may  form  at  the  bottom  of  each.  The  worst  cases  are  those  which  are  the 
-most  septic,  not  the  best  vaccinated  and  by  no  means  the  best  protected. 

The  fever  develops  with  the  appearance  of  the  vesicle,  about  the  third 
to  the  fifth  day,  and  attains  its  maximum  of  100-101°  F.,  occasionally 
105°  F.,  with  the  maturation  of  the  pock  about  the  ninth  or  tenth  day, 
then  slowly  subsiding.  It  usually  lasts  from  three  to  five  days,  and  may 
be  absent.     The  axillary  glands  are  often  enlarged. 

Insusceptibility  is  rare.  Failures  are  due  to  inert  lymph,  inefficient 
operation,  the  production  of  too  much  bleeding  which  washes  away  the 
vaccine,  washing  the  skin  after  inoculation,  and  occasionally  to  anaemia 
•or  the  incubation  of  a  specific  fever.  No  child  can  be  regarded  as  insus- 
ceptible unless  there  have  been  three  complete  failures  with  different 
brands  of  lymph.  An  interval  of  a  month  should  elapse  between  each 
vaccination  for  even  inert  lymph  may  cause  a  certain  local  immunity. 
Inert  lymph  may  produce  bullae  which  leave  no  scars,  instead  of  pocks 
(vaccinia  pemphigoides).  Partial  failures  are  due  to  similar  causes  as 
complete  ones.  One  or  more  inefficient  pocks  are  produced  and  cause 
further  attempts  to  fail.  Such  a  child  is  imperfectly  protected  and  should 
be  re-vaccinated  at  6-7  years  of  age. 

In  rare  instances  the  latent  period  lasts  for  10-16  days,  after  which  the 
"vaccinia  runs  a  normal  course.  This  is  probably  due  to  defective  lymph. 
Washbourn  (1902)  reported  a  case  of  latent  vaccinia,  the  pocks  coming  out 
■during  scarlatina  2  years  after  vaccination  in  which  only  one  place  took 
and  that  very  slightly.  Latency  has  also  been  recorded  of  2  months 
duration  (Brierly),  4-5  months  (Metail),  one  year  (G.  Harley),  and 
14  years  (Sir  T.  Watson). 

Complications. — Extra  vesicles,  bullae,  ulcers  with  indurated  bases,  and 
gangrene  have  been  noted  as  local  abnomalities.  Suppuration,  ulceration 
and  lymphangitis,  with  secondary  adenitis  and  perhaps  abscess,  are  due  to 


Vaccinia.  95T 

pyogenic  organisms  in  the  lymph,  and  infection  at  operation  or  subsequent 
to  rupture  of  the  pock.  Vesicles  are  liable  to  get  rubbed,  broken  and 
infected.  The  local  process  may  end  in  gangrenous  dermatitis 
(v.  gangrenosa).  Suppurative  adenitis  is  not  uncommon.  Pyaemia  is  not 
unknown.  Tetanus  is  usually  due  to  contaminated  lymph,  probably 
through  the  glycerine.  Occasionally,  like  erysipelas,  it  results  from 
secondary  infection. 

Secondary  vaccinia  arises  from  rupture  of  the  pocks  and  accidental 
infection.  It  is  possible  up  to  the  ninth  or  tenth  day.  Multiple  pocks 
are  produced  down  the  arm  and  forearm,  and  sometimes  on  other  parts 
of  the  body.  Generalised  vaccinia  is  due  to  blood  infection  or  auto-inocu- 
lation. It  begins  on  the  eighth  day.  The  rash  is  symmetrical,  scattered 
all  over  the  body,  and  may  resemble  variola  or  vary  in  character,  suggesting^ 
erythemata,  urticaria  or  measles.  Occasionally  a  lichen  comes  out  in 
crops  of  small,  red,  conical  papules  about  the  end  of  the  first  week,  and 
may  become  vesicular  or  even  pustular.  Possibly  some  of  these  rashes  are 
toxic  or  co-incident,  or  are  analogous  to  serum  rash.  If  there  is  pyogenic 
infection  and  suppuration,  the  usual  sequels  of  these  may  arise.  In  one 
instance  encephalitis,  ending  in  microcephalic  idiocy,  appeared  due  to  this 
cause.     A  few  cases  of  nephritis  are  on  record. 

The  Effect  on  other  Diseases.— Vaccination  during  the  incubation 
period  of  variola  runs  a  typical  course  and  renders  it  milder.  The 
paroxysms  of  pertussis  disappear  as  the  pocks  develop.  Vaccinia  seems 
to  render  bronchitis  and  broncho-pneumonia  less  severe.  It  does  not 
increase  the  virulence  of  scarlatina  or  measles,  but  may  be  delayed  until 
defervescence,  and  may  become  confluent  and  sloughing.  It  is  sometimes 
decidedly  beneficial  to  existing  rashes,  does  not  make  eczematous  con- 
ditions worse,  yet  is  supposed  to  excite  dormant  eczema  and  impetigo. 
Its  effect  on  gastro-enteric  affections  is  unfavourable.  Small  nsevi  can  be- 
cured  by  vaccinating  them. 

Prognosis. — In  healthy  children  normal  vaccination  produces  no 
ill  effects.  It  does  not  impair  vitality  or  contribute  to  mortality.  Death 
is  rare  and  almost  invariably  due  to  erysipelas,  cellulitis  or  pysemia  from 
dirt  or  neglect.  I  have  never  seen  syphilitic  or  tuberculous  infection  of 
the  wound.  Keloid  and  hypertrophic  scars  are  uncommon.  The  mortality 
is  higher  among  unvaccinated  than  vaccinated  babies,  probably  because 
debility  leads  to  postponement. 

Treatment. — Attend  to  local  and  general  cleanliness,  and  keep  the 
bowels  open.  Protect  the  pocks  from  injury.  Wire  shields  are  unsafe 
for  they  are  often  dirty,  are  handed  on  from  child  to  child,  and  by  keeping 
the  parts  moist  and  warm  favour  rupture.  For  local  inflammation  powder 
freely,  apply  lead  lotion  or  cold  water  compresses  every  J  hour,  and  keep 
the  limb  at  rest.  In  ordinary  cases  dust  with  boric  acid  before  or  when 
the  pocks  burst,  and  use  antiseptic  fomentations  and  iodoform  for 
suppuration  and  ulceration. 


•958  Chapter  LX  VIII. 

VARIOLA. 

Syn.  :  Smallpox. 

This  affection  differs  little  in  unvaccinated  children  from  the  disease 
in  adults  and  is  rare,  except  when  there  is  an  epidemic.  The 
nature  of  the  virus  in  vaccinia  and  variola  is  uncertain.  According 
lo  Klein  and  Copeman  it  is  a  spore-bearing  bipolar  bacillus.  A 
parasite  in  the  form  of  spores,  sporidium  or  amoeba,  encysted  parasite 
.and  morula  body,  has  been  described.  Guarnieri  gave  these  bodies  the 
name  Cytoryctes  variola?.  In  vaccinia  they  do  not  reach  as  full  develop- 
ment. According  to  Funk  of  Brussels  they  are  present  in  human  and 
-glycerinated  calf  lymph,  and  in  the  skin  during  the  incubation  stage.  They 
must  be  sought  in  hanging  drop  preparations. 

Congenital  variola  does  not  vary  directly  in  severity  with  the  virulence 
in  the  mother.  The  pustular  stage  is  of  the  same  character  as  after  birth 
but  the  pustules  are  usually  larger.  Apparently  the  course  may  be  much 
prolonged.  It  has  been  said  to  have  been  transmitted  by  an  infected  father, 
the  mother  showing  no  signs  of  the  disease,  but  this  is  improbable. 

Variable  Severity. — The  virulence  of  the  disease  depends  on  racial  and 
family  resistance  ;  acquired  immunity,  from  intra-uterine  infection  or  the 
transmission  of  immunity  from  the  mother  to  the  foetus  ;  age,  being  most 
severe  under  1  and  over  30  and  mildest  about  10  years  of  age  ;  and  nutrition, 
the  fat  having  pocks  which  are  large  and  run  a  typical  course,  while  in  the 
lean  and  ill-nourished  they  often  abort.  The  social  status  has  little  influence. 
Antecedent  varicella  is  supposed  to  attenuate,  and  scarlet  fever  and 
diphtheria  to  exaggerate  the  severity  of  the  attack.  Small-pox  may  be 
very  mild  in  some  unvaccinated  children,  for  there  is  always  a  small 
percentage  of  insusceptibility.  It  is  mild  in  the  vaccinated  in  whom 
immunity  is  waning.  The  type  varies  in  different  epidemics  and  is  less 
severe  toward  the  end  of  an  epidemic. 

Variola  sine  variolis  is  not  rare  in  the  vaccinated.  More  often  one  or 
two  pocks  are  present.  In  unmodified  cases  the  number  varies  from  a  few 
hundred  to  thousands.  In  modified  variola  there  are  less  than  20.  It  is 
often  called  varioloid.  The  incubation  period  is  13  full  days  and  the  first 
symptoms  appear  on  the  fourteenth  day.  It  must  be  regarded  as  infectious 
from  the  onset  until  the  complete  separation  of  the  scabs. 

Symptoms. — In  varioloid  the  patient  is  "  out  of  sorts  "  or  "off  his 
food  "  for  a  day  before  the  eruption  comes  out.  Or  there  may  be  epigastric 
pain,  vomiting  and  slight  fever  for  a  day.  Occasionally  there  is  a  prodromal 
scarlatiniform  rash.     The  eruption  comes  out  on  the  second  day.     It  is 


Variola.  959 

•distributed  irregularly  in  infants,  and  may  be  limited  to  the  thighs  and 
buttocks.  The  rash  frequently  does  not  pass  beyond  the  papular  stage, 
and  the  child  may  be  free  from  scabs  in  14  days. 

Severe  attacks  are  ushered  in  by  headache,  chilliness  or  rigors,  great 
backache,  nausea,  anorexia,  vomiting,  vertigo,  malaise  and  fever.  The 
vomiting,  sacral  pain  and  high  temperature  are  the  most  characteristic 
features.  Incontinence  of  urine  and  faeces  is  not  infrequent.  Initial 
symptoms  appear  early,  are  marked,  and  may  be  as  severe  in  mild  or 
modified  cases  as  in  the  unvaccinated.  Convulsions,  delirium  and  stupor 
may  be  present. 

Prodromal  rashes  are  probably  vasomotor  in  origin  and  due  to  toxsernia. 
They  are  rare  under  10  years'of  age,  and  are  scarlatiniform,  morbilliform  or 
purpuric.  They  appear  first  in  the  inguinal  regions,  sometimes  in  the 
axillary  or  submammary.  The  scarlatiniform  or  "lobster"  rash  is  a 
uniform  brilliant  redness,  rarely  punctate.  It  comes  out  on  the  second  or 
third  day,  is  partial  or  general,  brick-red  in  colour  and  becomes  dusky  or 
purplish  in  the  flexures.  It  is  most  common  in  the  groins,  flanks  and 
.axilla,  rare  on  the  neck  and  chest,  and  may  be  present  on  the  face.  It 
is  of  bad  prognosis  and  may  be  associated  with  pufnness  of  the  face,  sub- 
conjunctival ecchymoses,  multiple  haemorrhages  and  blood  blisters.  A 
less  common  and  unimportant  type  is  a  punctate  rash  with  little  erythema. 
The  purpuric  rash  takes  the  form  of  small,  pin-head  petechias,  usually  on  the 
lower  part  of  the  abdomen. 

The  true  rash  appears  on  the  third  or  fourth  day  and  is  preceded  by 
invisible,  shotty,  subcutaneous  nodules.  It  consists  of  small  red  papules 
and  is  most  marked  on  the  face,  arms  and  legs,  especially  the  backs  of  the 
wrists  where  it  feels  like  shotty  papules.  It  comes  out  first  on  the  chin 
•or  forehead,  is  more  profuse  on  the  back  than  the  chest  or  abdomen,  and 
appears  on  the  palate  and  mucous  membranes.  The  papules  are  large  and 
become  vesicular.  The  vesicles  are  round  or  pea  shaped,  not  oval  like  many 
varicella  vesicles,  and  take  4-5  days  for  full  development.  They  are 
multilocular,  umbilicated,  filled  with  clear  serum,  and  do  not  collapse  on 
puncture.  They  may  become  dome  shaped  when  pustular.  By  the 
■eighth  day  the  rash  is  distinctly  pustular  and  then  the  pocks  enlarge,  each 
being  situated  on  a  swollen  inflamed  base  with  a  deep  red  areola.  In 
another  3  days  the  contents  of  the  pocks  are  discharged  and  scabbing 
•commences. 

Thus  the  average  sequence  of  events  is  eruption  of  papules  on  the 
third  day,  vesiculation  on  the  sixth,  pustulation  on  the  ninth,  and  the 
■commencement  of  scabbing  on  the  twelfth  day. 

The  temperature  rises  at  the  onset,  and  falls  on  the  appearance  of  the 
rash,  often  to  normal  when  the  rash  is  fully  out,  but  only  to  about  100°  F. 
if  it  is  confluent.  It  rises  again  as  the  contents  of  the  vesicles  become 
purulent  (maturation  fever),  and  then  slowly  subsides  in  about  another 


960  Chapter  L  XVIII. 

week.  Possibly  suppuration  depends  on  pyogenic  infection  and  can  be 
prevented  by  appropriate  treatment.  During  the  stage  of  maturation,  or 
secondary  fever,  the  constitutional  symptoms  return  and  are  proportionate 
to  the  severity  of  the  attack. 

For  complications  and  sequels  reference  must  be  made  to  the  usual 
text-books  on  medicine. 

Diagnosis. — It  is  of  the  utmost  importance  to  distinguish  between 
chicken  pox  and  modified  small  pox.  At  the  onset  it  may  be  mistaken  for 
influenza,  typhus  fever,  scarlet  fever,  measles,  varicella  or  meningitis. 
Stress  must  be  laid  on  the  suddenness  and  severity  of  the  onset  with 
headache  and  backache;  the  absence  of  throat  symptoms  and  marked 
vomiting;  and  no  catarrhal  signs  or  buccal  spots.  Prodromal  rashes  are  rare, 
whereas  scarlatina  and  measles  are  common  under  10  years.  In  measles 
the  polymorphs  in  the  blood  reach  75  per  cent,  and  the  temperature  rises 
as  the  rash  comes  out.  In  variola  the  polymorphs  fall  to  40-50  per  cent., 
and  to  15-20  per  cent,  in  heemorrhagic  types,  and  the  temperature  falls 
with  the  appearance  of  the  rash. 

Mild  variola  closely  resembles  varicella.  Good  recent  vaccination 
scars  are  strong  presumptive  evidence  against  variola.  In  varicella  the 
rash  and  fever  are  synchronous,  vomiting  and  sacral  pain  uncommon, 
mental  symptoms  are  absent,  and  the  forearms  and  hands  are  usually 
spared.  The  differences  in  the  description  of  the  rash  and  its  course  in 
the  two  diseases  must  be  noted.  In  varioloid  the  rash  is  present  in  more 
than  one  stage,  just  as  in  varicella,  many  papules  never  become  vesicles, 
others  are  vesicular  in  1-3  days,  and  umbilication  is  slight  or  absent.  Hence 
the  difference  in  these  two  affections  is  extremely  small  and,  if  small  pox  is 
prevalent,  it  is  advisable  to  regard  every  doubtful  case  as  variola,  to 
vaccinate  the  child,  and  to  isolate  it  or  send  it  to  a  small-pox  hospital. 

Prognosis. — The  severity  depends  on  the  efficiency  and  recency  of 
vaccination.  General  prodromal  rashes  are  of  bad  omen.  Local  ones  may 
be  present  in  trivial  cases.     Eruption  on  the  second  day  indicates  gravity. 

Treatment  is  essentially  the  same  as  in  adults.  The  application  of  pure 
carbolic  acid  with  a  camel's  hair  brush  to  the  vesicles  will  abort  them. 
Xylol,  m.  10-30,  given  three  times  daily  in  wine  or  milk,  is  said  to  prevent 
the  rash  coming  out  fully  and  so  stop  the  smell  and  disfiguration.  Of  these 
remedies  I  have  no  experience.  Ordinary  cases  of  modified  small-pox 
are  treated  on  the  same  lines  as  those  of  varicella.  The  bed  and  body  linen 
must  be  changed  daily  and  the  body  sponged  with  tepid  water.  Cold 
compresses  may  be  applied  to  the  face  and  hands  if  the  rash  is  copious. 
Or  the  skin  may  be  dabbed  freely  with  carbolic  oil,  1  in  40.  This  also  softens 
and  assists  the  removal  of  scabs  in  later  stages.  They  should  be  removed 
early,  by  poulticing  if  necessary,  should  pus  be  forming  underneath.  The 
rest  of  the  treatment  is  symptomatic. 


CHAPTER    LXIX. 

PERTUSSIS. 

Syn.  :    Whooping  cough — Chin   Cough. 

Whooping  cough,  an  infectious  disease,  is  characterised  by  catarrhal 
congestion  of  the  larynx  and  trachea  and  a  typical  paroxysmal  cough. 
It  may  prove  fatal  apart  from  complications  or  may  leave  permanent 
physical,  mental  or  nervous  defects.  It  is  quite  as  serious  as  scarlet  fever. 
De  Baillou  (1578)  described  an  epidemic  which  occurred  in  Paris  in  1573 
and  called  it  La  Quinta  or  Tussis  Quint  ana.  Willis  (1667)  described  it 
under  the  name  of  "  chin  cough,"  possibly  a  corruption  of  "  Quintana  " 
meaning  a  5-hourly  cough.  It  occurs  in  all  countries  and  in  epidemics, 
being  less  frequent  and  less  fatal  in  warm  climates. 

Bacteriology. — Various  organisms  are  present  in  the  sputum. 
Sprengler  andEppendorf  (1897)  found  a  gram-negative  bacillus  very  closely 
resembling  Pfeiffer's  influenza  bacillus  morphologically  and  culturally. 
Jochmann  and  Krause,  Wollstein,  Davis,  Reyler,  and  Albrecht  have 
found  a  similar  organism.  According  to  Albrecht  it  was  invariably 
present  in  200  fatal  and  70  non-fatal  cases.  Hensel  and  Czaplewski  found 
an  allied  gram-negative  bacillus.  One  of  the  experimenters  developed 
whooping  cough  during  the  investigation  and  large  numbers  of  bacilli  were 
found  in  the  sputum.  They  could  predict  whooping  cough  from  the 
presence  of  the  organism  before  the  whoop  developed.  On  the  other  hand 
the  scrum  of  patients  during  the  attack  and  in  convalescence  did  not 
agglutinate  this  bacillus.  Borclet  and  Gengou  (1906)  obtained  a  pure 
culture  of  a  very  small,  ovoid,  aerobic  bacillus,  gram-negative  and  non- 
sporing.  It  was  obtained  from  the  viscid  pellet  coughed  up,  and  sub- 
cultured  from  the  bare  places  on  the  medium  between  colonies  of  extraneous 
organisms,  for  it  grows  very  slowly.  It  was  most  abundant  on  the  fifth 
day  of  the  disease.  The  serum  of  children  recovering  from  pertussis  had  a 
marked  agglutinating  effect  on  the  organism  while  that  of  healthy  children 
had  none.  Klimenko,  a  Russian,  claims  that  he  has  obtained  this  organism 
from  the  sputum  of  5  early  cases  in  children,  and  produced  the  disease  in 
puppies  by  inoculation.  Taken  as  a  whole  the  evidence  is  in  favour  of  a 
gram-negative  bacillus  closely  allied  to  the  influenza  bacillus. 

Pathology. — The  causation  of  the  whoop  is  somewhat  doubtful. 
Probably  there  is  a  specific  laryngo-tracheitis.  It  is  a  general  infectious 
disease  which  starts  in  the  larynx  and  produces  its  characteristic  symptoms 

3    Q 


962  Chapter  LXIX. 

partly  through  the  local  conditions  and  partly  through  toxins.  According 
to  observations  made  by  von  Herff  on  himself,  a  small  pellet  of  mucus  can 
be  seen  on  the  posterior  wall  of  the  larynx  at  the  level  of  the  glottis  during 
a  paroxysm,  and  the  removal  of  this  stops  the  paroxysm.  Irritation  of  this 
part  induced  a  coughing  fit,  whereas  other  parts  could  be  touched  with 
impunity.  On  examination  with  a  spatula  a  paroxysmal  cough  may  be 
caused  from  reflex  irritation  of  the  larynx,  even  though  a  whoop  has  not 
been  noted  before.  These  facts  indicate  that  the  spasmodic  cough  is  due  to 
local  irritation  of  the  larynx  or  pharynx,  and  is  somewhat  similar  to  the 
cough  induced  by  a  crumb  going  the  wrong  way.  According  to  other 
theories  it  is  due  to  inflammation  of  the  vagus,  superior  laryngeal  or 
phrenic  nerve  ;  compression  of  nerves  by  tracheo-bronchial  structures ; 
increased  excitability  of  the  vagus  nerve  system  ;  a  spasmodic  bronchitis  ; 
a  general  inflammation  of  the  larynx ;  or  a  mixed  disease  of  catarrh  and 
neuritis. 

Etiology. — It  may  occur  in  the  newborn,  even  at  the  very  moment  of 
birth  (Sir  Thomas  Watson),  and  is  not  rare  under  6  months.  During  the 
suckling  period  infants  are  less  liable  because  they  are  less  exposed  to 
infection.  It  is  much  more  common  in  the  first  than  in  the  second  5  years 
of  life,  and  is  infrequent  afterwards.  About  80  per  cent,  are  under  5  years 
old  and  half  of  these  under  2  years.  Females  are  somewhat  more  liable 
than  males.  The  seasonal  incidence  depends  on  conditions  likely  to 
induce  catarrh.  It  is  most  common  in  spring  and  autumn,  and  most 
fatal  in  winter.  It  is  more  fatal  in  urban  and  mining  centres  than  in 
country  districts.  The  predisposing  factors  are  all  those  which  give  rise 
to  catarrh  of  the  air  passages,  notably  measles  with  which  it  may  be 
coincident.  The  incubation  period  varies  from  3-15  days  and  is  usually 
2  weeks,  sometimes  it  may  be  as  long  as  3  weeks.  The  cough  may  begin  a 
week  before  the  whoop. 

It  is  infectious  by  contact  from  the  very  commencement  of  the  catarrhal 
stage  and  before  the  whoop  is  recognised.     A  very  short  contact  is  necessary. 
The  infective  agent  is  present  in  the  sputa  and  is  spread  by  coughing.     It 
may  be  spread  by  a  third  person,  through  secretions  adhering  to  the 
clothes,  and  possibly  by  the  domestic  cat.     Probably  it  is  only  contagious 
during  the  catarrhal  stage  and  the  child  may  be  free  from  infection  as  soon 
as  the  whoop  has  developed.     Thus,  it  very  rarely  spreads  in  hospitals 
from  cases  in  which  there  are  serious  complications.     Perhaps  this  is  due 
to  the  patient  being  in  bed  and  the  infection  localised.     In  practice  it  is 
advisable  to  regard  it  as  contagious  as  long  as  there  is  expectoration  and  to 
isolate  the  child  for  6  weeks  from  the  onset.     The  virus  remains  active  after 
drying,  for  epidemics  have  broken  out  on  ships  some  weeks  after  leavrn 
land.     The  presence  of  a  whoop  does  not  necessarily  indicate  whoopin 
cough  or  that  the  child  is  infectious.     One  attack  produces,  almost  in 
variably,  complete  immunity.     Secondary  attacks  are  very  rare  and  mild 


Pertussis.  963 

•but  it  is  by  no  means  uncommon  for  a  child  to  whoop  again  during  a 
•subsequent  attack  of  bronchitis. 

Symptoms. — It  may  be  divided  into  three  stages,  catarrhal,  spasmodic, 
and  the  period  of  convalescence  ;  an  artificial  distinction  not  maintained 
•clinically.  Occasionally  in  very  young  infants  it  begins  as  acute  laryngitis. 
Usually  there  is  a  stage  of  catarrh  for  1-2  weeks  before  the  typical  cough 
•develops.  The  early  signs  may  be  erythema  of  the  fauces,  sneezing, 
respiratory  catarrh,  cough,  conjunctivitis  and  slight  fever.  Often  there 
are  no  abnormal  signs  in  the  pharynx  and  chest.  Sometimes  whooping  is 
present  from  the  beginning.  More  commonly  the  cough  becomes  gradually 
paroxysmal.  It  is  usually  afebrile  in  its  course  but  preceded  by  a  mild 
fever  and  leucocytosis.  The  blood  almost  invariably  shows  leucocytosis, 
varying  with  the  intensity  of  the  course  of  the  disease.  This  begins  with  the 
catarrh,  generally  before  the  whoop,  and  is  at  its  maximum  in  the  paroxys- 
mal stage.  It  is  greatest  in  the  very  young  and  increased  by  complications. 
There  is  no  eosinophilia.  According  to  Churchill  (1906)  it  is  a  lymphocytosis. 
Lumbar  puncture  shows  an  excess  of  mononuclears. 

A  typical  attack. — The  chest  is  first  filled  with  air  and  then,  or  without 
this  preliminary  process,  a  series  of  violent  expiratory  efforts  are  followed 
by  a  noisy  crowing  inspiration.  The  fits  of  coughing  recur  and  are  followed 
by  another  and  more  prolonged  inspiratory  whoop.  The  child  then 
brings  up  some  thick,  glairy,  viscid  mucus,  and  often  vomits.  In  severe 
•cases  there  is  a  third  bout  of  coughing  and  whooping  before  the  expulsion 
■of  mucus  and  vomiting.  During  bad  attacks  the  chest  assumes  the  position 
of  complete  expiration  ;  the  eyes  are  injected,  full  of  tears  and  protrude  ; 
the  face  is  swollen  and  livid  ;  the  tongue  projects  and  its  edges  are  curved 
upward  ;  the  lips  are  dusky  to  purple  in  colour  ;  and  the  general  appearance 
borders  on  asphyxia.     There  may  be  involuntary  micturition  or  defsecation. 

An  attack  is  often  preceded  by  nervous  disturbance.  The  child  seems 
frightened,  runs  to  its  mother  or  nurse,  or  stops  playing  and  seizes  hold  of 
some  support.  Paroxysms  arise  spontaneously  or  are  induced  by  emotion, 
■excitement,  and  any  kind  of  reflex  irritation.  They  are  sometimes  preceded 
by  tickling  in  the  throat,  a  feeling  of  compression,  suffocation  or  choking, 
and  anxiety.  Deglutition,  spasm  and  salivation  have  been  noted  by 
Meredith  Young  to  follow  severe  paroxysms.  Saliva  is  gulped  down  as 
•quickly  as  possible  for  a  minute  or  two  and  the  stomach  becomes  distended 
with  air.  Paroxysms  last  from  1-5  minutes.  If  there  is  no  complication, 
the  child  seems  well  between  the  attacks.  If  the  fit  is  mild,  the  child  goes  on 
playing  with  its  toys  as  if  nothing  had  happened.  In  severe  attacks  he  is 
exhausted,  sweats  freely,  breathes  more  rapidly,  has  an  accelerated  pulse, 
and  lies  quiet  for  a  time. 

The  number  of  paroxysms  and  the  number  of  whoops  in  each  is  very 
variable.  In  a  severe  case  there  are  hourly  attacks,  rarely  over  20  in  24 
hours,  though  as  many  as  60  may  occur.     The  total  number  of  whoops 


964  Chapter  LXIX. 

may  reach  300-400  daily.  In  some  paroxysms  there  is  no  whoop.  During 
subsidence  of  the  disease  the  whoops  often  cease  before  the  spasmodic 
cough.  The  paroxysms  are  more  frequent  during  the  day,  unless  they  are 
increased  from  fatigue  at  bedtime.  They  decrease  during  inflammatory 
complications  with  fever.  The  whoop  may  disappear  in  severe  broncho- 
pneumonia or  pneumonia. 

Babies  under  6  months  of  age  do  not  whoop.  They  have  paroxysms 
of  cough  and  turn  red,  or  more  or  less  black,  in  the  face.  In  older  children  the 
whoop  is  absent  or  abortive,  if  the  glottis  is  not  much  narrowed. 

Physical  Signs. — Between  the  paroxysms,  due  to  distension  of  blood 
and  lymph  vessels  in  the  attacks,  we  find  the  face  congested  and  puffy, 
perhaps  bloated,  swollen  eyelids,  pufhness  under  the  eyes,  suffusion  of  the 
eyes,  dilated  veins  on  the  head  and  forehead,  and  possibly  haemorrhages. 
Examination  of  the  chest  shows  catarrhal  sounds  in  the  lungs,  emphysema, 
accentuation  of  the  pulmonary  second  sound,  and  increased  cardiac  dulness 
to  the  right,  unless  obscured  by  emphysema. 

Secondary  effects  and  complications  are  mainly  mechanical.  Sublingual 
ulcer  on  the  frsenuni  is  present  in  25-35  per  cent.  It  is  rare  under  1  year 
of  age  and  most  common  in  the  second  year.  It  is  usually  due  to  mechanical 
injury,  from  scraping  of  the  frsenuno.  against  the  lower  incisor  teeth  during 
the  spasm,  but  it  may  occur  in  the  absence  of  teeth.  The  ulcer  is  single, 
variable  in  size,  and  rarely  painful.  It  is  not  typical  of  whooping  cough 
and  may  occur  in  other  varieties  of  spasmodic  cough.  It  may  give  rise  to 
severe  haemoptysis. 

Severe  vomiting. — Although  vomiting  is  present  as  a  symptom  in  at 
least  half  the  cases,  in  severe  forms  it  must  be  regarded  as  a  complication. 
It  leads  to  refusal  of  food  and  malnutrition.  Some  looseness  of  the  bowels, 
diarrhoea  or  ileo-colitis,  is  fairly  common.  Involuntary  evacuations, 
rectal  prolapse,  and  inguinal  or  umbilical  hernia,  depend  on  the  violence  of 
the  cough. 

Subconjunctival  haemorrhage  occurs  in  2-3  per  cent,  and  may  be 
associated  with  haemorrhage  into  the  eyelids,  producing  a  black  eye.  It 
is  a  very  suggestive  symptom  but  not  pathognomonic.  Haemorrhage  may 
take  place  from  the  nose,  mouth,  ears,  bronchi  and  lungs  ;  and  exceptionally 
into  the  skin,  substance  of  the  eye  and  brain. 

Post-nasal  and  laryngeal  catarrh  are  occasionally  present.  Glottic 
spasm,  with  rigidity  and  cyanosis,  may  occur.  Bronchitis  is  usually  added. 
As  it  extends  downward  it  sets  up  broncho-pneumonia,  perhaps  from 
secondary  infection.  It  is  a  common  cause  of  death  in  infants.  Collapse 
of  the  lung  is  frequent  in  infants  and  may  be  accompanied  by  rise  of 
temperature.  In  the  paroxysms  the  lungs  are  unduly  emptied,  and  the , 
viscid  mucus  prevents  the  free  entrance  of  air  through  the  narrowed  glottis. 
Acute   emphysema  is   common   even   in   early  stages.     Occasional  com- 


Pertussis.  965 

plications  are  mediastinal,  sub-pleural,  and  subcutaneous  emphysema  of  the 
upper  half  of  the  body,  pleurisy,  pleural  effusion,  empyema,  haemorrhage 
into  the  substance  of  the  lung,  bronchiectasis,  and  tuberculosis  of  the 
lymph  nodes  and  lungs.  Sputum  is  often  bloody.  The  strain  of  coughing 
produces  dilatation  and  hypertrophy  of  the  right  side  of  the  heart.  All 
the  cardiac  cavities  may  be  dilated,  especially  in  ill-nourished  children, 
partly  from  cough  and  partly  from  toxaemia  and  malnutrition  of  the 
cardiac  muscle.     Endocarditis  and  pericarditis  are  exceptional. 

Nephritis  is  rare,  though  albuminuria  is  not  uncommon.  The  urine 
is  pale  yellow,  specific  gravity  1022-1032,  highly  acid,  and  contains  much 
free  uric  acid.  It  frequently  reduces  copper  salts.  This  property  is  most 
common  in  the  convulsive  stage.  It  is  sometimes  due  to  glucose,  a  true 
glycosuria,  and  more  often  depends  on  protein  derivatives.  It  has  no 
clinical  significance. 

Cerebral  complications  and  sequels  are  infrequent  and  varied.  They 
depend  on  hyperaemia  or  asphyxia,  thrombosis,  haemorrhage,  sinus  throm- 
bosis, meningitis,  and  local  or  general  encephalitis.  Most  of  them  are  due 
to  encephalitis.  Only  in  rare  instances  are  they  caused  by  extra-dural, 
meningeal,  or  intra-cerebral  haemorrhage.  Minute  haemorrhages  may 
produce  small  foci  of  sclerosis. 

A  mild  form  of  meningitis  is  characterised  by  subnormal  temperature, 
slow  pulse,  unequal  pupils,  headache  and  torpor.  The  cerebrospinal  fluid, 
on  lumbar  puncture,  is  under  pressure  and  contains  about  80  per  cent,  of 
mononuclear  cells.  Many  cerebral  complications  are  ushered  in  by  con- 
vulsions, generally  multiple  and  often  associated  with  stupor,  rigidity  of  the 
neck,  and  perhaps  opisthotonos.  Severe  general  convulsions  may  be  due 
to  cerebral  oedema  from  venous  stasis  while  whooping. 

Cerebral  palsies  usually  arise  in  the  convulsive  stage  from  haemorrhage 
when  the  paroxysms  are  violent.  During  the  stage  of  decline  they  are 
more  likely  to  be  due  to  encephalitis.  They  are  ushered  in  by  fits,  which 
may  end  in  coma  and  death.  Or  the  unconsciousness  passes  off  and  leaves 
behind  hemiplegia,  less  often  diplegia,  monoplegia  and  aphasia,  and 
rarely  bulbar  symptoms,  ophthalmoplegia,  and  nuclear  palsy  of  the  sixth 
nerve.  Transitory  blindness  depends  on  acute  oedema  of  the  cerebral 
centres.  If  the  pupillary  reflex  is  present,  the  lesion  is  between  the  corpora 
quadrigemina  and  the  occipital  lobes,  and  the  prospect  of  recovery  is  good  ; 
if  it  is  absent,  the  lesion  is  lower  down  and  the  prognosis  bad.  Should  coma 
be  also  present,  the  child  dies.  Eare  complications  are  double  optic 
neuritis,  blindness  due  to  haemorrhage  into  the  anterior  chamber  or  retinal 
■detachment ;  otitis  media,  deafness  and  deaf-mutism  ;  cancrum  oris  ; 
gluteal  and  ischio-rectal  abscess  ;  and  various  psychoses,  neuroses  and 
scleroses.  The  psychoses  include  delirium,  screaming,  hallucinations, 
delusions,  apathy,  imbecility,  and  weakness  of  intellect  or  memory. 
Paraplegia  and  peripheral  polyneuritis  have  occurred. 


^66  Chapter  LXIX. 

Course. — The  catarrhal  stage  is  often  very  short  in  infants.  During  the 
first  year  of  life  the  characteristic  whooping  is  frequently  absent,  and 
the  lack  of  deep  inspiration  (apncea)  may  induce  fatal  syncope.  Occasion- 
ally paroxysmal  sneezing  ushers  in  the  paroxysm  and  very  rarely  replaces  it.. 
The  paroxysmal  stage  increases  in  severity  to  a  maximum,  and  then 
gradually  decreases  in  the  severity  rather  than  in  the  number  of  the  attacks. 
Next,  the  number  of  paroxysms  falls  to  1-3  daily,  and  finally  to  1  every 
few  days,  eventually  ceasing.  During  subsidence  there  is  an  increase  in 
catarrh  and  muco-purulent  expectoration. 

The  duration  varies  from  1-3  months.  Mild  cases  recover  in  3-4  weeks, 
leading  to  undue  credit  being  given  to  treatment.  A  prolonged  duration 
is  partly  due  to  habit,  and  partly  to  constitutional  debility,  cold  weather,, 
dyspeptic  troubles,  etc.     Relapses  depend  on  mismanagement. 

Convalescence  is  tedious,  because  of  malnutrition,  anaemia  and  cardiac 
dilatation.  The  child  is  susceptible  to  catarrhal  affections,  influenza, 
measles,  caseation  of  thoracic  glands  and  tuberculosis. 

Diagnosis. — Pertussis  can  occur  without  whooping  in  the  very  young 
and  in  the  presence  of  grave  lung  complications  ;  and  whooping  can  occur 
without  pertussis.  The  crow  of  laryngospasm  may  be  mistaken  for  a 
whoop.  The  diagnosis  is  based  on  a  history  of  possible  infection,  the 
presence  of  cough  in  other  members  of  the  household,  and  the  hard,  irritable, 
paroxysmal  cough  in  conjunction  with  puffiness  under  the  eyes,  coryza. 
sublingual  ulcer  and  vomiting.  A  paroxysmal  cough,  without  vomiting,, 
may  be  a  sign  of  influenza.  The  cough  produced  by  enlarged  tonsils  and 
adenoids,  or  pressure  on  the  trachea  or  recurrent  laryngeal  nerve,  is  similar 
in  character.  The  spasmodic  cough  of  bronchiectasis  is  most  marked  in 
the  morning,  and  is  associated  with  expectoration,  clubbed  fingers  and 
certain  physical  signs.  Haemoptysis  is  common  in  pertussis  and  rare  in 
tuberculous  lung  disease.  In  acute  tuberculosis  the  child  is  much  more 
ill  than  the  physical  signs  warrant ;  in  pertussis  the  reverse  holds  good. 
Expectoration  in  childhood  is  most  frequently  seen  in  pertussis  and 
bronchiectasis.  In  the  former  it  is  thick,  tenacious  and  hangs  from  the 
lips  ;  in  the  latter  it  may  be  offensive.  Stress  can  be  placed  on  the  good 
health  of  the  child  between  the  paroxysms.  The  introduction  of  a  spatula 
may  bring  on  choking,  retching,  and  a  typical  paroxysm  ;  so,  too,  tickling 
the  nasal  mucosa  or  the  external  ear,  and  pressure  on  the  thyroid  cartilage. 
A  hysterical  cough  is  barking  in  type,  ceases  during  sleep,  and  does  not 
impair  the  general  health.  Vomiting  is  common  in  many  diseases,  but 
in  pertussis  it  is  frequent  and  usually  brought  on  by  cough.  The  initial 
nervous  symptoms,  preceding  the  paroxysms,  are  a  useful  aid  to  diagnosis 
in  some  instances. 

Prognosis. — In  itself  the  disease  is  rarely  fatal,  but  death  is  common 
from  its  complications.  The  outlook  depends  on  the  age.  Although 
unusually  mild  in  the  first  few  weeks  of  life,  it  is  very  fatal  in  the  first  year, 


Pertussis.  967 

about  25  per  cent,  dying  of  those  affected,  whereas  after  that  age  only 
3-7  per  cent.  die.  Two-thirds  of  the  fatal  cases  are  under  1  year  old. 
The  number  of  paroxysms  per  diem  is  a  measure  of  the  severity  of  the 
disease,  but  the  frequency  of  the  cough  is  no  measure  of  the  severity  of  the 
paroxysm.  The  prognosis  is  worst  in  the  first  6  months  of  life  and  in 
rachitic  infants  under  2  years  of  age,  because  of  the  liability  to  pulmonary 
and  cerebral  complications.  Uncomplicated  cases,  over  2  years  of  age, 
generally  recover.  Complications  increase  the  gravity.  Usually  they 
come  on  during  the  first  2  weeks,  and  after  that  the  prognosis  becomes  more 
favourable.  The  common  causes  of  death  are  bronchitis  and  broncho- 
pneumonia, terminating  in  cardiac  failure.  This  accounts  for  half  the 
deaths  of  hospital  patients.  Others  die  from  anorexia  and  frequent 
vomiting,  asthenia,  general  malnutrition,  or  convulsions  due  to  cyanosis, 
cerebral  hsemorrhage,  etc.  A  few  die  from  syncope  during  a  violent 
paroxysm,  and  the  right  side  of  the  heart  is  found  much  distended  after 
death.  It  is  essential  to  keep  a  careful  watch  for  evidence  of  cardiac 
dilatation. 

Post  mortem  examination  reveals  hyperemia  and  congestion  of  the 
respiratory  mucosa  from  the  posterior  nares  to  the  bifurcation  of  the 
trachea,  especially  of  the  posterior  wall  of  the  larynx  between  the  vocal 
cords  and  the  under  surface  of  the  epiglottis.  The  thoracic  glands  are 
enlarged  and  the  right  side  of  the  heart  dilated.  There  is  more  or  less 
emphysema  and  signs  of  complications,  if  any. 

Treatment. — Prophylaxis  consists  in  isolation  for  14  days  after 
exposure  to  infection,  for  6  weeks  of  an  attack,  and  disinfection  of  the  sputa. 

Maintain  general  health,  prevent  inanition  from  vomiting,  guard 
against  lung  complications,  try  and  reduce  the  frequency  and  intensity  of 
the  paroxysms,  and  lessen  the  duration  of  the  disease.  Both  the  mechanical 
strain  and  the  toxsemia  are  enfeebling.  Let  the  supply  of  fresh,  pure,  mild 
air  be  as  liberal  as  possible  in  view  of  climatic  conditions.  If  the  weather 
is  suitably  mild,  open  air  treatment  throughout  is  most  beneficial.  The 
child  need  not  be  confined  to  bed  nor  to  the  house,  if  the  weather  is  mild 
and  dry  and  the  case  uncomplicated.  Sea  air  is  the  best.  Avoid  dust, 
draughts,  wet,  cold  and  wind.  If  there  is  pulmonary  mischief  keep  the 
child  in  a  warm,  even  temperature,  55-65°  F.,  protected  from  draughts  and 
from  excitement.  Two  well  ventilated  rooms  are  required.  Older 
children  should  be  encouraged  to  restrain  the  cough  and  to  cough  with  the 
lungs  full.     Bed  is  necessary,  if  there  is  fever  or  debility. 

The  diet  must  be  soft,  light,  easily  digestible,  and  not  irritating  to  the 
pharynx.  Avoid  fermentable  foods.  If  there  is  much  vomiting,  give 
small  meals  after  each  paroxysm  or  feed  the  child  again  shortly  after  the 
vomiting.  Attend  to  the  state  of  the  digestive  tract  and  be  sure  to  avoid 
nauseous  drugs.  Keep  the  bowels  open  with  rhubarb,  soda  and  grey 
powder,  if  the  tongue  is  furred. 


968  Chapter  LXIX. 

Permit  no  thoracic  compression  by  clothes  or  poultices.  An  abdominal 
belt,  4-8  ins.  deep,  worn  day  and  night,  is  comforting,  prevents  vomiting 
and  reduces  the  paroxysms  (Kilmer).  It  is  made  of  linen  or  flannel,  with 
an  insertion  of  elastic  webbing  or  stockinette,  2  ins.  wide,  on  each  side,  and 
laces  up  the  back.  It  should  be  3  ins.  in  length  less  than  the  girth  at  the 
navel  and  applied  moderately  tightly.  Much  care  is  required  in  the  use 
of  such  a  bandage  in  infancy,  for  compression  of  the  abdomen  is  apt  to 
include  compression  of  the  lower  ribs,  press  up  the  diaphragm,  and  interfere 
with  expansion  or  lead  to  collapse  of  the  lower  portions  of  the  lungs. 

Of  the  Paroxysm. — An  attack  can  be  cut  short  by  dashing  cold  water 
in  the  face  ;  by  inducing  vomiting,  e.g.  with  a  finger  or  tickling  the  fauces 
with  a  feather  ;  or  by  pulling  the  lower  jaw  downward  and  forward 
(Naegele,  1889).  The  last  method  must  not  be  used  if  there  is  food  in  the 
mouth  or  oesophagus.  It  is  most  successful  in  older  children  ;  and  may 
overcome  expiratory  spasm  in  cases  without  whoop. 

Specific  Treatmeyit. — Leuriaux  prepared  a  serum  by  inoculating  horses 
with  broth  cultures  of  his  gram-positive  bacillus  and  gave  injections  of 
5  c.c.  to  children  with  good  results.  Manicatide  has  also  prepared  a 
serum.  Several  observers  have  noted  that  vaccination,  during  the  first 
or  beginning  of  the  second  stage,  lessens  the  number  and  severity  of  the 
paroxysms.     The  symptoms  abate  as  the  pocks  mature. 

Local  Treatment. — Keep  the  nose  and  throat  clean  with  sprays  of  salt 
solution,  boric  acid,  sod.  bicarb.,  H202  in  glycerine  and  water,  or  with 
DobelPs  solution.  Irrigate  if  the  child  is  old  enough.  Or  insert  into  each 
nostril  a  portion  of  ointment  containing  bismuth  salicyl.,  boric  acid, 
quinine,  menthol,  or  various  antiseptics.  Syringing  the  ears  night  and 
morning  with  boric  a&d  solution,  and  painting  the  tympanic  membrane 
and  external  auditory  meatus  with  a  solution  of  cocaine  and  perch loride 
of  mercury,  have  been  claimed  as  efficacious  measures  ;  so,  too,  painting 
the  fauces  once  daily  with  a  solution  of  cocaine  5  per  cent,  or  hydarg. 
perchlor.  0-1  per  cent.;  and  the  application  of  resorcin  1-3  per  cent,  to  the 
glottis  or  larynx. 

For  inhalation  use  oxygen  for  cyanosis,  especially  at  night ;  a  formalin 
or  cresolin  lamp  ;  carbolic  acid  spray,  1  in  40,  twice  daily  for  20  minutes, 
1  yard  from  the  child's  head,  protecting  the  eyes  by  bandaging  ;  iodide  of 
ethyl;  carbolic  acid  0-5-2-0  per  cent., thymol  0-2,  benzol  0-1,  cresol,  cresolin, 
eucalyptus,  terebene,  tr.  benzoin  co.,  etc.  The  drawback  to  these  methods 
is  the  limitation  of  fresh  air,  and  the  advantages  are  uncertain. 

Drugs. — The  most  useful  antispasmodics  are  assafcetida,  belladonna, 
bromides,  phenazone,  bromoform,  codeine,  morphine,  heroin,  citrophen  and 
fluoroform.  A  simple  cough  mixture  is  often  as  good  as  anything.  Alkaline 
carbonates  are  useful  in  early  stages,  and  expectorants  if  there  is  much 
bronchitis. 


Pertussis.  969 

Belladonna  and  bromides  must  be  given  in  large  doses.  Belladonna 
reduces  spasms,  checks  secretion  of  mucus,  and  is  a  cardiac  and  respiratory 
stimulant.  It  is  given  in  doses  sufficient  to  produce  erythematous  flushing 
of  the  cheeks  and  marked  dilatation  of  the  pupils,  e.g.  m.  4  at  1  year  of 
age  and  m.  10  at  5  years.  After  a  variable  period  it  loses  its  effect.  It  is 
advisable  to  combine  pot.  citrate  as  a  diuretic  with  large  doses.  Sedatives 
ward  off  complications  by  diminishing  the  number  and  severity  of  the 
paroxysms.  A  mixture  of  chloral  hydrate,  phenazone,  and  vin.  ipecac, 
bromides  and  syrup  is  very  useful.  Eustace  Smith  recommends  butyl- 
chloral  hydrate  gr.  1  every  2-6  hours. 

Bromoform  is  somewhat  dangerous.  Its  high  specific  gravity  causes 
it  to  sink  to  the  bottom  of  the  bottle  and  the  final  dose  is  an  overdose. 
From  m.  1-4  for  each  year  of  life  are  given  3-4  times  daily  in  pure  form 
on  sugar,  or  in  an  emulsion  ;  e.g.  bromoform  q.s.,  sp.  vin.  rect.  dr.  1,  pulv. 
a,cacise  drs.  2,  syr.  aurant.  oz.  J,  aquse  ad.  oz.  4  ;  or  bromoform  q.s.,  ol. 
amygdal.  drs.  6,  tragacanth  dr.  \,  gum  arabic  dr.  1,  aq.  laurocerasi  dr.  1, 
aqua?  ad  oz.  3.  It  must  be  dispensed  in  dark,  glass-stoppered  bottles, 
kept  in  the  dark,  and  shaken  before  taken.  Duncan's  syr.  bromoform. 
co.  contains  bromoform  m.  2,  aconite,  codeine,  tolu  etc.  per  drachm.  A 
poisonous  dose  of  bromoform  produces  narcosis,  slow  breathing,  soft  and 
intermittent  pulse,  diminished  corneal  reflex  and  an  erythematous  rash.  It 
is  treated  by  artificial  respiration,  mustard  baths,  faradisation,  coffee, 
alcohol,  etc. 

Phenazone  is  given  in  doses  of  gr.  1  per  year  of  life  every  4  hours, 
sometimes  in  much  larger  doses  or  combined  with  other  drugs.  It  rarely 
causes  rash  in  children  and  does  not  produce  depression.  It  stops  the 
vomiting  and  reduces  the  frequency  of  the  paroxysms.  Tussol  is  a  com- 
pound of  phenazone,  so  is  Duncan's  elixir  pro  pertussi,  grs.  2  per  drachm. 
Pertussin  is  a  thyme  preparation  of  little  value.  Fluoroform  is  expensive 
and  difficult  to  obtain.  A  saturated,  2-0-2-5  per  cent.,  solution  in  water 
is  colourless,  odourless,  tasteless  and  apparently  harmless.  In  doses  of 
drs.  1-8  hourly  it  is  said  to  reduce  the  duration  of  the  whoop  to  6-18  days. 
For  small  infants  give  m.  1  daily  after  each  paroxysm,  and  increase  by 
m.  1  daily  up  to  m.  100  per  diem. 

Quinine  gr.  ^  per  month  of  life,  or  gr.  1|  per  year,  up  to  grs.  6,t.d.s., 
by  mouth  or  rectum,  is  sometimes  efficacous.  Other  remedies  are  codeine, 
morphine,  and  heroin  hydrochlor.  in  doses  of  gr.  -jVAj  ac.  carbolici 
Sr-  tV>  benzol  m.  1,  hyoscyamus,  conium,  valerian,  tr.  grindelia  robusta, 
cannabis  indica,  and  aristochin,  alone  or  in  various  combination,  t.d.s.  at 
1  year  of  age.  Antispasmine,  a  mixture  of  sod.  salicyl.  and  a  compound  of 
sodium  and  narcine,  5-10  per  cent,  solution  in  Avater,  is  given  in  doses  of 
m.  3  under  6  months  and  m.  5-10  at  6-12  months  of  age.  Creosote  and 
carbolic  acid  are  useful  for  gastric  and  intestinal  fermentation.  Oxygen, 
strychnia  and  digitalis,  or  strophanthus,  are  necessary  for  cardiac  dilatation, 


970  Chapter  LXIX. 

cyanosis  and  albuminuria;  and  often  stimulants  are  essential.  The- 
usual  methods  of  treatment  for  dilatation  of  the  right  side  of  the  heart,, 
if  present,  must  be  adopted.  Minute  doses  of  opium  can  be  given  for 
insomnia  and  excitement,  if  there  is  not  much  bronchitis.  Lumbar 
puncture  relieves  convulsions.  Cod-liver  oil,  iron  and  nux  vomica  are^ 
needed  during  convalescence,  and  wise  management  in  guarding  against 
exposure  to  cold,  infection,   and  cardiac   strain. 


CHAPTER    LXX. 

MUMPS. 

Syn.  :'  Specific  or  Contagious  Parotitis — Cynanche  parotidea. 

Mumps  is  a  specific,  highly  contagious  affection  of  the  salivary  glands, 
chiefly  the  parotid,  with  usually  slight  constitutional  symptoms  and 
infrequent  complications.  It  is  most  common  in  cold  weather.  Epidemics 
are  frequent  in  schools.  Infants  arc  remarkably  immune  and  the  disease 
is  rare  in  early  childhood.  It  has  been  recorded  in  the  newborn,  but  is 
most  frequent  from  the  fourth  to  the  fourteenth  years  of  life. 

It  is  spread  almost  always  by  direct  contact,  probably  through  the 
medium  of  the  breath;  possibly  by  infected  articles  of  clothing,  toys,  etc.; 
and  exceptionally  by  intermediaries,  such  as  nurses,  doctors,  visitors  and 
cats.  The  infective  agent  and  mode  of  entry  are  unknown.  Peculiarly 
shaped  micrococci  have  been  found  in  the  blood  and  urine  by  Capelan  and 
Charrin,  and  diplo-streptococci  by  Michaelis  (1897).  Probably  the  infective 
agent  enters  the  mouth  or  naso-pharynx,  travels  up  the  ducts  to  the  glands, 
and  passes  into  the  circulation.  Hence,  because  of  their  large  ducts,  the 
parotids  are  particularly  susceptible  to  infection.  The  ducts  become 
swollen  and  obstructed,  and  the  glands  enlarged  by  hyperemia  and  oedema. 
All  the  salivary  glands  may  be  involved,  sometimes  only  the  submaxillary, 
more  often  the  parotids  alone.  The  inflammation  is  peri-glandular  and 
inter-acinous,  the  glandular  epithelium  being  unaffected.  Suppuration  may 
result  from  a  mixed  pyogenic  infection. 

Injectivity. — Apparently  it  is  infectious  during  the  prodromal  period, 
for  as  long  as  4  days  before  the  onset,  and  remains  infectious  for  2-3  weeks. 
No  patient  should  be  allowed  to  return  to  school  or  mix  with  others  until 
3  weeks  after  the  onset  and  at  least  a  week  after  the  subsidence  of  all 
swelling. 

The  incuhalion  period  is  14-21  days.  Dukes  (1899)  states  that  it 
is  13-25  days,  in  the  majority  of  cases  17-20  days.  In  1906  he  reported 
that  22  out  of  23  cases  began  on  the  sixteenth  to  nineteenth  day.  Cases 
have  occurred  as  late  as  the  thirty-third  day  after  exposure.  Quarantine 
should  be  maintained  for  25  days  after  exposure,  but  need  not  be  enforced 
during  the  first  half  of  that  time. 

Symptoms. — The  prodromal  period  is  indefinite,  often  absent. 
Symptoms  may  exist  in  the  form  of  irritability,  languor,  fever,  general 
malaise,  and  diarrhoea  or  vomiting  for  a  day  or  two  in  bad  cases.  Usually 
the  first  indication  is  stiffness  of  the  jaws,  difficulty  in  opening  the  mouth, 
pain  on  eating,  and  pricking  in  the  ear  or  otalgia.      Perhaps  there  is 


972  Chapter  LXX. 

dulness  of  hearing  or  stiff-neck.  Occasionally  the  onset  is  acute,  with 
vomiting,  high  fever,  and  even  a  rigor  or  convulsions.  Gastro-mtestinal 
symptoms,  possibly  due  to  pancreatitis,  may  be  severe.  The  pain  is  dull, 
aching,  and  localised  in  the  temporo-maxillary  articulation.  Like  the 
swelling  it  is  often  unilateral.  It  is  not  always  present,  even  in  cases  where 
the  swelling  is  pronounced,  and  the  child  may  have  no  discomfort 
throughout. 

The  parotid  swelling  begins  on  one  side  in  front  of  and  below  the  ear, 
elevating  and  pushing  out  the  lobe.  In  shape  it  is  that  of  the  gland.  It 
varies  in  extent,  and  may  involve  almost  half  the  face  and  extend  to  the 
clavicle.  The  lateral  pharyngeal  wall  and  tonsil  may  be  bulged  inward. 
It  attains  its  maximum  in  3-4  days  and  gradually  subsides  in  about  the 
same  time.  The  opposite  gland  is  occasionally  affected  simultaneously, 
generally  in  2-3  days,  and  rarely  not  for  2-3  weeks.  One  side  is  almost 
invariably  larger  than  the  other.  The  swelling  feels  doughy  or  elastic. 
It  may  be  limited  to  the  submaxillary  glands.  The  skin  is  somewhat  tense 
and  shiny,  and  there  is  rarely  any  redness  or  tenderness  on  pressure. 
The  facial  aspect  is  altered,  especially  if  both  the  parotid  and  submaxillary 
glands  are  much  swollen.  The  mouth  is  dry  for  it  is  kept  partly  open. 
Salivary  secretion  is  normal,  deficient,  or  rarely  excessive.  The  tongue  is 
furred.  Stomatitis  and  pharyngitis  may  be  present.  Sometimes  there  is 
deafness.  The  swelling  may  cause  sufficient  venous  pressure  to  induce 
congestion  of  the  face,  headache  and  delirium. 

Fever  may  be  absent.  Generally  the  temperature  rises  with  the 
swelling,  up  to  102°  F.  in  mild  cases  and  in  severe  ones  to  104°  F.,  or 
higher.  Its  course  is  irregular,  not  characteristic,  and  it  comes  down  to 
normal  in  a  few  days.  Usually  the  illness  lasts  a  few  days  to  a  week  ; 
longer,  if  the  glands  are  successively  involved  or  complications  arise. 
Diarrhoea  may  be  pronounced  at  the  onset  and  throughout.  Gastro- 
intestinal symptoms  are  marked  in  some  epidemics.  The  spleen  is  enlarged 
in  severe  cases  and  the  cervical  lymph  nodes  may  be  engorged. 

The  Blood. — Leucocytosis  was  absent  in  7  cases  (Cabot),  slight  in  15 
(Sacquepee,  1902).  Both  Krestnikow  and  Pick  (1902)  found  lympho- 
cytosis from  the  onset.  Wile's  results  (1906),  based  on  20  cases,  yielded 
a  total  leucocytosis ;  a  lymphocytosis,  as  a  relative  and  absolute  constant 
sign  from  the  onset  until  the  subsidence  of  the  swelling,  most  marked 
in  bilateral  cases  and  in  children  at  puberty  ;  a  relative  decrease  in  poly- 
morphs, except  in  orchitis ;  and  no  eosinophilia.  He  regarded  the 
lymphocytosis  as  a  diagnostic  feature  between  mumps  and  adenitis, 
provided  the  relative  lymphocytosis  of  early  life  is  not  forgotten.  Average 
relative  percentages  in  these  affections  were  : — 


Lymphocytes. 

Polymorphs. 

Eosinophiles. 

Basophiles 

Mumps 

. .     59-37 

38-32 

2-28 

0-43 

Adenitis 

. .     35-32 

62-75 

2-26 

0-37 

Mumps.  973 

Complications  and  Sequels. — Before  the  age  of  puberty  these  are 
uncommon.  Orchitis  is  exceptional  under  12  years  of  age.  It  is  more 
frequent  in  some  epidemics,  comes  on  at  the  end  of  the  first  or  beginning  of 
the  second  week,  generally  about  the  eighth  day,  and  lasts  about  a  week. 
It  is  sometimes  ushered  in  with  vomiting,  is  usually  unilateral,  and  may  be 
followed  by  testicular  atrophy.  Occasionally  in  adults  it  is  unassociated 
with  parotid  swelling,  begins  acutely,  and  lasts  2-3  weeks.  Oophoritis 
(ovaritis)  and  mammary  swelling  have  been  noted  in  girls,  usually  on  one 
side,  e.g.  13  out  of  33  cases,  in  8  of  which  the  menses  had  appeared 
(Troitsky,  1906).  It  may  lead  to  atrophy,  parenchymatous  or  interstitial 
changes.  Occasionally  the  labium  major  is  swollen.  Both  oophoritis 
and  orchitis  may  precede  the  parotid  swelling. 

Meningoencephalitis  of  a  mild  type  is  not  very  rare.  It  appears  to  be 
limited  to  the  region  of  the  medulla  and  pons,  and  probably  accounts  for 
occasional  sequels  such  as  headache,  optic  neuritis,  deafness,  facial  palsy,, 
and  herpes  of  the  fifth  nerve.  Bradycardia  and  Kernig's  sign  are  symptoms. 
It  has  been  verified  in  adults  with  bradycardia,  headache  and  fever 
(ChaufTard  and  Boidin,  1904).  An  excess  of  lymphocytes  was  found  in  the 
blood  and  cerebrospinal  fluid.     Deafness  is  unilateral  and  permanent. 

Bare  complications  are  paralysis  of  accommodation,  iritis,  nyctalopia, 
optic  atrophy,  facial  palsy,  peripheral  neuritis,  herpes  zoster  ;  labyrin- 
thitis ;  temporary  dementia  and  loss  of  memory,  convulsions,  delirium  ; 
endocarditis,  myocardial  degeneration;  acute  nephritis,  usually  hemorrhagic 
and  benign,  beginning  during  convalescence,  occasionally  chronic  and 
fatal  :  and  the  results  of  secondary  infection,  viz.  suppuration,  sloughing 
and  gangrene  of  the  gland  ;  nephritis,  pericarditis  and  pneumonia.  It  is 
uncommon  to  find  complications  in  young  children. 

Pancreatitis. — The  pancreas,  or  abdominal  parotid,  is  sometimes 
involved  in  the  metastases  of  mumps.  The  connection  was  noted  in  1817 
by  Schmackpeffer.  It  is  more  frequent  in  adults  but  may  occur  in  boys, 
even  apart  from  parotitis. 

The  attack  is  usually  mild,  comes  on  about  the  third  to  sixth  day 
(first  to  twelfth),  lasts  2-7  days,  and  runs  a  similar  course  to  that  of  the 
parotid  swelling.  Pain  is  felt  in  the  epigastrium  and  left  hypochondrium. 
At  first  it  is  dull  and  deep  seated,  but  it  increases  in  severity  and  may  cause 
syncope.  Usually  it  is  paroxysmal,  midway  between  the  navel  and 
ensiform  cartilage,  and  radiates  to  the  back  or  toward  the  floating  ribs.. 
There  is  much  tenderness  on  pressure  and  deep  palpation  is  impossible. 
The  swelling  is  palpable  or  obscured  by  abdominal  distension  ;  or  may  be 
felt  after  the  tenderness  has  subsided.  Nausea  and  vomiting  are  rarely 
absent.  The  vomiting  varies  in  degree,  and  may  be  intractable  and 
hfemorrhagic.  Diarrhoea  occurs  in  half  the  cases,  and  blood  and  fat 
have  been  found  in  the  stools.  Constipation  is  present  in  some.  Jaundice 
is  uncommon.         Cammids,e's  reaction,   acetone  and  diacetic  acid,   and 


-974  Chapter  LXX. 

■calcium  oxalate  crystals  (often  present  in  pancreatitis),  may  be  present  in 
the  urine.  There  is  no  glycosuria.  The  temperature  varies  from  100-102°  F. 
•or  may  be  normal.  The  parotid  swelling  subsides  rapidly.  Fever,  vomiting 
and  pain  disappear  in  succession ;  and  there  is  no  evidence  of  subsequent 
atrophy.     The  complication  has  proved  fatal. 

Simple  acute  pancreatitis  may  result  from  injury,  catarrh  of  the 
gut,  duodenal  ulceration,  or  infection  of  the  biliary  passages.  It  may 
terminate  in  chronic  parenchymatous  or  interstitial  inflammation  ;  or  in 
an  abscess  discharging  through  the  duct  or  ending  in  cyst  formation.  The 
general  symptoms,  often  absent  for  a  small  portion  of  the  gland  may  carry 
on  its  functions,  are  (1)  tenderness  on  palpation ;  (2)  colicky  pains ; 
(3)  steatorrhea,  greyish  white  stools  containing  fatty  acid  crystals,  globules 
of  fat  and  clots  of  soap  ;  (4)  azotorrhcea,  undigested  muscle  fibres  in  the 
feces  ;  (5)  diabetes,  often  with  acetonuria.  Diabetes  can  occur  in  children 
as  a  functional  pancreatic  disorder  without  histological  changes  in  the 
gland. 

The  treatment  of  acute  attacks  consists  of  rest,  light  diet,  local 
applications  of  heat  or  cold,  and  opium  for  severe  pain.  Fat  must  be 
omitted  in  pancreatic  affections  and  the  amount  of  meat  reduced,  if  there 
is  no  diabetes. 

Diagnosis. — Glandular  hyperplasia  is  more  apt  to  be  mistaken  for 
mumps  than  mumps  for  adenitis,  except  in  the  primary  submaxillary  cases 
which  can  be  distinguished  by  the  course  of  the  disease.  Swollen  glands  are 
small,  circumscribed,  of  slow  development,  and  do  not  extend  on  to  the 
face.  The  association  of  pain  and  difficulty  about  the  angle  of  the  jaw 
with  a  parotid  swelling  is  usually  conclusive,  especially  if  there  is  no  redness 
of  the  skin  or  faucial  affection.  Blood  examination  is  of  assistance  in 
doubtful  cases.  Catheterisation  of  Steno's  duct  has  been  recommended. 
Parotid  fluid  is  normally  free  from  cells.  In  mumps  it  is  full  of  polymorphs, 
large  mononuclears,  and  some  cells  peculiar  to  the  salivary  glands. 

Prognosis  is  excellent.  Complications  are  rare  and  the  course  usually 
very  mild.  About  puberty  the  disease  is  more  serious  than  commonly 
admitted.  Eelapses  are  rare  ;  second  attacks  unknown.  A  secondary 
rise  of  temperature  indicates  extension  or  a  complication. 

Treatment. — Keep  the  child  in  bed  until  constitutional  symptoms  have 
subsided ;  for  10  days,  if  over  9  years  of  age.  Younger  children  with  mild 
attacks  must  be  kept  indoors  until  the  swelling  has  subsided.  Give 
a  saline  purge,  or  calomel  and  scammony  ;  sod.  salicyl.,  or  quinine  in 
•effervescence  (p.  80)  ;  and  liquid  or  semi-solid  diet.  Apply  locally  hot 
fomentations,  lin.  belladon.,  methyl  salicyl.,  or  a  mixture  of  guiacol  1, 
lanolin  10,  vaseline  10  parts,  twice  a  day  and  covered  with  oiled  silk  (useful 
.also  for  orchitis).     Disinfect  the  nose,  mouth  and  pharynx. 


CHAPTER    LXXI. 

THE    EYE. 

Blepharitis — Styes —  Conjunctivitis — Phlyctenules —  Trachoma —  The  Lachry- 
mal Apparatus — The  Ocular  Muscles — The  Eyeball — Buphthahnos — 
Keratomalacia  —  Nyctalopia  —  Retinitis  pigmentosa  —  Glioma  — 
Amblyopia. 

The  newborn  child  is  particularly  liable  to  infection,  because  there  is  no 
•secretion  of  tears  to  wash  away  micro-organisms.  The  common  signs  of 
•eye  mischief  are  irritation  and  rubbing  of  the  eyes,  photophobia,  blepharo- 
spasm, and  watery,  muco-purulent  or  purulent  secretions,  with  more  or 
less  congestion  of  the  conjunctiva?,  and  swelling  of  the  eyelids.  Opacities 
indicate  old  corneal  ulceration. 

Mode  of  Examination. — Use  no  unavoidable  force  for  the  hyperemia 
of  crying  is  injurious  to  an  inflamed  eye.  If  necessary,  the  child  is  placed 
•on  its  back,  held  by  the  nurse,  and  the  head  fixed  between  the  examiner's 
knees.  Photophobia  results  from  irritation  of  the  fifth  nerve.  If  present, 
the  child  must  be  examined  with  its  back  to  the  light  after  instillation  of  a 
few  drops  of  cocaine  2  per  cent,  solution. 

For  supposed  blindness  or  amblyopia  try  the  "  flash-test,"  i.e.  note  if 
the  eyes  will  follow  a  bright  light  reflected  from  a  mirror  in  a  dark  room. 
A  negative  result  at  3  months  of  age  is  due  to  blindness  or  mental  defect. 

The  pupils  are  naturally  small  and  do  not  dilate  much,  even  in  the 
•shade.  In  the  blindness  of  optic  atrophy. the  eyes  are  wide-open,  the 
pupils  large,  nystagmus  often  present,  and  the  expression  is  wandering. 
Acuity  of  vision  is  tested  by  simple  measures  suited  to  the  age  of  the  child  ; 
so,  too,  colour  vision,  red  being  the  colour  first  distinguished. 

Ophthalmoscopic  examination  requires  considerable  skill  unless  the 
child  is  unconscious.  Ethyl  chloride  can  be  given.  The  pupil  should  be 
fully  dilated  by  homatropine  1,  euphthalmine  5,  or  mydrine  10  per  cent, 
solution,  a  drop  being  inserted  into  each  conjunctival  sac  above  the  inner 
■canthus.  For  estimating  refraction  insert  ung.  atrophia?,  grs.  2-4  ad  oz.  1, 
t.d.s.,  for  3  days  before  but  not  on  the  day  of  examination.  It  paralyses 
accommodation  and  the  effects  take  some  days  to  wear  off,  interfering  with 
observations  on  the  light  reflex  and  inequalities  etc.  Mydrine  and  euph- 
thalmine dilate  the  pupil  quickly  and  interfere  little  with  accommodation. 

Note  whether  there  is  nystagmus,  squint,  normal  pupillary  reflexes, 
stigmata  of  degeneration,  or  cranial  defects,  and  the  state  of  mental  and 


976  Chapter  LXXI. 

physical  development.  Congenital  defects  include  cysts  of  the  orbit, 
defects  in  the  eyelids,  abnormalities  of  the  eye  or  portions  of  the  eye,  and 
ocular  palsies. 

Shades  should  be  thick,  black,  dark  green  or  dark  blue  in  colour, 
and  dull  on  the  inner  surface.  They  should  be  worn  whenever  atropine  is 
used  or  if  light  irritates  the  eyes. 

The  Eyelids. —  Coloboma  is  rare.  It  is  usually  limited  to  one  eyelid 
or  the  two  lids  of  one  eye,  exceptionally  affecting  all  4  eyelids,  and 
occasionally  double.     Other  malformations  are  often  present. 

Blepharitis. — Syn.  :  Ciliary  blepharitis — Tinea  tarsi. — Marginal  or 
ciliary  blepharitis  is  an  inflammation  or  hypereemia  of  the  edges  of  the 
evelids,  which  may  progress  to  ulceration.  In  the  first  stage,  B.  squamosa, 
the  lids  are  red,  slightly  swollen,  and  show  branny  desquamation  or  perhaps 
yellow  crusts.  The  skin  under  the  scales  is  hyperfemic.  Eyelashes  are 
easily  pulled  out  but  grow  again.  In  the  second  stage,-  B.  ulcerosa,  there 
is  more  swelling,  small  ulcers  beneath  crusts,  and  diseased  hair  follicles, 
and  the  lashes  are  stunted,  irregular,  and  come  out  but  do  not  grow  again. 
It  is  a  suppuration  of  the  hair  follicles  and  sebaceous  glands.  Ulceration 
may  extend  to  adjacent  skin.  % 

It  depends  on  delicacy,  bad  hygiene,  measles,  and  microbial  or  parasitic 
infection,  e.g.  pediculi.  A  mild  error  of  refraction,  notably  myopic  astig- 
matism, is  a  predisposing  factor.  Sometimes  the  disease  is  unilateral  and 
due  to  chronic  catarrh  of  the  lachrymal  sac.  It  is  often  associated  with 
phlyctenules,  and  occasionally  due  to  eczema.  The  eyelids  on  waking 
are  stuck  together  by  tenacious  secretion  and  can  only  be  efficiently  opened 
after  bathing  with  warm  water.  The  lids  are  red  and  swollen,  and  may 
show  pustules,  ulcers,  cicatrices,  and  matting  of  the  cilia.  In  bad  and 
prolonged  cases  the  ulceration  may  destroy  the  hair  follicles  and  cause 
complete  loss  of  the  eyelashes.  Other  sequels  are  hypertrophy  of  the  lid 
border  (tylosis),  chronic  conjunctivitis,  closure  of  the  puncta  lachrymalia 
with  epiphora  and  eczema,  ectropion  of  the  lower  lid  and  epiphora,  with 
eventual  contraction,  entropion,  trichiasis  and  secondary  superficial 
keratitis. 

Treatment. — Suitable  glasses  alone  may  cure  mild  cases.  Remove 
crusts  and  scabs,  after  softening  them  by  prolonged  bathing,  borated 
starch  poultice,  or  olive  oil  followed  by  an  alkaline  lotion.  Bathe  with  the 
alkaline  lotion  and  apply  ung.  hydrag.  arum.,  grs.  8  ad  oz.  1,  t.d.s.  ;  or 
ung.  hyd.  oxid.  flav.,  grs.  4-8  ad  oz.  1,  or  ung.  hyd.  nitrat.  dil.  (B.P.),for 
an  hour  every  morning  along  the  edges  of  the  lids.  If  there  is  pus  oozing  from 
a  raw  surface,  paint  with  silver  nitrate  1-2  per  cent,  or  protargol  15  per  cent., 
with  the  eyes  closed,  wash  with  salt  solution,  and  then  apply  the  ointment. 
The  solid  stick  of  silver  nitrate  is  sometimes  preferable.  If  pus  can  be 
pressed  out  of  the  lachrymal  sac,  the  canaliculus  must  be  slit  up.  Open 
pustules  daily,  and  epilate  involved  cilia  and  those  abnormal  in  colour, 


The  Eye.  977 

thickness  or  direction  of  growth,  and  remove  scales.     Give  iron  and  cod- 
liver  oil,  and  attend  to  general  hygiene. 

Styes. — A  stye,  or  hordeolum,  is  a  furuncle  of  the  lid  margin,  beginning 
in  a  sebaceous  gland  of  an  eyelash  and  forming  a  hard  swelling.  It  may 
cause  considerable  oedema  of  the  lid  and  chemosis.  If  near  the  outer 
canthus,  the  cause  of  the  oedema  is  not  always  obvious.  The  pre-auricular 
lymph  nodes  may  be  enlarged  and  tender.  The  boil  points  on  the  margin 
of  the  lid  as  a  small  yellow  area  from  the  centre  of  which  a  hair  protrudes. 

Predisposing  causes  are  refractive  errors,  chiefly  hypermetropia  or 
hypermetropic  astigmatism.  Some  children  have  recurrent  attacks  on 
account  of  a  constitutional  peculiarity,  the  so-called  strumous  diathesis, 
constipation,  general  ill-health  or  a  susceptibility  to  acne.  Others  appear 
strong  and  healthy,  and  are  perhaps  overfed.  The  exciting  cause  is  a 
staphylococcal  infection. 

Treatment. — Attend  to  the  general  health  and  the  state  of  the  alimen- 
tary tract.  Some  children  need  a  mild  aperient,  tonics,  ol.  morrhuse  and 
liberal  diet ;  others  require  less  food  and  mild  saline  purgatives.  For 
immediate  relief  apply  hot  compresses  of  boric  acid,  lead  lotion  1  per  cent. 
or  alum  1  per  cent.,  give  a  purge,  and  if  the  stye  points  pull  out  the  hair. 
If  necessary,  incise  in  the  long  axis  of  the  lid  margin,  squeeze  out  the 
pus  gently,  and  apply  hot  fomentations.  Another  suitable  preparation  is 
ac.  borici  dr.  1,  ext.  hamamelis  liq.  drs.  2,  aq.  ad  oz.  4,  applied  on  wool 
several  times  daily.  "For  recurrent  cases  apply  ung.  hyd.  nit.  and  white 
vaseline,  p. a.,  or  ung.  hyd.  oxid.  flav.  1  and  vaseline  2  parts,  to  the  eyelids 
night  and  morning.  The  administration  of  yeast  or  grape  ferment  is 
sometimes  beneficial.  Should  the  frequent  recurrence  be  very  troublesome, 
a  vaccine  may  be  tried. 

Meibomian  or  Tarsal  Cyst  is  due  to  blockage  of  a  duct  with  secretion. 
It  forms  a  pimple  on  the  eyelid  and,  if  suppurating,  points  on  the  con- 
junctival or  skin  surface.  An  incision  should  be  made  on  the  conjunctival 
surface  and  the  contents  gently  evacuated  by  squeezing. 

Conjunctivitis. — The  purulent  variety,  due  to  the  gonococcus,  has 
been  described  (p.  137).  The  membranous  type  is  commonly  diphtheritic. 
Simple  catarrh  is  a  frequent  complication  of  a  'l  cold  in  the  head,"  hay 
fever,  measles,  cerebrospinal  fever,  and  many  forms  of  local  inflammation, 
and  is  due  to  various  micro-organisms.  The  discharge  is  watery,  muco- 
purulent or  purulent.     A  unilateral  one  may  be  due  to  a  foreign  body. 

Bacteriology. — Take  a  little  secretion  on  a  platinum  loop,  make  a 
film  and  stain  by  Gram's  method.  The  organisms  in  order  of  frequency 
are  (1)  Koch- Weeks  bacillus,  decolourised  by  Gram  and  like  the  influenza 
bacillus  ;  (2)  Morax-Axenfeld  bacillus,  a  large,  broad  bacillus  or  diplo- 
bacillus,  gram-negative  ;  (3)  Gonococcus  ;  (4)  Fraenkel's  pneumococcus, 
not      very    contagious ;  (5)     Streptococci,     staphylococci,     Friedlander's 

3   R 


978 


Chapter  LXXI. 


bacillus  and  b.  diphtheria?,  all  of  which  are  sometimes  normally  present 
without  symptoms  ;    (6)  B.  coli  and  the  meningococcus. 

Muco-yurulent  Conjunctivitis,  commonly  due  to  the  Koch- Weeks 
bacillus,  is  very  contagious  and  the  cause  of  school  ophthalmia  or  :;  pink 
eye."  It  is  characterised  by  injection  or  hyperaemia,  followed  by  chemosis, 
a  discharge  containing  flakes  of  muco-pus,  catarrhal  ulcers  of  the  cornea, 
and  sometimes  phlyctenules  and  iritis.  The  ulcers  are  often  multiple, 
along  the  margins  of  the  cornea,  and,  if  they  deepen  and  extend  more  or 
less  completely  round  the  cornea,  may  cause  its  necrosis.  The  Koch-"Weeks 
bacillus  may  set  up  toxic  iritis. 

Angular  or  Follicular  Conjunctivitis,  due  to  the  Morax-Axenfeld 
bacillus,  is  chronic  in  character  and  causes  aching  of  the  eyes,  heaviness  of 
the  lids,  a  feeling  of  sand  in  the  eyes,  and  glueing  together  of  the  lids  in 
the  morning.  The  lids  are  red  and  macerated  at  the  canthi,  and  the 
discharge  is  soapy,  scanty  and  not  purulent.  It  is  often  associated  with 
refractive  error.     Corneal  ulceration  is  rare. 

Membranous  Conjunctivitis  is  due  to  a  streptococcus,  staphylococcus, 
pneumococcus,  gonococcus  or  the  diphtheria  bacillus.  The  streptococcal 
type  is  unilateral  or  bilateral,  of  variable  severity,  with  a  thin  or  purulent 
discharge  and  sometimes  a  pellicle  or  membrane  on  the  conjunctiva.  It 
may  cause  oedema  of  the  lids,  ulceration  of  the  lid  margins,  chemosis,  nasal 
discharge,  adenitis,  and  a  temperature  up  to  101°  F.  Infiltration  of  the 
cornea,  amaurosis,  toxic  iritis,  corneal  ulcer,  hypopyon,  staphyloma  and 
loss  of  the  eye  are  sequels.  These  results  may  occur  apart  from  membrane 
formation. 

A  staphylococcal  infection  produces  the  same  symptoms,  complications 
and  results,  except  that  it  is  less  serious  and  rarely  causes  staphyloma  or 
loss  of  the  eye.  The  discharge  is  usually  glairy  and  watery,  rather  than 
purulent.  The  S.  albus  is  milder  than  S.  aureus  in  its  effects.  In 
diphtherial  infection  albuminuria  is  more  frequently  present,  and  the 
pre-auricular  and  often  other  glands  are  enlarged.  Differential  diagnosis 
depends  on  cultural  examination  of  the  discharge. 

Treatment. — In  mild  cases  apply  hourly  with  a  tampon  of  cotton 
wool  boracic  lotion,  zn.  sulphat.  gr.  1  or  alum  grs.  4  ad  oz.  1,  and  vaseline 
along  the  edge  of  the  lids  to  prevent  gumming.  Zinc  sulph.  grs.  2  ad  oz.  1 
destroys  the  Koch- Weeks  and  Morax-Axenfeld  bacilli.  It  can  be  used 
4-6  times  daily  in  the  more  severe  purulent  forms,  until  the  flow  of  pus 
ceases,  first  irrigating  with  normal  saline  solution  or  washing  freely  with 
absorbent  wool  dipped  in  water.  After  the  washing  instil  a  few  drops  into 
the  inner  canthus  of  hyd.  perchlor.  gr.  rg-,  or  acid,  boric,  grs.  10  and  zn. 
sulph.  grs.  2,  or  sod.  biborat.  grs.  6  and  ac.  salicyl.  grs.  2,  or  silver  nitrate 
gr.  1-2,  each  made  up  with  an  ounce  of  water.  In  very  severe  cases,  without 
ulceration  of  the  lids  or  membrane  formation,  brush  the  conjunctiva 
with  silver  nitrate  1  per  cent,  daily,  and  irrigate  every  4-6  hours  with 


The  Eye.  979 

1  in  10,000  perchloride  lotion.  Or  irrigate  with  normal  saline  and  paint 
-with  argyrol  20  per  cent.,  a  measure  often  efficacious  if  there  is  membrane. 
Use  boric  acid  fomentations  for  ulceration  of  the  lids.  For  the  treatment 
of  gonococcal  infection  vide  ophthalmia  neonatorum  (p.  139). 

Phlyctenular  Ophthalmia. — Syn.  :  Phlyctenular  conjunctivitis  or 
keratitis  —  Phlyctenule  —  Lymphatic  or  eczematous  conjunctivitis. — A 
phlyctenule  is  a  minute  infiltration,  elevation  or  nodule,  single  or  multiple, 
composed  of  cellular  elements,  situated  on  the  ocular  conjunctiva  and 
■occasionally  on  the  palpebral,  with  dilated  blood  vessels  (vascular  triangles) 
radiating  outward  from  it.  The  common  situation  is  the  juncture  of  the 
cornea  and  sclerotic.  One  on  the  cornea  (P.  keratitis)  is  superficial  and  of  a 
uniform  greyish  colour.  If  central,  it  may  leave  an  opacity,  lessening 
acuity  of  vision  or  inducing  squint.  Occasionally  a  fascicular  ulcer 
travels  across  the  cornea,  healing  as  it  goes  but  leaving  a  terminal  opacity. 

Phlyctenules  have  been  ascribed  to  malnutrition,  defective  assimilation 
and  excretion,  improper  food,  e.g.  sweets  between  meals,  intestinal 
toxcemia  and  bad  hygiene.  They  are  most  prevalent  under  10  years  of 
age  and  often  follow  measles.  Possibly  they  represent  the  local  reaction 
■of  the  tissues  to  the  tuberculous  toxin,  or  are  due  to  infarction  of  dead  or 
attenuated  tubercle  bacilli.  Giant-cells  have  been  found  by  Leber  and 
Wintersteiner.  Nevertheless  it  would  be  rash  to  assume  that  there  is 
reliable  evidence  in  favour  of  a  tuberculous  foundation. 

Symptoms. — Discomfort,  lachrymation  and  photophobia  are  present, 
and  greatest  when  the  phlyctenule  is  corneal.  Blepharospasm  and  eczema 
of  the  lids  are  secondary  effects.  The  nodule  is  usually  reabsorbed  and 
well  in  7-10  days.  Recurrence  is  common  and  may  persist  for  years. 
Ulceration,  due  to  infection  by  pyogenic  organism,  leads  to  muco-purulent 
conjunctivitis  and  local  cicatrisation,  perhaps  corneal  perforation  or 
permanent  infiltration. 

Treatment. — Prescribe  high  bracing  or  sea  air,  but  not  the  seaside 
because  of  the  glare,  salt  baths,  liberal  diet  with  omission  of  sweets  and 
pastries,  general  hygiene,  and  tonics  such  as  ol.  morrh.,  malt,  hypophos- 
phites,  iodide  of  iron,  iron  and  arsenic.  Attend  to  the  state  of  the  alimen- 
tary tract.  For  mild  cases  use  ung.  hyd.  ox.  flav.  dil.  (grs.  4  ad  oz.  1), 
together  with  atropine,  grs.  4,  if  there  is  photophobia.  Boric  acid  lotion, 
:grs.  10  ad  oz.  1,  can  be  used  as  a  cold  application  to  reduce  inflammation. 
Atropine  has  an  antiphlogistic  action,  besides  limiting  the  movements  of 
the  iris  and  coincident  alterations  in  the  curve  of  the  cornea.  Instil  a  few 
drops  of  a  1  per  cent,  solution,  if  the  cornea  is  involved.  Cocaine  is  added 
if  there  is  much  pain  or  photophobia.  Finely  divided  calomel,  applied 
with  a  brush,  can  be  used  if  iodide  is  not  given  internally.  Do  not  apply 
solid  nitrate  of  silver  for  it  may  produce  a  dense  silver  deposit  in  the  cornea. 
If  the  ulcer  is  purulent  and  threatening  to  perforate,  use  eserine  gr.  1-2  ad 


980  Chapter  LXXI. 

oz.  1,  4-6  times  daily.     In  bad  cases  apply  hot  fomentations,  t.d.s.,  for 
15-20  minutes.     A  large,  thick  shade  or  tinted  glasses  should  be  worn. 

For  photophobia  permit  no  dark  room,  no  bandages,  no  lying  on  the- 
face.  Sponge  with  cold  water  or  plunge  the  face  in  cold  water  ;  and 
introduce  a  speculum  and  expose  the  eye  to  light  for  15  minutes.  Severe- 
blepharospasm  may  necessitate  shading  the  eyes  from  light,  or  even  the- 
division  of  the  outer  canthus  with  scizzors.  No  ansesthetic  is  needed^ 
The  wound  soon  heals  and  leaves  no  obvious  mark.  After  recovery 
correct  any  error  of  refraction.  If  there  is  opacity,  massage  gently  with  the 
yellow  oxide  ointment  for  10  minutes  twice  daily. 

Trachoma. — Syn.  :  Granular  Lids — Follicular  Conjunctivitis. — 
Granular  lids  are  the  result  of  a  chronic  contagious  inflammation  which 
responds  readily  to  treatment.  It  is  acute  or  chronic.  At  first  it  is  a 
follicular  conjunctivitis,  and  later  it  passes  into  the  condition  known  as- 
trachoma,  granular  lids  or  granular  ophthalmia.  Mild  cases  show  a  few 
follicles  (roundish  granulations)  and  a  little  conjunctival  hyperemia.  In 
more  severe  ones  there  are  numerous  follicles,  a  red  and  opaque  con- 
junctiva, swollen  lids,  photophobia,  and  a  variable  amount  of  discharge,, 
sometimes  muco-purulent.  Chronic  granules  look  like  sago  grains.  The 
sequels  are  cicatrisation  leading  to  entropion,  trichiasis  etc.  ;  cloudiness  of 
the  cornea  and  impaired  vision. 

Treatment. — In  acute  stages  use  the  ordinary  remedies  for  conjunc- 
tivitis. In  the  chronic  stage  paint  the  lids  with  cocaine,  holding  them 
from  the  eye.  Then  crush  and  empty  the  follicles  by  pressure  with  one 
thumb  nail  on  the  conjunctiva  and  the  other  outside  the  lid.  After- 
expression  paint  with  argyrol  20  per  cent,  or  silver  nitrate  2  per  cent.,  and 
in  2-3  minutes  brush  with  adrenalin,  1  in  1000,  to  prevent  the  blood  and 
serum  washing  away  the  silver  salt.  A  lotion  of  cyanide  of  mercury,. 
1  in  10,000,  is  ordered  for  home  use,  a  few  drops  being  allowed  to  trickle 
in  between  the  lids  when  washing  the  eyes  with  it.  The  treatment  is. 
repeated  every  third  day  and  the  patient  cured  in  3  weeks.  Other  methods 
are  the  application  of  tannic  acid  grs.  20,  glycerine  oz.  1,  or  sulphate  of 
copper  grs.  2-3,  glycerine  oz.  1,  or  tr.  iodi  and  glycerine  p. a.,  over  the 
inner  surface  of  the  lids  daily  or  on  alternate  days.  The  child  can  attend 
school,  if  he  never  touches  his  eyes  without  washing  his  hands  in  a  basin  of 
antiseptic  lotion. 

Tuberculosis  of  the  Eyelids. — Small  miliary  tubercles,  which  may 
caseate,  ulcerate  and  coalesce,  occur  occasionally,  more  often  on  the 
palpebral  than  the  bulbar  conjunctiva.  The  ulcer  is  round,  oval  or  saucer- 
shaped,  and  not  indurated,  and  causes  some  discomfort  or  pain.  The 
eyelids  may  be  red  and  swollen,  the  pre-auricular  glands  enlarged  and 
tender,  and  the  discharge  purulent.  Such  an  ulcer  may  simulate  chancre. 
It  is  treated  by  scraping  and  constitutional  measures.  Rarer  varieties  are- 
grey  or  yellow   subconjunctival  nodules,   often  mistaken  for  trachoma ^ 


The  Eye.  981 

and  usually  arising  from  the  fornices  and  forming  granulomatous  masses  ; 
"'  cockscomb"  excrescences  in  the  fornices,  with  swelling  of  the  pre-auricular 
•and  parotid  lymph  nodes ;  polypoid  tumours  and  extensions  from  lupoid 
growths. 

The  Lachrymal  Apparatus. — The  puncta  lachrymalia  may  be  absent 
or  duplicated.  Fissure  of  the  gland  or  sac  is  a  rare  congenital  anomaly. 
Unilateral  and  bilateral  absence  of  tears  have  been  recorded.  "  Bloody  " 
•or  sanguineous  tears  come  from  the  conjunctivae  ;  some  possibly  due  to 
vicarious  menstruation. 

Dacryo-adenitis,  inflammation  of  the  gland,  may  be  primary,  secondary 
to  a  stye,  or  associated  with  mumps,  influenza,  measles  or  gonorrhoea.  It 
is  acute  or  chronic,  and  terminates  in  resolution,  suppuration  or  fistula. 
The  physical  signs  are  tenderness  and  swelling  in  the  upper  and  outer  part 
of  the  orbit,  oedema  of  the  upper  eyelid,  and  chemosis  of  the  conjunctiva 
■of  the  upper  fornix. 

Dacryo-cystitis,  inflammation  of  the  sac,  is  more  common  and  is  not 
xare  in  babies  under  6  months  old.  In  them  it  is  due  to  an  impermeable 
nasal  duct,  catarrh  (blenorrhcea),  or  the  retention  of  secretory  products, 
which  become  mucopurulent  from  mild  pyogenic  infection  at  or 
shortly  after  birth.  Other  cases  follow  injury,  nasal  affections,  measles, 
scarlatina,  etc. 

In  babies  it  is  generally  bilateral  and  present  from  birth.  By  the  time 
the  child  comes  under  observation,  it  is  often  unilateral  through  subsidence 
•of  the  affection  on  one  side.  The  physical  signs  are  slight  ill-defined  fulness 
at  the  side  of  the  root  of  the  nose,  swollen  caruncles,  epiphora,  and  some- 
times a  speck  of  muco-pus  in  the  inner  canthus.  On  squeezing  the  swelling 
a  little  serum  or  muco-pus  can  be  pressed  out  through  the  puncta  into  the 
conjunctival  sac  or,  occasionally,  through  the  nostril  on  the  same  side. 
An  acute  attack  may  cause  chilliness,  fever,  severe  local  pain,  redness  and 
oedema.  The  local  swelling  is  defined  and  very  tender.  Later  it  may 
•extend  and  simulate  erysipelas. 

Many  cases  get  well  spontaneously.  Others  require  gentle  compression 
•of  the  sac,  twice  a  day,  to  evacuate  the  contents,  and  perhaps  it  may  be 
necessary  to  probe  the  duct  and  clear  away  obstruction.  For  acute 
inflammation  apply  lead  and  opium  lotion,  or  a  leech,  and  give  a  purge. 
Neglected  cases  may  rupture  externally  and  end  in  fistula,  if  the  nasal  duct 
is  impermeable.  In  older  children  inflammation  and  abscess  may  be 
■syphilitic  or  tuberculous. 

Tears. — Normally  the  secretion  is  only  enough  to  keep  the  con- 
junctiva moist,  and  there  is  no  epiphora,  even  if  the  nasal  duct  is  blocked. 
Excess  is  due  to  emotion,  overflow  from  obstruction  of  the  canaliculi  or 
displacement  of  the  puncta,  irritation  of  the  ophthalmic  branch  of  the 
fifth  nerve,  foreign  body,  reflex  irritation,  and  hypersecretion  occasionally 
.seen  in  exophthalmic  goitre. 


982  Chapter  LXXI. 

Extrinsic  Ocular  Muscles. — Paralysis  depends  on  congenital  defects  ; 
injury  to  the  head  and  cerebral  affections,  such  as  meningitis,  polio- 
encephalitis inferior,  cerebral  syphilis  and  tumour  ;  and  toxins,  notably 
those  of  diphtheria,  measles,  typhoid  and  influenza.  Polioencephalitis 
inferior  may  affect  the  third,  fourth  or  sixth  nerve  alone,  on  one  or  both 
sides.  In  palsy  of  the  third  nerve  the  pupil  is  dilated,  and  reacts  to  light 
but  not  to  accommodation.  Squint  is  due  to  paralysis,  weakness  or 
congenital  defect  of  the  muscle,  or  visual  deficiencies.  A  convergent  squint 
suggests  hypermetropia.     Treat  the  refractive  error. 

Complete  Ophthalmoplegia  may  be  hereditary  and  congenital.  Gourfein 
reported  one  family  in  which  the  father  and  5  sons,  aged  8  months  to 
12  years,  were  affected  and  3  daughters  unaffected.  The  man's  mother 
showed  a  like  defect  and  a  sister  had  convergent  squint.  The  signs  were 
complete  ptosis,  inability  to  move  the  eyeball,  rotatory  nystagmus,  and  a 
certain  amount  of  amblyopia. 

Congenital  Ptosis  is  usually  bilateral  and  associated  with  defective 
upward  and  downward  movements  of  the  eyes,  weak  lateral  and  good 
convergent  ones.  Sometimes  the  oblique  muscles  are  inert.  There  is  no 
affection  of  the  intrinsic  muscles  and  no  association  with  other  congenital 
defects.  It  depends  on  imperfect  development  of  the  muscles  or  nerve 
nuclei. 

The  Eyeball. — Microphthalmos  has  been  noted  as  a  congenital  and 
familial  affection.  It  was  associated  with  cataract  in  a  man  and  4  out  of 
his  8  children,  and  in  a  woman  and  all  her  4  children  (A.  Bronner,  1902).. 
A  translucent  globule  in  the  hinder  part  of  the  vitre.ous  humour  is  regarded 
by  S.  Stephenson  as  a  common  defect.  Lang  and  Collins  have  described 
"  little  rounded  bodies  of  a  steel-grey  colour  which  appear  to  be  fluid- 
containing  cysts  attached  to  the  optic  nerve."  They  are  situated  in  the 
fundus  in  the  immediate  neighbourhood  of  the  optic  disc,  and  possibly 
have  some  connection  with  the  embryonic  hyaloid  artery  of  the  sheath. 
No  change  has  been  noted  in  them  as  age  advances.  The  iris  may  be 
absent  on  one  or  both  sides,  or  show  a  coloboma,  which  may  involve  the 
choroid  and  optic  disc,  on  one  or  both  sides.  Anterior  staphyloma,  often 
bilateral,  is  due  to  failure  of  development  of  the  anterior  chamber  or  infec- 
tion via  the  amniotic  fluid.     It  is  decidedly  rare. 

The  lens  may  be  congenitally  dislocated,  as  a  familial  defect.. 
Congenital  cataract,  of  a  partial  and  stationary  type,  has  been  recorded 
by  Nettleship  and  Ogilvie  (1906)  in  20  members  in  4  generations  of  one 
family.  The  sight  was  little  affected.  Lamellar  or  zonular  cataract  is  not 
infrequently  associated  with  enamel  defects  in  the  permanent  teeth  and  a 
history  of  infantile  fits.  It  is  not  due  to  mercury,  for  it  may  be  present 
without  such  a  past  history. 

Congenital  Glaucoma,  or  Buphthalmos,  may  be  present  at  birth  or 
develop  very  early  in  life,  and  in  several  members  of  a  family.     One  or 


The  Eye.  983 

both  eyes  look  unusually  large  or  "  ox-eyed,"  and  the  child  is  said  to  have 
"  a  fine  pair  of  eyes."  It  is  the  result  of  increased  ocular  tension  from 
developmental  defect  or  an  inflammation  of  the  iris  and  adjoining  parts, 
probably  of  syphilitic  origin.  Evidence  of  congenital  syphilis  is  often 
obtained.  The  increased  tension  leads  to  progressive  uniform  enlargement 
of  the  whole  eye,  owing  to  its  distensibility  in  infancy.  The  cornea  is 
increased  in  size,  altered  in  curvature,  and  cloudy.  The  anterior  chamber 
is  deepened.  The  optic  disc  is  abnormally  cupped  and  atrophic,  the  visual 
fields  contracted,  and  the  sight  defective.  The  iris  is  thinned,  stretched, 
and  may  be  torn.  Mild  cases  show  abnormally  large  eyes,  increased 
tension,  a  little  cloudiness  and  photophobia.  They  are  liable  to  hsemorrhage, 
detachment  of  the  retina,  sub-luxation  of  the  lens,  escape  of  the  vitreous, 
corneal  ulceration,  choroidal  degeneration  and  cataract. 

It  must  be  diagnosed  from  slight  congenital  opacities  of  the  cornea, 
interstitial  keratitis,  and  the  buphthalmos  secondary  to  ophthalmia 
neonatorum  or  severe  interstitial  keratitis.  Some  cases  get  well,  with  or 
without  treatment.  Others  end  in  blindness.  The  treatment  consists 
in  the  prolonged  use  of  myotics  and  mercurials  in  mild  cases.  Iridectomy 
is  of  great  value  prior  to  enlargement,  and  sclerotomy  subsequently. 

The  Cornea. — Injury  at  birth  may  cause  subconjunctival  or  retinal 
hajmorrhage,  dislocation  of  the  eyeball,  retroversion  of  the  lens  and  vitreous, 
or  traumatic  keratitis.  The  cornea  may  exhibit  at  birth  an  opacity  in  its 
anterior  layers,  with  dulness  of  the  surface  but  no  vascularity.  The  lids 
and  conjunctiva!  show  some  bruising.  This  is  due  to  injury  by  forceps  or 
by  a  contracted  pelvis.  It  may  be  present  in  non-forceps  cases.  A 
diffuse  temporary  opacity  depends  on  oedema.  A  central,  oblique  or 
vertical,  linear,  white  scar  with  an  adjacent  area  of  fainter  haze,  as  a 
permanent  sequel,  is  due  to  fibrosis  secondary  to  rupture  of  the  posterior 
elastic  lamina  of  the  cornea. 

Keraiomalacia  is  a  softening  or  gangrene  of  the  cornea,  usually  bilateral, 
sometimes  found  in  marasmic  infants  3-12  months  old.  It  is  identical 
with  ';  Hikan,"  prevalent  in  Japan  during  the  diarrhoeal  season,  and  with 
the  Ophthalmia  Braziliana  of  South  America.  It  is  common  in  Russia 
during  the  great  Lenten  Fast.  It  is  rare  in  the  breast-fed  unless  the 
mother  has  undergone  starvation.  In  London  hospitals  it  is  associated 
with  dangerous  marasmus  from  tuberculosis,  congenital  syphilis,  ileo- 
colitis, broncho-pneumonia  and  bad  feeding.  S.  Stephenson  found  the 
treponema  pallidum  in  the  scrapings  from  4  cases.  Probably  it  can  be  set 
up  by  many  different  organisms.  Infiltration  is  followed  by  ulceration, 
sloughing,  sometimes  pus  in  the  anterior  chamber,  and  perforation,  with 
extrusion  of  the  contents  and  collapse  of  the  eyeball.  Symptoms  are 
limited  to  athrepsia,  central  ulceration  and  sloughing  of  the  cornea,  slight 
local  reaction,  and  perhaps  a  little  swelling  of  the  lids  and  blepharospasm. 
Sensation  appears  blunted.     The  prognosis  is  that  of  the  constitutional 


984 


Chapter  LXXI. 


state.  About  two-thirds  of  these  babies  die,  generally  before  the  disease 
has  progressed  to  perforation. 

Family  Corneal  Degeneration  is  very  rare.  Discrete  grey  dots  or 
nodules,  or  a  lattice-like  system  of  lines  with  intervening  minute  dots, 
appear  in  the  cornea  about  puberty.  The  degeneration  is  bilateral,  central, 
unassociated  with  syphilis  or  inflammation,  of  slow  progress,  and  seriously 
impairs  sight. 

Treatment  of  Corneal  Affections. — Use  atropine  drops,  1  per  cent, 
strength,  for  abrasions  or  infiltration  ;  ung.  atropines  for  ulceration,  with 
the  addition  x>f  iodoform,  dr.  1  ad  oz.  1,  if  it  is  septic.  In  keratomalacia 
attend  to  the  general  health,  keep  the  eyes  bandaged  up  and  use  the 
greatest  gentleness.  Douche  frequently  with  warm  boric  acid  lotion, 
and  instil  physostigmine  sulphate,  gr.  1  ad  aquam  oz.  1,  every  4-6  hours, 
causing  the  sloughs  to  be  cast  off.  For  corneal  opacities  massage  with 
ung.  hyd.  oz.  flav.  dil.  for  10  minutes,  bis  die. 

The  Iris  is  affected  with  inflammation  in  the  same  way  as  in  adults. 
Sometimes  it  is  tuberculous.  Miliary  tubercles  may  be  scattered  over 
its  surface.  They  disappear  or  fuse  into  a  mass  of  granulation  tissue, 
and  may  lead  to  perforation  of  the  corneoscleral  juncture  and  loss  of  the 
eye.  Occasionally  confluent  or  conglomerate  tubercle  forms  a  definite 
yellowish  tumour  with  smaller  surrounding  satellites.  Or  a  tuberculous 
iritis  may  occur.  The  ciliary  body  may  be  affected  primarily  by  tuber- 
culosis, or  secondarily  to  the  iris  or  choroid.  The  retina  is  affected 
secondarily  to  the  uveal  tract  or  the  optic  nerve. 

The  Choroid. — Miliary  tubercles,  up  to  70  in  number,  are  found  in 
both  eyes,  shortly  before  death  in  75  per  cent.  (Litten)  or  82*7  per  cent. 
(Bock),  of  all  cases  of  general  tuberculosis.  They  vary  from  pin-point 
specks  to  tubercles  2  mm.  in  diameter.  Often  there  is  only  one  small 
tubercle,  and  only  in  one  eye.  Solitary  tubercles,  or  more  than  one,  are 
not  infrequent  in  chronic  tuberculosis,  possibly  in  about  10  per  cent. 
Chronic  forms  exist  in  which  there  is  an  extensive  area  of  inflammation  and 
much  granulation  tissue  ;  or  a  single  large,  conglomerate,  circumscribed 
tumour  simulating  a  glioma.  Chronic  tuberculosis  of  the  choroid  may  be 
associated  with  tuberculosis  of  the  conjimctiva ;  may  cause  retinal 
detachment ;  may  become  obsolescent  or  re-absorbed,  leaving  patches  like 
those  of  albuminuric  retinitis,  without  residual  pigment ;  or  may  gradually 
extend  and  destroy  the  eye.  Tubercle  of  the  choroid  is  often  single  and 
central,  whereas  gummata  are  commonly  multiple  and  peripheral. 

Night-Blindness  or  Nyctalopia,  and  Day-Blindness  or  Hemeralopia. — 

In  night-blindness  the  child  sees  well  in  the  daytime,  i.e.  if  the  light  is- 
good,  and  badly  in  the  dark  or  when  passing  into  a  shadow.  In  hemeralopia 
the  sight  is  better  by  night  or  in  a  feeble  light,  because  central  vision  is 
impaired  and  the  child  is  dependent  on  peripheral  vision,  seeing  better  when 


The  Eye.  985 

the  pupils  are  dilated.  It  is  due  to  central  corneal  opacities  or,  in  older 
patients,  to  central  scotoma,  e.g.  in  tobacco  poisoning. 

Night-blindness  may  be  familial,  congenital  or  acquired ;  and 
■stationary  or  progressive.  One  variety,  due  to  "  torpor  retinae,"  is  common 
in  India  and  in  Russia  during  the  Lenten  Fast.  It  has  been  ascribed  to 
malnutrition  and  to  deficient  alkalinity  of  the  blood.  This  may  be 
associated  with  xerosis  and  conjunctivitis  pigmentosa,  ulceration  of  the 
•cornea  and  keratomalacia.  Malannah  (1908)  states  that  urotropin  is 
beneficial. 

The  Stationary  Type  is  familial  and  shows  no  ophthalmoscopic  changes. 
Possibly  there  is  a  deficiency  of  visual  purple  in  the  reds  and  cones  of  the 
Tetina.  Cunier  published  the  history  of  a  remarkable  family  (600  members, 
7  generations),  but  the  nature  of  the  affection  was  only  diagnosed  in 
1906.  Nettleship  (1907)  studied  this  family,  and  his  chart  embraces  10 
generations  and  2121  individuals.  The  disease  was  traced  to  an  ancestor, 
Jean  Nougaret,  born  in  1637.  It  passed  from  parent  to  child,  was  rather 
more  common  in  females,  not  due  to  consanguinity,  and  was  not  associated 
with -blindness,  other  defects  or  peculiarities.  In  this  family  it  must  be 
regarded  as  a  dominant,  for  only  the  affected  transmitted  the  peculiarity. 
In  other  instances  it  has  been  transmitted  by  the  unaffected. 

The  Progressive  Type  is  due  to  retinitis  pigmentosa  and  is  associated 
with  progressive  atrophy  of  the  optic  nerve.  It  is  a  slow  degeneration  or 
atrophy  of  the  retina,  with  deposition  of  black  pigment  along  the  blood 
vessels.  Possibly  it  depends  on  atrophy  of  the  rods  and  cones  and 
secondary  migration  of  the  pigment.  A  4-year  old  boy  had  a  very  granular 
appearance  of  the  fundus,  as  if  the  pigment  was  escaping  from  the 
•epithelium.  The  pigmentation  is  not  always  present.  Snell  (1907) 
reported  it  as  a  familial  affection  in  12  out  of  ^64  members  in  4  generations  ; 
'9  males,  3  females.  The  males  transmitted  the  affection  to  the  daughters 
and  the  females  to  the  sons, ,  the  other  sex  being  normal  in  each  case. 
Syphilitic  retinitis,  or  retino-cJioroiditii,  may  cause  night-blindness  which 
progresses  for  a  time  and  then  becomes  stationary.  It  is  not  always 
syphilitic  and  is  sometimes  associated  with  microcephalus  or  cerebral 
•degeneration. 

Glioma  also  occurs  as  a  familial  disease,  e.g.  10  out  of  16  children  in  one 
family  (R.  Earle  Newton,  1902),  2  being  dead  and  4  unaffected.  The  sexes 
were  equal.  It  was  unilateral  in  3,  bilateral  in  7.  Six  were  unoperated 
on  and  the  eye  ruptured  in  all.  A  unilateral  growth  was  removed  in  one 
•case,  but  death  ensued  from  recurrence  at  5  years.  The  others  died  under 
4  years  of  age.  The  prognosis  is  very  bad.  Snell  (1904)  reported  2  cases  in 
•one  family.  One  was  bilateral,  unoperated  on  and  fatal.  The  other  was 
unilateral,  removed,  and  had  not  recurred  in  6  months.  In  another  case 
the  first  eye  was  removed  at  22  months,  the  second  one  2  months  later, 
and  the  child  was  alive  and  well  5  years  afterwards.     A  unilateral  case 


986  Chapter  LXXI. 

operated  on  in  the  fifth  month  showed  no  recurrence  at  18  months.  A 
girl  under  my  care  had  the  right  eye  removed  at  16  months,  and  showed 
recurrence  8  months  later  in  the  form  of  multiple,  rounded,  smooth, 
softish  nodules  fixed  to  the  skull  and  not  adherent  to  the  scalp.  Some 
became  purplish  in  colour.  The  left  eye  was  partially  proptosed  and 
showed  a  white  growth  in  the  posterior  chamber,  with  the  retinal  vessels 
running  over  it ;  and  the  left  cheek  was  white,  waxy  and  swollen.  Next 
the  eyelids  became  purplish.  Death  ensued  2  months  later.  Nodules  of 
growth  had  appeared  in  the  groins.  The  only  hope  is  immediate  removal. 
It  must  not  be  mistaken  for  a  tuberculous  tumour. 

Optic  Nerve. — Congenital  optic  atrophy  occurred  in  55  members  of 
16  families  (Leber),  chiefly  but  not  exclusively  in  males  and  transmitted 
by  females.  It  began  usually  after  puberty,  in  one  patient  at  5  years  of 
age.  Dimness  of  vision  comes  on  suddenly  and  increases  rapidly,  rarely 
to  complete  blindness.  Apparently  it  is  a  neuritic  atrophy  and  may  be 
induced  by  toxins,  tobacco  or  congenital  syphilis.  The  nerve  may  be 
affected  by  tuberculosis  spreading  from  the  choroid.  Miliary  tubercles  are 
found  in  the  sheath  and  septa  in  general  tuberculosis.  No  special 
reference,  beyond  allusions  in  the  text,  is  necessary  concerning  the  ordinary 
forms  of  optic  neuritis,  choked  disc  and  atrophy. 

Amblyopia. — The  "  acute  cerebral  amaurosis  "  of  William  Gay,  or 
"  fleeting  amaurosis,"  is  a  loss  of  sight,  without  ophthalmoscopic  changes, 
due  to  basal  meningitis.  Post-eclamptic  amaurosis  (Ashby  and  Stephenson) 
is  similar  in  character,  but  seeing  that  it  is  sometimes  associated  with 
aphasia  or  hemiplegia,  it  may  depend  on  cerebral  changes,  the  visual 
cortical  centres  being  involved.  Meningitis  or  encephalitis,  with  papillitis,. 
is  the  most  probable  explanation  of  bilateral  "  incomplete  post-papillic 
atrophy  of  the  optic  discs  ;  it  may  be  very  slight,  or  associated  with  squint 
and  nystagmus."  There  is  usually  a  past  history  of  fits,  headache, 
vomiting,  constipation,  retracted  head,  palsy,  squint  and  unconsciousness,, 
with  partial  or  total  blindness  which  has  been  more  or  less  recovered  from. 

Refractive  errors  are  described  in  works  on  ophthalmology.  For 
2  hours  to  2  days  after  birth  there  is  frequently  4-7  D.  of  myopia,  with 
dilated  pupils  and  almost  immobile  eyeballs  (Elshnig,  1906).  It  disappears 
after  instillation  of  atropine  and  is  replaced  by  hypermetropia  or  emme- 
tropia.  Refractive  errors,  notably  astigmatism,  are  a  cause  of  headache. 
Myopia  is  often  hereditary,  but  generally  is  the  result  of  undue  use  of  the 
eyes  in  reading  badly  printed  school-books  in  an  unsuitable  light. 


CHAPTER    LXXIT. 

THE    EAR. 

Hearing— Congenital    Defects — Affections  of  the   External   Ear — Foreign 
Bodies —  Otitis  Media —  Earache —  Otorrhea — Mastoiditis. 

Perfect  hearing  is  essential  to  the  perfect  acquirement  of  speech,  and  for 
intellectual  and  moral  development.  Children  with  defective  hearing  learn 
speech  slowly,  often  slur  the  consonants,  and  have  a  somewhat  toneless 
voice.  Primarily  sounds  are  registered  in  the  cortical  auditory  centres 
and  sense  memories  of  them  are  there  stored  up.  In  the  next  stage  the 
child  attempts  motor  reproductions  of  these  memories  (echolalia),  and 
gradually  develops  intelligent  speech. 

Physiology  -  and  Anatomy. — The  blood  vessels  of  the  auricle  are 
superficial  and  susceptible  to  cold.  Chilblains  and  frost-bite  are  common. 
The  nerve  supply  is  abundant.  The  auricular  branch  of  the  vagus  is  partly 
distributed  to  the  external  auditory  meatus.  Hence,  local  irritation  of  the 
meatus  may  cause  "  ear  cough.''''  The  epidermis,  lining  the  auditory  canal, 
contains  sebaceous  and  ceruminous  glands  and  many  short  hairs,  and  is 
continued  over  the  drum  as  a  very  thin  layer. 

The  middle  ear  consists  of  the  tympanum  or  tympanic  cavity,  the  bony 
part  of  the  Eustachian  tube,  and  the  mastoid  antrum.  The  continuity  of 
these  parts  is  easily  made  out  in  infancy  and  early  childhood.  The 
tympanum  and  Eustachian  tube  are  the  remains  of  the  first  post-oral 
visceral  cleft,  and  the  antrum  is  also  developed  from  this  cleft.  The 
cavity  is  a  small  irregular  space  between  the  drum  and  internal  ear.  It  is 
lined  with  ciliated  epithelium  on  its  floor  and  toward  the  Eustachian  tube, 
through  which  it  communicates  with  the  pharynx.  The  mucous  membrane 
is  closely  adherent  to  the  bone,  which  becomes  readily  affected  in  disease. 
The  plate  of  bone  separating  the  tympanum  from  the  meninges  is  extremely 
thin  and  sometimes  congenitally  absent.  Inflammation  may  readily 
spread  from  one  to  the  other.  The  petro-squamous  suture  runs  across  the 
roof  of  the  tympanum  and  is  not  obliterated  until  the  end  of  the  first  year, 
and  not  always  then.  The  close  relationship  of  the  mastoid  cells  to  the 
internal  ear  is  also  of  much  importance.  During  early  life  the  mastoid  bone 
is  small  and  its  cells  undeveloped.  In  children  the  external  lamina  of  this 
bone  is  thin  and  easily  perforated. 

The  Eustachian  tube  maintains  equality  of  pressure  in  the  tympanum 
with  that  of  the  external  atmosphere,  and  is  the  channel  by  which  the 


•988  Chapter  LXXII. 

secretions  of  the  mucous  membrane  escape  from  the  middle  ear.  Obstruc- 
tion to  its  orifice  or  canal  induces  distension  with  secretion,  indrawn 
drum,  deafness,  tinnitus  etc.  It  is  nearly  horizontal  at  birth.  It  opens 
into  the  pharynx  at  the  level  of  the  hard  palate  until  the  age  of  9  months, 
then  a  little  higher.  Though  it  is  wider  than  in  adults,  catheterisation  is 
almost  impossible,  for  the  fossa  of  Eosenmuller  is  nearly  imperceptible. 

The  external  auditory  canal  is  almost  straight,  running  a  little  forward 
and  inward ;  and  the  tympanic  membrane  is  placed  more  horizontally 
than  in  adults,  being  almost  horizontal  at  birth.     . 

Examination  of  the  Ear  and  Hearing. — Enquire  into  the  family  history. 
Seek  for  evidence  of  congenital  syphilis,  a  previous  attack  of  scarlatina  or 
measles,  etc.,  nasal  or  respiratory  affections,  earache  and  otorrhoea. 
Ascertain  the  mode  of  onset  and  duration  of  symptoms.  Note  the  general 
■condition  of  the  child,  its  mode  of  life,  diet  and  environment,  and  its  facial 
■aspect.  Examine  the  throat  and  nose  for  enlarged  tonsils,  adenoids,  post- 
nasal catarrh  and  nasal  obstruction.  Syringe  away  any  wax  or  discharge 
present. 

Apart  from  dulness  of  hearing,  the  ears  should  be  examined  in  the 
first  year  of  school  life  and  after  exanthemata.  The  usual  tests  are  whis- 
pered speech,  ordinary  speech,  a  bell,  watch,  Galton's  whistle  and  the 
tuning  fork.  The  whispered  voice  is  heard  by  the  normal  ear  at  a  distance 
of  18-27  feet.  The  ear  should  be  turned  toward  the  examiner,  the  other 
one  plugged  with  wool,  and  the  eyes  covered  or  closed.  Cases  are  classified 
■as  bad  deafness  when  the  whisper  cannot  be  heard  at  a  distance  of  over 
2  yards  ;  medium,  at  2-4  yards  ;  and  slight,  if  heard  over  4  yards  away. 
Sibilants,  s  and  sch,  are  usually  heard  badly  in  disease  of  the  conducting 
•apparatus,  r  in  defects  of  the  drum,  and  /  in  labyrinthine  disease.  A 
watch  is  not  a  reliable  testing  instrument,  for  its  tick  varies  and  is  a  com- 
pound of  sound  and  noise.  The  tuning  fork  only  gives  satisfactory  results 
in  very  intelligent  children.  If  it  is  not  heard  in  the  deaf  ear,  when  applied 
to  the  vertex  or  on  the  mastoid,  there  is  probably  serious  disease  of  the 
auditory  nerve  or  nucleus,  fortunately  rare  in  childhood.  For  infants  and 
the  very  deaf  reliance  must  be  placed  on  sudden  sounds,  e.g.  that  of  a  bell 
with  the  clapper  fixed  by  a  spring  to  the  outer  surface,  and  noting  whether 
the  eyes  are  attracted  toward  the  sound.  Care  must  be  taken  to  eliminate 
the  effects  of  vibration.  It  is  important  to  note  what  escapes  the  child, 
quite  as  much  as  what  he  hears.  Inability  to  hear  soft  sounds,  the  murmur 
of  the  breeze,  the  shivering  of  the  leaves,  and  the  buzzing  or  humming  of 
insects,  is  a  serious  drawback  to  the  intellectual  appreciation  of  life  and 
nature. 

Note  the  characters  and  appearance  of  the  pinna  and  external  auditory 
meatus,  and  if  there  is  otorrhcea.  Affections  of  the  canal  can  generally  be 
•diagnosed  without  a  speculum,  by  simple  inspection  in  a  bright  light. 
For  examining  the  drum  use  Brunton's  otoscope,  containing  a  lens,  or  a 


The  Ear.  989« 

speculum  and  reflected  light  from  a  forehead  or  hand  mirror.  Warm  the 
speculum  first.  An  infant  or  young  child  should  be  held  sideways  on  the 
nurse's  lap  with  the  head  against  her  breast.  Under  4  years  of  age,  the 
canal  is  straightened  by  pulling  the  auricle  outward,  downward  and 
forward,  or  downward  and  backward.  Above  that  age  it  is  pulled  upward 
and  backward.  Wipe  away  discharge,  if  present,  with  a  dry  antiseptic 
mop  ;  and  gently  syringe  out  any  wax  which  impedes  the  view.  Look  for 
a  relaxed  or  depressed  membrane,  inflammation,  perforation,  and  a 
"  dancing  bubble,"  a  minute  speck  which  pulsates  and  is  due  to  perforation. 

Inflation  is  used  for  diagnosis  and  treatment.  In  Valsalva's  method 
the  patient  holds  the  nose,  shuts  the  mouth  and  swallows  suddenly.  If 
the  tube  is  patent,  air  rushes  up  into  the  tympanum.  In  Politzer's  method 
a  small  rubber  bag  with  a  soft  nozzle  is  used.  The  patient  takes  a  mouthful 
of  water,  with  the  nozzle  of  the  bag  in  one  nostril  and  the  nostrils  com- 
pressed by  the  finger  and  thumb,  and  swallows  as  the  operator  compresses 
the  bag.  If  the  child  can  be  taught  to  puff  out  the  cheeks,  swallowing  is 
not  always  necessary.  A  rubber  tube,  with  an  ear  piece  at  each  end,  is 
inserted  into  the  ears  of  the  patient  and  operator.  Complete  absence  of 
sound  and  no  improvement  in  hearing  indicate  Eustachian  obstruction. 
A  "  pop  ':  is  heard,  if  the  obstruction  is  relieved  ;  "  bubbling,"  if  there  is 
mucus  in  the  tube  or  fluid  in  the  tympanum  ;  and  "  whistling,"  if  there 
is  perforation. 

Children,  especially  when  young  and  nervous,  must  be  examined  with 
great  care  and  tenderness.  Otherwise  they  may  be  hurt  or  frightened  and 
it  is  impossible  to  form  accurate  conclusions.  If  there  is  great  tenderness, 
an  anaesthetic  is  necessary.  No  probe  or  director  should  be  used  in 
examining  for  a  foreign  body,  without  full  illumination.  If  the  drum 
cannot  be  seen  because  of  swelling,  reduce  the  swelling  and  examine  later. 
Catheterisation  is  rarely  advisable. 

Congenital  Abnormalities.- -Developmental  errors  chiefly  affect  the 
auricle.  It  is  formed  by  the  coalescence  of  6  tubercles  on  the  margin  of 
the  first  branchial  cleft.  The  ear  may  be  represented  by  a  lump  of  skin. 
Supernumerary  auricles  are  not  uncommon,  usually  in  the  form  of  one  or 
more  small  tubercles  of  skin  near  the  lobule  of  the  ear  or  on  the  side  of 
the  neck.  Rarely  one  is  modified  to  imitate  a  second  pinna.  They  are 
due  to  persistence  or  modification  of  the  primary  tubercles  and  should  be 
removed.  Inequality  in  size  results  from  excessive  or  defective  develop- 
ment of  one  pinna.  A  very  small  ear  may  be  associated  with  facial  hemi- 
atrophy. Peculiarities  in  shape  are  present  in  many  idiots  and  are 
regarded  as  stigmata  of  degeneration.  Protruding  ears  are  due  to 
developmental  defects,  ill-fitting  caps,  strings  behind  the  ears,  or  pressure 
on  the  turned-over  ear  during  sleep.  A  suitable  apparatus  worn  at  night 
cures  some  cases.  Or  a  plastic  operation  can  be  done,  a  piece  of  skin  being 
removed  from  the  auriculo-mastoid  juncture.     Congenital  defects  of  the- 


990  Chapter  LXXII. 

pinna  are  often  combined  with  occlusion  of  the  canal  and  branchial  fistula, 
imperfections  in  the  deeper  aural  structures,  and  sometimes  with  con- 
genital morbus  cordis  and  other  malformations.  The  meatus  may  be 
closed  by  a  membranous  septum. 

External  Ear. —  Erythema  amis,  the  result  of  sunburn,  may  need  a 
cooling  lotion  or  soothing  powder  for  its  relief.  Intertrigo  is  a  superficial 
erythema,  often  due  to  binding  the  auricle  to  the  head  before  it  is  properly 
washed  and  dried  or  to  the  use  of  irritating  powders  and  lotions.  Wash  the 
part  gently  twice  a  day,  dry  by  dabbing,  and  dust  with  emol  keleet,  or 
zinc  oxide  and  starch.  Eczema  is  common  in  all  its  forms,  acute  and 
chronic.  It  is  dry,  vesicular,  papular  or  pustular,  and  often  secondary  to 
facial  eczema  or  local  irritation  from  otorrhcea.  The  pustular  variety  is 
sometimes  of  the  nature  of  an  impetigo,  and  called  impetigo  auris,  and  is 
due  to  microbial  infection.  Chronic  eczema  leads  to  thickening  and 
deformity  of  the  pinna,  and  extends  into  the  meatus,  causing  swelling  and 
•obstruction.  Other  affections  include  herpes,  erysipelas,  gangrene,  Eay- 
naud's  disease  and  tuberculous  ulceration  around  ear-rings. 

Treatment. — For  details  refer  to  the  section  on  eczema.  Protect  the 
■ear  from  air,  water  and  injury.  Do  not  allow  remedies  to  get  to  the 
tympanum.  For  the  cure  of  a  very  chronic  eczema  it  may  be  necessary  to 
set  up  an  acute  attack. 

Foreign  Bodies  are  frequently  unsuspected,  giving  rise  to  no  symptoms. 
Some  are  soft,  e.g.  peas,  and  tend  to  swell  after  insertion.  Others  are 
hard,  smooth  or  rough,  e.g.  beads,  stones,  slate  pencil,  fruit  stones,  etc. 
Occasionally  insects  of  various  kinds  or  maggots  are  found.  Foreign 
bodies  more  often  give  rise  to  injurious  consequences  from  the  attempts 
made  to  remove  them  than  when  left  alone.  Both  hearing  and  life  have  been 
sacrificed  to  unskilful  management.  In  the  case  of  a  bead  or  pebble  there 
is  no  urgency,  for  there  is  normally  a  tendency  to  spontaneous  extrusion 
by  the  growth  of  the  epidermis  outward. 

Insects  can  be  killed  by  filling  the  ear  with  warm  carbolic  lotion  or  a 
pledget  of  wool  soaked  in  chloroform.  Maggots  are  killed  by  carbolic- 
lotion,  or  a  mixture  of  chloroform  1,  sp.  vin.  rect.  2  parts,  and  then  removed 
by  syringing.  For  bodies  which  do  not  swell,  syringe  with  warm  water  ; 
for  peas  and  similar  soft  substances,  syringe  with  warm  oil,  instilling 
glycerine  in  the  intervals  to  induce  shrinkage.  Always  direct  the  stream 
against  the  upper  wall  of  the  canal,  with  the  head  inclined  toward  the 
affected  side.  Inject  the  fluid  regularly,  not  in  jerks.  Do  not  syringe  unless 
the  body  has  been  seen.  Therefore,  examine  first  in  a  good  light  and  do 
not  try  to  locate  it  by  probing  in  the  dark.  Attempts  to  remove  it  by 
forceps  are  more  likely  to  push  it  further  in.  If  there  is  inflammatory 
swelling  reduce  it  first  by  antiseptic  and  sedative  lotions  before  trying  to 
remove  the  body.  If  syringing  fails,  recourse  is  had  to  the  use  of  a  wire 
loop  for  hard  bodies  and  a  fine  crochet  hook  for  soft  ones. 


The  Ear.  991 

Impacted  Wax. — The  insertion  of  water  into  the  ear,  as  in  bathing  and 
plunge  baths,  hardens  the  wax  into  a  mass  which  is  retained.  Another 
cause  is  the  use  of  appliances,  such  as  a  small  sponge  on  a  stick,  for  cleaning 
the  ears.  Wax  is  protective  and  only  the  excess  should  be  removed. 
Obstruction  of  the  canal  and  catarrh  of  the  middle  or  external  ear  are 
predisposing  factors.  Impaction  produces  dulness  of  hearing,  actual 
deafness  and  noises  in  the  ear,  but  rarely  any  injury  to  the  drum.  The 
wax  is  easily  removed,  for  it  rarely  forms  the  hard,  massive  plug  found  in 
adults.  A  plug  of  compressed  scales,  due  to  desquamative  dermatitis,  is 
more  irregular  and  lighter  in  colour.  On  syringing  it  swells  up  and  causes 
increased  pressure  and  headache.  It  can  be  removed  by  forceps,  after 
softening  it  for  2  days  by  instillation  of  ac.  salicyl.  gr.  5,  sp.  vin.  rect.  m.  90, 
glycerine  oz.  -|.  For  the  removal  of  wax  use  a  syringe  with  a  fine  nozzle,  a 
lotion  of  sod.  bicarb,  or  borax,  good  light  and  a  forehead  mirror.  The 
wax  can  be  softened  by  dropping  in,  5-6  times  daily,  a  few  drops  of  sod. 
bicarb,  grs.  20,  glycerine  m.  30,  water  to  oz.  1.  The  stream  from  the 
•syringe  must  be  directed  toward  the  roof  of  the  canal.  As  soon  as  the 
wax  is  evacuated,  the  hearing  returns  and  is  often  very  acute.  Afterwards 
insert  a  plug  of  wool  for  a  few  hours  to  protect  from  cold.  If  the  hearing  is 
not  improved,  examine  for  disease  of  the  middle  or  internal  ear. 

Furunculosis. — A  boil  in  the  canal  is  very  painful  and  may  cause 
inflammatory  swelling  over  the  mastoid.  Insert  a  pledget  of  wool  soaked 
in  ichthyol  and  glycerine,  p. a.,  with  another  pledget  to  keep  in  the  solution 
without  exerting  pressure,  once  or  twice  daily  until  the  boil  dries  up.  It 
prevents  further  infection  and  eczema  of  the  meatus,  if  the  boil  suppurates, 
bursts  or  is  opened.  Should  incision  be  necessary,  use  a  special  knife  so 
shaped  that  the  point  is  directed  outward. 

Earache  is  a  symptom  not  always  easy  to  diagnose  in  infants.  Keliance 
must  be  placed  on  the  troubled  face,  resting  the  head  on  the  nurse,  refusal 
to  rest  it  on  the  affected  side,  rolling  the  head  on  the  pillow,  rubbing  or 
pulling  the  ear,  putting  the  hand  to  the  ear  or  side  of  the  head,  and  "crying 
on  sudden  change  in  position  of  the  head,  on  touching  the  ear,  and  on 
pressure  below  the  meatus.  It  is  not  always  due  to  ear  disease,  being  some- 
times reflex,  e.g.  along  the  auriculo-temporal  nerve  from  dental  caries  or 
during  dentition. 

Cocaine,  followed  by  large  hot  fomentations,  is  the  best  treatment. 
Or  insert  a  few  drops  of  (1)  warm  olive  oil  and  chloroform,  p. a.  ;  (2)  cocaine, 
'2  per  cent,  in  aniline  oil  and  sp.  vin.  rect.  p. a.  ;  (3)  adrenalin  1  in  2000  ; 
(4)  ac.  carbolici  grs.  5-10,  glycerine  oz.  1.  Never  use  cold  applications  and 
avoid  spirituous  lotions.  Other  remedies  are  irrigation  with  hot  lysol  or 
lysoform  lotion,  fomentations,  mustard  leaf  over  the  mastoid,  and  possibly 
a  few  drops  of  tr.  opii  internally.  Paracentesis  is  unnecessary  and 
Politzerisation  unsuitable. 

Otitis  Media. — Inflammation  of  the  middle  ear  is  of  grave  importance 
in  early  life.     During  infancy  it  may  cause  deaf-mutism  or  be  the  starting 


992  Chapter  LXXII. 

point  of  ear  disease  at  a  later  age.  It  is  acute  or  chronic,  primary  or 
secondary,  and  gives  rise  to  earache,  fever  and  subsequent  otorrhcea.  The 
discharge  is  serous,  seropurulent  or  purulent. 

Etiology. — It  is  extremely  common  under  2  years  of  age  and  bilateral 
in  50  per  cent.  Rasch  (1894)  found  no  exudation  before  the  third  day  of 
life.  Primary  cases  are  exceptional ;  the  cause  may  be  overlooked.  Few 
are  due  to  blood  infection.  Nearly  all  are  secondary  to  direct  infection, 
via  the  Eustachian  tube  or  lymphatics,  from  the  throat,  nose  and  naso- 
pharynx, especially  adenoids.  Often  it  complicates  an  acute  catarrhal 
respiratory  or  pneumonic  affection.  Of  the  infective  fevers  scarlatina  is 
the  great  cause,  measles  next,  and  less  frequently  diphtheria,  varicella,, 
variola  and  typhoid  fever. 

It  complicates  cerebrospinal  and  pneumococcal  meningitis,  influenza, 
pertussis,  various  throat  affections,  stomatitis  and  other  mouth  affections. 
Ill-health  and  bad  hygiene  are  predisposing  causes.  It  is  frequent  in 
infants  dying  from  congenital  syphilis,  tuberculosis,  marasmus  and  disorders 
of  the  alimentary  tract. 

Bacteriology. — The  pneumococcus  is  present  in  80-90  per  cent,  in 
infancy.  Preysing  (1906)  found  it  in  almost  all  of  81  cases,  73  bilateral, 
in  100  children,  aged  1  day  to  3  years,  examined  after  death.  The  otitis, 
was  pneumococcal  in  112  out  of  125  positive  results. 

Miller  (1907)  examined  after  death  the  ears  of  50  children  under 
4  years  old,  and  found  20  bilateral  pus,  17  unilateral  pus,  and  13  normal ;. 
the  pneumococcus  present  in  nearly  all ;  and  that  29  out  of  the  37  with 
otitis  had  broncho-pneumonia.  Under  10  years  of  age  this  organism 
predominates,  and  the  younger  the  child  the  more  probably  is  it  the  cause- 
of  the  disease.  Pyogenic  organisms  are  often  found  in  secondary  cases  and 
the  tubercle  bacillus  in  a  few. 

Morbid  Anatomy. — As  soon  as  the  mucous  membrane  undergoes  catar- 
rhal inflammation,  it  appears  to  lose  its  bactericidal  properties  and  may 
become  secondarily  septic.  There  are  3  types  of  otitis,  serous,  suppurative, 
and  necrotic,  all  of  which  are  seen  in  scarlatina.  The  mucosa  is  swollen 
and  injected,  and  secretes  serum,  sero-pus  or  pus,  and  becomes  thickened 
by  small-celled  infiltration.  The  exudation  fills  the  cavity,  causes  necrosis, 
and  ulceration,  and  rupture  of  the  drum  and  otorrhcea.  In  bad  cases  the 
disease  produces  destruction  of  the  drum,  loosening  and  detachment  of  the 
ossicles,  periostitis,  caries  or  necrosis  of  bone,  involvement  of  the  internal 
ear,  total  deafness,  and  palsy  of  the  seventh  and  eighth  nerves.  The 
inflammation  may  extend  to  the  meninges,  via  the  lymphatics  or  the 
squamo-petrosal  fissure,  and  cause  meningitis  ;  or  may  set  up  mastoiditis, 
or  labyrinthitis. 

Symptoms. — Otitis  can  exist  without  earache  or  pain,  notably  when 
it  complicates  acute  general  disease.  Or  the  expression  of  pain  may  be 
absent  on  account  of  the  mental  state,  and  even  in  normal  children.     In. 


The  Ear.  993 

infants  acute  pain  is  constantly  absent  or  unrecognisable,  and  indeed  all 
signs  may  be  lacking.  Usually  there  is  restlessness,  insomnia  and  sharp 
cries,  and  rarely  mastoid  tenderness.  Sometimes  the  pain  is  agonising, 
throbbing,  and  causes  incessant  shrieking.  High  fever,  coated  tongue  and 
delirium  are  not  uncommon  ;  and  there  may  be  convulsions,  head-retrac- 
tion, vomiting,  and  rapid  breathing.  Meningitis  is  often  suspected  in 
infantile  otitis,  generally  a  bilateral  and  purulent  one,  because  of  the  head 
retraction  and  cerebral  symptoms.  The  drum  should  be  punctured  in 
doubtful  cases.  The  otitis  may  be  an  antecedent  or  a  sequel  of  meningitis1 
(p.  644). 

The  onset  is  often  insidious,  with  dulness  of  hearing  or  deafness  as  the 
only  symptom.  Subjective  noises  are  difficult  to  ascertain  in  the  young. 
Many  cases  are  mild  or  sub-acute.  Possibly  the  child  complains  of  slight 
earache  and  noises  in  the  head,  and  appears  dull  of  hearing,  otorrhoea 
developing  in  a  few  days.  These  children  are  generally  delicate  and  have 
some  catarrh  of  the  nose  or  fauces. 

The  temperature  varies.  In  mild  and  subacute  cases,  and  those  in 
the  course  of  acute  disease,  there  may  be  no  fever.  Generally  the  tempera- 
ture rises  abruptly  to  101-105°  F.,  and  falls  sharply  as  soon  as  the  drum 
is  perforated.  The  fall  is  not  necessarily  simultaneous  with  the  relief 
of  tension.     Usually  the  fever  lasts  1-5  days. 

Otorrhoea  is  the  confirmatory  sign  ;  "an  abscess  has  broken  in  the 
head  "  is  the  common  description.  The  discharge  may  be  so  scanty  and 
tenacious  as  not  to  be  visible  externally.  Wipe  out  the  meatus  with  a 
pledget  of  absorbent  wool.  Insert  a  smaller  pledget  for  a  short  distance. 
If  on  removal  it  is  moist  with  mucus,  there  is  a  perforation,  for  mucus  is 
not  secreted  in  the  canal. 

Physical  Signs. — If  the  meatus  and  canal  are  swollen,  inflamed  and 
tender,  it  is  impossible  to  make  a  satisfactory  examination.  At  first  the 
large  capillaries  of  the  drum  are  seen  to  be  congested  ;  next  the  minute 
capillaries  on  the  periphery  become  visible  ;  and  finally  the  whole  drum  is 
vividly  red  or  almost  purple  in  colour,  and  the  individual  vessels  indis- 
tinguishable. This  vivid  redness  is  not  often  seen,  for  desquamation  of  the 
epidermis  in  the  form  of  minute  dots  begins  about  the  same  time.  The 
membrane  becomes  so  dotted  with  white  epidermis  that  the  redness  is 
not  visible.  The  drum  in  early  stages  is  thickened,  cedematous  and 
opaque,  from  serous  exudation,  rendering  the  ossicles  eventually  invisible. 
Sometimes  it  bulges.  In  infants  it  is  often  deficient  in  lustre,  sodden. 
and  does  not  bulge.  The  presence  of  rhinitis  in  such  cases  is  a  suspicious 
indication. 

On  perforation  discharge  is  visible  and  must  be  removed  by  mopping, 
in  order  to  see  the  deeper  structures.  A  perforation  looks  like  a  small 
drop  of  muco-pus  on  the  drum,  which  if  wiped  away  at  once  re-appears. 
On  inflation  by  Valsalva's  method  the  drop  is  enlarged.     It  is  usually 

3  s 


994  Chapter   LXXII. 

situated  above  and  behind,  or  in  front  and  below  the  centre  of  the  drum. 
At  times  the  whole  drum  is  destroyed,  especially  in  scarlet  fever.  This 
may  be  preceded  by  membranous  deposit  on  the  drum  or  in  the  middle  ear. 
The  odour  is  foetid. 

Varieties. — All  the  signs  and  symptoms  may  be  present  in  a  severe 
form  and  yet  subside  spontaneously  without  perforation  or  formation  of 
pus.  In  some  of  these  the  pus  escapes  through  the  Eustachian  tube.  In 
others  no  pus  is  found  on  paracentesis.  A  non-purulent  exudation  may 
become  purulent.  After  a  variable  period  of  earache,  the  temperature 
rises,  pain  becomes  worse,  and  the  drum  is  found  swollen  and  cedematous 
at  first,  then  deep  red  or  purple,  and  later  of  a  yellowish  colour. 

Scarlatinal  otitis  varies  in  frequency  with  the  severity  of  the  throat 
symptoms,  and  the  presence  of  adenoids,  carious  teeth,  and  septic  mouth 
conditions.  It  is  either  due  to  the  specific  organism  or  to  the  spread  of 
non-specific  ones  from  the  naso-pharynx  to  the  tympanum  and  antrum. 
It  is  usually  bilateral,  though  not  necessarily  simultaneous  on  the  two  sides. 

An  acute  catarrhal  otitis  may  occur  at  the  time  of  the  rash  or  within 
the  first  10  days.  The  mastoid  antrum  is  only  affected  secondarily.  The 
perforation,  if  present,  is  small  and  high  up  in  ShrapnelPs  membrane. 

A  suppurative  variety,  due  to  pyogenic  infection  of  the  catarrhal  one, 
commonly  begins  in  the  second  week,  sometimes  not  until  the  fourth  week 
or  during  convalescence,  and  occasionally  in  the  acute  stage.  It  may  give 
rise  to  no  symptoms,  being  only  recognised  when  the  otorrhcea  begins  ; 
to  earache,  deafness  and  rise  of  temperature  ;  to  increasing  delirium  and 
coma  ;  or  merely  signs  of  aural  discomfort  or  a  rise  of  temperature. 
Perforation  may  result  within  24  hours  or  after  a  slower  course.  The 
perforation  is  large  and  in  the  inferior  segment.  There  is  no  Eustachian 
obstruction  or  tinnitus,  and  deafness  is  usually  slight  unless  adenoids  are 
present. 

Some  attacks  pass  into  acute  necrotic  inflammation,  rapid  destruction 
of  the  tympanum,  separation  and  discharge  of  the  ossicles,  and  permanent 
deafness.  The  cavity  is  filled  with  pus  and  granulation  tissue,  perhaps 
in  large  masses  forming  aural  polypi  which  may  be  even  present  at  the 
meatus.  The  discharge  is  profuse  and  soon  becomes  foetid.  The  seventh 
and  eighth  nerves  may  be  involved,  and  meningitis  may  supervene. 

Infection  of  the  mastoid  cells  and  antrum,  an  osteitis  of  the  antrum 
and  cells,  occurs  early.  Sometimes  there  is  a  primary  otorrhcea  which 
subsides  and  is  followed  by  a  secondary  offensive  discharge,  due  to 
accumulation  in  the  antrum.  Other  sequels  are  perforation  of  the  labyrinth, 
caries  and  necrosis,  cerebral  and  cerebellar  abscess,  thrombosis  of  the 
lateral  sinus,  permanent  deafness  and  deaf-mutism. 

About  half  the  cases  recover  in  2  weeks  to  2  months.  Adopt  intra- 
tympanic  treatment  for  a  month  and  then,  if  there  is  no  improvement,  open 
the  antrum  or  do  a  radical  operation. 


The  Ear.  995 

Typhoidal  Otitis  begins  in  the  third  to  the  fifth  week  with  otorrhoea 
■and  rarely  pain.  Occasionally  it  is  acute,  unilateral,  and  may  involve  the 
mastoid.  The  deafness  of  typhoid  is  generally  of  central  origin,  and 
:sometimes  due  to  catarrh  of  the  fauces  and  Eustachian  tube.  The  otitis 
■of  measles,  diphtheria  and  pneumococcal  infections  has  no  distinctive 
-features.  In  measles  it  generally  occurs  during  desquamation,  with  rise  of 
temperature  and  earache,  and  rarely  ends  in  ulcerative  destruction  or 
mastoiditis. 

Influenza  gives  rise  to  hsemorrhagic  otitis,  primary  mastoiditis,  or  rapid 
•caries  or  necrosis  of  the  ossicles  or  mastoid.  In  this  otitis  the  pain  is  sudden 
in  onset,  neuralgic  in  character,  intermittent,  the  paroxysms  being  longer 
.and  more  frequent  at  night,  and  is  little  or  not  at  all  relieved  by  perforation. 
Deafness  comes  on  more  gradually  than  in  simple  otitis,  is  little  relieved 
by  inflation,  and  lasts  for  3  weeks  or  more.  The  drum  is  swollen  and 
.intensely  congested,  showing  punctate  or  diffuse  ecchymoses.  The 
tympanic  mucosa  is  much  swollen  and  forms  flabby  cedematous  granulations. 
The  discharge  varies  in  character  from  scanty  sero-sanguineous  to  profuse 
purulent  fluid.     Nervous  prostration  and  insomnia  are  marked. 

Tuberculosis  of  the  middle  ear  is  sudden  in  onset,  chronic  in  course  and 
practically  painless.  It  chiefly  affects  the  poor  in  large  towns.  The 
bacillus  reaches  the  tympanum  via  the  Eustachian  tube,  or  possibly  by  the 
blood.  The  discharge  is  thin,  semi-purulent  and  very  foetid,  sometimes 
thick  and  curdy,  and  the  bacillus  may  be  found  in  it.  The  drum  is  pale, 
.sodden  and  cedematous,  and  perforations  have  indolent  edges.  There 
is  a  tendency  to  flabby  granulations,  and  caries  of  the  mastoid  and  inner 
tympanic  wall.  The  facial  nerve  is  soon  involved.  Early  operation  is  the 
proper  treatment. 

Course  and  Complications. — An  ordinary  case  of  otitis  gets  well  and 
leaves  no  permanent  effects.  Deafness  is  most  likely  to  follow  scarlet 
fever  ;  or  after  mild  but  recurrent  attacks.  The  ossicles  may  be  detached 
and  thrown  off.  Other  complications  are  caries  and  necrosis  of  the  walls 
■of  the  tympanum,  mastoiditis,  labyrinthitis,  sinus  thrombosis,  meningitis, 
•cerebral  abscess,  and  abscess  in  the  neck.  A  cervical  abscess  may  be 
.glandular,  in  the  cellular  tissue  and  due  to  direct  infection  from  diseased 
bone,  or  a  collection  of  pus  in  the  jugular  vein. 

Chronic  Otorrhoea  is  not  infrequent.  Otorrhoea  is  a  sign  of  suppura- 
tion. If  it  comes  from  a  meatal  boil,  it  is  intermittent  and  lasts  for  a  day 
•or  two.  If  due  to  a  foreign  body,  it  is  associated  with  swelling  and  may  be 
continuous.  A  discharge  of  6  weeks  duration  is  "  chronic,"  and  in  90  per 
•cent,  comes  from  the  middle  ear,  indicating  perforation  and  chronic  inflam- 
mation of  the  tympanum,  and  caries  or  necrosis  of  the  mastoid.  The  signs 
of  chronic  disease  are  a  constant  foetid  discharge,  exuberant  granulations, 
,and  caseous  foci.  The  longer  its  duration,  the  greater  is  the  probability  of 
.bone  disease  in  and  around  the  cavity.     It  is  generally  septic  or  tuberculous. 


996  Chapter  LXXII. 

Mastoiditis  is  primary  or  secondary.  The  primary  influenzal  form 
gives  rise  to  local,  lancinating  pain,  tenderness  over  the  mastoid  antrum, 
local  heat,  and  possibly  fever.  It  often  causes  rapid  destruction.  Primary 
caries  of  the  mastoid,  ending  in  abscess,  is  not  uncommon.  The  patch  of 
caries  is  usually  along  the  line  of  the  masto-squamosal  suture.  It  is  a  slow 
painless  formation,  sometimes  taking  a  month,  without  fever,  and  pro- 
duces a  swelling  behind  and  perhaps  pushing  forward  the  ear,  generally 
extensive  destruction  of  bone,  and  no  intracranial  symptoms.  There  is  no 
history  of  otorrhcea,  no  earache,  and  the  membrane  is  normal.  Secondary 
mastoiditis  begins  2-8  weeks  after  tympanic  suppuration.  It  may  start 
acutely  with  rise  of  fever,  rigors  and  severe  pain.   • 

The  signs  of  mastoiditis  in  infancy  are  restlessness,  crying,  paroxysmal 
pain  which  is  worse  at  night,  rubbing  the  occiput,  tremor  of  the  lower 
jaw  during  pain,  fever  up  to  105°  F.,  cessation  of  otorrhcea,  glandular 
swelling  and  torticollis.  In  older  children  there  is  often  no  fever  and  no 
local  signs,  but  the  pulse  is  generally  accelerated  and  pus  constantly  oozes- 
through  the  perforation  in  the  drum,  after  mopping,  showing  that  there  is. 
accumulation  and  retention.  Local  signs  indicate  that  the  inflammation 
has  reached  the  surface.  They  include  swelling,  heat,  redness,  oedema  and 
tenderness  over  the  antrum  or  pre-mastoid  lamina,  if  it  has  started  as  a. 
periostitis.  When  due  to  extension  from  the  tympanum  the  signs  and 
symptoms  are  less  acute.  There  may  be  persistent  and  deep-seated  pain,, 
increased  discharge,  and  bogginess  or  bulging  of  the  posterior  superior 
wall  of  the  meatus,  just  external  to  the  drum.  The  mastoid  cells  form  the 
outer  wall  of  the  lateral  sinus.     If  they  are  diseased,  thrombosis  may  ensue. 

Treatment. — Apply  leeches  or  cold.  Make  an  incision  down  to  the 
bone,  or  trephine  the  process  if  the  symptoms  persist.  A  permanent 
fistula  indicates  caries.  The  earlier  the  operation,  the  less  is  its  severity,, 
the  more  rapid  the  cure,  and  the  smaller  the  loss  of  hearing. 

Labyrinthitis  may  be  primary  in  mumps,  or  secondary  to  tuberculous 
infection  or  otitis  media.  It  leads  to  destruction  of  the  labyrinth  and 
deafness,  or  deaf-mutism  if  it  is  bilateral  and  occurs  in  an  infant.  Loss  of 
bone  conduction  is  the  sign  of  inflammation  or  destruction  of  the  labyrinth. 
Occasionally  it  is  due  to  pressure  on  the  nervous  structures  and  is  relieved 
by  perforation  of  the  drum. 

Treatment  of  Otitis  and  Otorrhcea. — Prevention  consists  in  the  removal 
of  adenoids  and  large  tonsils,  attention  to  carious  teeth,  and  hygiene  of  the 
mouth  and  nose,  especially  in  exanthemata.  The  mouth  must  be  kept  clean 
during  illness,  the  throat  sprayed  and  the  nose  syringed  with  a  mild 
antiseptic  lotion,  e.g.  ac.  carbolici  grs.  30,  sod.  bicarb,  grs.  30,  water  1  pint,, 
warmed  by  dilution  with  hot  water. 

In  acute  otitis  make  use  of  the  measures  for  the  relief  of  earache 
(p.  991)  and  give  bromides.  Let  an  infant  lie  on  a  large  pillow  on  the 
nurse's  lap,  with  the  affected  ear  uppermost.     It  must  not  be  rocked  or 


The  Ear.  997 

jogged  up  and  down.  Keep  the  room  dark,  cool  and  quiet.  Feed  with  a 
spoon,  for  sucking  causes  pain.  Give  liquid  diet  and  a  purge.  Similar 
measures  are  suitable  for  older  children,  together  with  liq.  quin.  salicyl. 
m.  10-15.  q.i.d.  Examine  the  ear,  under  anaesthesia  if  necessary.  Try  and 
reduce  acute  inflammation,  so  that  it  does  not  end  in  suppuration,  by 
1-3  leeches  on  the  inner  side  of  the  concha,  the  meatus  being  plugged  with 
wool,  or  in  front  of  the  ear,  or  over  the  mastoid  if  pain  is  felt  there  as  well. 
If  an  infant  is  teething,  blood  may  be  abstracted  by  lancing  the  gums. 
•Other  measures  are  hot  instillations  or  irrigations,  hot  fomentations 
•or  bran  bag,  etc.,  a  mercurial  and  saline  purge,  and  vin.  antimonialis. 

Paracentesis  does  no  harm,  if  the  meatus  is  kept  aseptic,  and  should  be 
•done  early  in  scarlatinal  cases  for  they  almost  always  suppurate.  Incise 
the  drum  if  it  is  red  and  bulging,  if  the  clinical  symptoms  are  severe,  or  if 
rolling  the  head  from  side  to  side  suggests  labyrinthine  trouble.  Enlarge 
-a  perforation,  if  it  is  too  small.  Cocaine  solution  2  per  cent,  in  aniline  oil 
and  sp.  vin.  rect.  p. a.,  5-10  drops,  produces  anaesthesia  in  5-15  minutes. 
Aqueous  solutions  do  not  penetrate  the  drum  and  reach  the  nerve  filaments, 
which  terminate  on  the  inner  layer.  Any  discharge  present  must  be 
iirst  syringed  away.  If  there  is  a  perforation,  the  solution  causes  a  burning 
pain  before  the  cocaine  takes  effect.  It  is  a  mistake  to  wait  for  perforation, 
for  the  pain  and  danger  are  prolonged,  and  the  resulting  hole  is  often  inade- 
quate for  drainage.  The  size  of  the  hole  is  of  more  importance  than  its 
■situation.  Select  a  spot  below  and  behind  the  handle  of  the  malleus,  and  be 
:sure  that  the  knife  is  sharp.  Keep  the  hole  open  until  exudation  into  the 
middle  ear  has  ceased.  Paracentesis  is  not  essential  in  serous  otitis,  but 
may  relieve  grave  symptoms  although  no  pus  escapes.  Afterwards  irrigate 
with  hot  boric  acid  lotion  for  a  few  minutes  every  hour  for  a  few  hours, 
instilling  a  few  drops  of  carbolised  glycerine,  5  per  cent.,  between  the 
irrigations.  Cover  with  a  pad  of  absorbent  wool  to  soak  up  the  discharge. 
After  3  weeks,  if  the  discharge  continues  in  spite  of  free  drainage, 
trephine  the  mastoid  although  there  may  be  no  evidence  of  mastoid  disease. 
It  is  the  only  means  of  securing  efficient  drainage  and  is  recommended  for 
purely  mechanical  reasons.  For  pain  and  profuse  discharge  in  otitis  of 
streptococcal,  influenzal  or  scarlatinal  origin,  operate  in  a  week,  because  of 
the  liability  to  bone  disease. 

Chronic  otorrhcea  depends  on  inefficient  treatment  of  acute  otitis, 
•debility,  tuberculous  infection,  recurrent  infection  from  the  naso-pharynx, 
.and  imperfect  drainage.  Therefore  enlarge  perforations,  get  rid  of 
•granulations,  polypi,  epithelial  debris  and  inspissated  pus,  and  treat  the 

nose  and  naso-pharynx.     Use  mops  or  a  suction  apparatus,  e.g.  Siegle's 
pneumatic  speculum,  for  cleaning  the  meatus.     Syringing,  politzerisation, 

and  hydrogen  peroxide  are  all  liable  to  drive  septic  matter  further  in. 

The  peroxide  is  very  useful  for  cleansing.     Fill  the   ear  until   bubbling 

ceases  and  leave  the  fluid  in  for  5  minutes.     Wash  it  away  with  warm  boric 
3otion  and  dry  by  mopping. 


998  Chapter  LXXII. 

As  a  rule  the  simplest  plan  is  to  illuminate  the  meatus  well,  mop  it  out 
with  a  dry  aseptic  mop  of  singed  wool,  and  clean  it  with  mops  dipped 
in  one  of  these  lotions  : — alcohol ;  biniodide  of  mercury  gr.  1  in  sp.  vin. 
rect.  oz.  6  :  bichloride  of  mercury  1  in  2000  ;  carbolic  acid  1  per  cent.,, 
salicylic  acid  or  boric  acid  or  resorcin  1-2  per  cent,  in  rectified  spirits- 
Spirituous  lotions  destroy  granulations  by  dehydration,  lessen  swelling,, 
and  are  antiseptic.  The  meatus  and  concha  must  be  anointed  first  to 
prevent  smarting  and  chapping.  The  discharge  usually  diminishes  in 
1-2  weeks.  Then,  if  there  is  no  bone  disease,  use  an  astringent  lotion  of 
lead  acetate  or  zinc  sulphate,  grs.  2  in  glycerine  oz.  1.  The  insufflation  of 
dry  powders  is  inadvisable  as  they  form  hard  masses  and  hinder  drainage. 
For  the  same  reason  do  not  insert  wool  into  the  meatus.  It  also  causes- 
maceration  and  excoriation.  A  gauze  drain  along  the  floor  of  the  meatus- 
up  to  the  drum  exerts  capillary  attraction  but  may  set  up  eczema.  AIL 
lotions  should  have  a  higher  specific  gravity  than  pus,  in  order  to  penetrate,, 
and  should  not  be  made  up  with  water  for  water  soddens  the  tissues  and 
promotes  the  growth  of  granulations  and  polypi. 

A  useful  method  is  to  syringe  with  a  boric  lotion  and  dry  by  mopping  ;. 
instil  freely  ac.  boric,  dr.  1,  sp.  vin.  rect.  drs.  2,  glycerine  ad  oz.  1,  and 
leave  it  in  for  a  few  minutes  ;  then  suck  it  out  with  an  eye-dropper  with 
a  rubber  bulb.    ATarious  antiseptics  can  be  used  in  a  similar  manner. 

Inflation  helps  to  drive  out  secretion  through  a  perforation.  If 
the  hole  is  large,  there  is  little  risk  of  driving  pus  into  the  antrum  and 
in  many  cases  the  antrum  is  already  infected.  It  is  better  avoided,  for  it  is 
unnecessary  if  drainage  is  efficient,  and  it  gives  shocks  to  inflamed  struc- 
tures and  may  drive  in  septic  material  from  the  pharynx.  If  the  discharge 
is  very  offensive  instil  daily,  or  every  other  day  for  a  week,  into  the  deepest 
part  of  the  meatus,  2-3  drops  of  a  warm  5  per  cent,  solution  of  the  double 
cyanide  of  zinc  and  mercury.  More  radical  measures  should  be  entrusted 
to  the  hands  of  a  surgeon  or  specialist  on  diseases  of  the  ear. 


Chapter  LXXIII. 

THE    SKIN. 

Dermatotherapy — Intertrigo — Erythema — Seborrhcea —  Eczema  —  Psoriasis 
—  Scleroderma —  Corns —  Warts  —  Molluscum  —  Lichen  —  Alopecia — 
Sudamina  —  Strophulus  —  Acne  —  Boils  —  Impetigo  Contagiosa  — 
Ecthyma  — Pemphigus  —  Herpes  —  Tuberculous  Affections  —  Parasitic 
Diseases. 

In  examining  the  skin  it  is  essential  to  inspect  the  whole  surface,  though 
not  necessarily  at  once.  Some  rashes,  e.g.  eczema,  assume  different  types 
in  different  regions.  The  examination  should  be  conducted  with  warm 
hands  in  a  good  light  and  warm  room.  Note  the  general  condition  of  the 
skin,  the  quality  and  texture  of  the  hair,  and  the  distribution  of  abnor- 
malities. A  dry,  lustreless  appearance  shows  a  tendency  to  xerodermia 
and  a  liability  to  eczema.  Icthyosis  appears  first  on  the  shins.  Look  for 
moles,  warts,  hairiness,  scratches,  and  patches  of  keratosis  pilaris  and 
lichen  spinulosus,  due  to  hypertrophy  of  hair  follicles.  A  fleeting  erythema 
is  a  sign  of  digestive  disturbance.  Dermatographia  indicates  vasomotor 
trouble. 

Dermatotherapy.— At  birth  the  skin  is  very  delicate  and  subjected  to 
a  great  change  in  its  surroundings.  The  vernix  caseosa  is  rubbed  off. 
Irritant  oil  or  fat,  caustic  soap,  water  of  unsuitable  temperature,  too 
vigorous  drying,  and  unsuitable  clothing  may  exert  their  injurious  influence 
at  the  time  of  the  first  bath  as  well  as  subsequently.  These  factors  are 
accentuated  by  irritant  powders,  sweating,  urine  and  fseces,  unclean  diapers 
and  general  lack  of  cleanliness.  Preventive  measures  consist  in  the  care 
of  the  skin  at  birth  and  the  use  of  baths  (p.  72).  The  special  measures 
include  soaps  (p.  72),  powders,  oils,  fats,  ointments,  pastes,  glues,  plasters, 
lotions,  and  baths  (p.  75). 

Powders  are  used  to  dry  up  secretions,  cool  the  skin,  and  reduce 
inflammation  and  swelling.  The  chief  kinds  are  the  starches  of  rice,  wheat, 
or  potato  ;  emol  keleet ;  lycopodium  ;  terra  silicea  ;  mag.  carb.  (calamine), 
mag.  silicat.  (talc),  zn.  oxid.,  zn.  oleat.  and  bism.  subnit.  To  any  one,  or 
mixtures,  of  these  boric  acid  is  often  added. 

Oils. — The  chief  ones  are  ol.  mor.,  ol.  olivse,  ol.  ric,  ol.  rapae  (cheap) 
ol.  amygdal.  dulce  (expensive)  ;  and  the  mineral  oils,  petroleum,  paraffin 
and  liquid  vaseline.  The  Fats  include  white  vaseline,  made  from  the 
residue  of  petroleum,  and  the  more  uniform  yellow  vaseline  ;    and  the 


1000  Chapter  LXXIII. 

animal  fats  lanoline  and  adeps  lanse,  lard  and  adeps  benzoat.,  cold  cream 
and  ung.  rosse,  wax,  and  ung.  cetacei. 

Ointments. — The  basis  of  an  ointment  must  be  non-irritating,  not 
rancid,  and  of  a  proper  consistency.  Cold  cream  and  ung.  rosse  are 
excellent,  if  fresh,  but  the  water  evaporates  and  they  may  go  rancid,  unless 
benzoin  2  per  cent,  or  carbolic  acid  1-2  per  cent,  is  added.  The  best 
emollient  is  fresh  pure  lard,  benzoated  to  prevent  decomposition.  Com- 
mercial lard  is  a  mixture  and  unsuitable.  Lard,  combined  with  an  animal 
or  vegetable  oil,  penetrates  into  but  not  below  the  skin.  Theobroma 
(cacao)  oil  is  the  best.  Lard  can  be  combined  with  wax  and  oil ;  or  with 
oleic  acid,  for  admixture  with  alkaloids.  Vaseline  is  protective  and  non- 
absorbent.  Its  irritant  effects,  if  any,  are  due  to  impurities  such  as  sulphur. 
It  is  the  proper  vehicle  for  antiseptics,  germicides,  parasiticides,  astringents 
and  counter-irritants.  If  it  is  desirable  for  the  active  constituent  to 
penetrate  and  pass  through  the  skin,  it  must  be  combined  with  pure  hydrated 
lanoline,  a  sebaceous  substance  which  is  practically  unalterable,  never 
becomes  rancid  and  is  unaffected  by  chemical  reagents.  Such  a  base  is 
required  for  mercury,  pot.  iod.,  quinine  and  narcotics.  It  is  rarely  suitable 
as  a  base  alone,  and  is  often  mixed  with  cacao  oil,  wax,  or  vaselin,  e.g. 
lanolin  pur.  65,  paraffin  30,  ceresin  5. 

Lubricants  include  mutton  tallow,  fats,  oils,  creams,  glycerine  of 
starch,  and  mixtures  such  as  boroglyceride  1,  lanolin  2,  ung.  rosse  6  parts. 
As  a  soothing  ointment  use  : — (1)  ac.  carbol.  gr.  5,  calamin.  gr.  20,  zn. 
oxid.  gr.  30,  ung.  rosse  ad  oz.  1  ;  (2)  zn.  oxid.  gr.  15-30,  ung.  picis  dr.  1-2, 
ung.  rosse  ad  oz.  1  ;  (3)  pulv.  camph.  gr.  30,  zn.  oxid.  dr.  2,  glycer.  dr.  2, 
adip.  benzoat.  oz.  1-2,  cochineal  gr.  1,  ol.  rosse  m.  1. 

Ointments  should  be  spread  freely  on  the  woolly  side  of  lint  and 
bandaged  on  ;  and  removed  by  means  of  a  dull  knife  or  absorbent  wool. 
At  first  the  strength  must  be  mild,  for  it  is  impossible  to  estimate  the 
susceptibility  of  the  skin.  The  ingredients  often  act  better  in  combination 
than  separately.     A  few  ointments  must  be  rubbed  in  vigorously. 

Creams. — An  excellent  cold  cream,  and  a  suitable  basis  for  an  oint- 
ment, consists  of  spermaceti  1,  cerse  alb.  1,  ol.  amygdal.  10,  aq.  rosse  10 
parts.  Carron  oil  is  a  mixture  of  ol.  olivse  and  aq.  calcis  p.a.,  and  forms  a 
suitable  cream  with  calamine  or  zn.  oxid.  10  per  cent. 

Pastes. — The  dry  parts  must  equal  the  fats.  Useful  ones  are  starch 
and  vaseline  p.a.;  zn.  oxid.,  starch,  vaseline,  lanoline,  p.a,  ;  zn.  oxid.,  ol. 
olivse,  p.a.  (Lassar's  zinc  oil)  ;  and  zn.  oxid.  1,  starch  1,  vaseline  2  parts 
(Lassar's  paste).  Pick's  paste  is  a  useful  excipient  for  applying  drugs 
without  the  necessity  of  bandaging.  It  is  made  of  tragacanth  powder  dr.  1, 
glycerine  dr.  |-1,  aq.  rosse  3  oz. 

Gelatines,  Glycogelatines,  Zinc  gelatines  or  Glues  are  composed  of  gelatine 
alb.  dr.  2-4,  zn.  oxid.  or  calamine  dr.  2-3,  glycerine  dr.  4,  water  1  oz.y 


The  Skin.  1001 

liquefied  in  a  glue  pot  and  painted  on.  Other  suitable  vehicles  for  ac.  salicyl. 
and  chrysarobin,  etc.,  are  collodion  and  traumaticin  (guttapercha  dr.  1, 
■chloroform  oz.  1). 

Salve  Muslins  are  made  by  spreading  muslin  with  lard  and  wax, 
lanoline  or  vaseline,  to  which  is  added  the  drug  required,  e.g.  ichthyol, 
.ac.  carbol.,  ac.  salicyl.,  resorcin,  sulphur,  etc.  It  is  trimmed  to  fit  the 
part.  A  cheaper  method  is  to  spread  a  thick  ointment  on  butter-cloth. 
Biersdorf's  plaster  mulls  contain  various  medicaments.  A  salve  stick  is 
made  of  cacao  butter  4,  wax  2,  lanolin  1  part. 

Lotions  are  cooling,  sedative,  antiseptic,  astringent  or  stimulant. 
"They  are  brushed  on,  or  applied  on  thin  gauze  to  permit  evaporation. 
Simple  soothing  lotions  are  warm  rice  water,  lime  water,  lead  lotion,  or 
solutions  of  boric  acid,  sod.  bicarb,  or  sod.  hypophosph.  dr.  1.-2  ad  water 
1  pint.  Calamine  lotion  consists  of  calamine  1,  zn.  oxid.  1-2,  glycerine  4, 
aq.  calcis  8,  aq.  rosse  32-64  parts.  A  mixture  of  calamine  1,  olive  oil  4, 
and  lime  water  4  parts,  is  very  soothing. 

Erythema  and  Intertrigo. — An  erythema  is  a  uniform  redness  of  the 
skin  of  varied  causation,  mainly  vasomotor  or  toxic.  Erythema  due 
to  irritation  by  the  sun  (E.  calorum),  lotions,  mustard  leaves,  etc.,  is  the 
first  stage  of  dermatitis.  E.  neonatorum  is  the  normal  redness  of  the  skin 
.at  birth.  Other  varieties  are  E.  pernio  or  chilblain  (p.  453),  E.  nodosum 
■(p.  535),  E.  infectiosum  (p.  950),  and  E.  multiforme. 

Erythematous  rashes  are  sometimes  caused  by  belladonna,  phenazone, 
quinine,  veronal,  resorcin,  iodoform  or  boracic  lotion.  Drug  rashes  are 
•often  polymorphous.  The  phenazone  rash  is  scarlatiniform,  burning  and 
itching,  and  may  involve  the  buccal  mucosa.  There  may  be  fever  and 
•subsequent  desquamation. 

Sometimes  it  is  morbilliform,  and  generalised,  or  mainly  on  the  limbs. 
Occasionally  one  or  more  small  red,  raised,  infiltrated  patches  of  "  fixed 
•erythema  "  come  out  in  a  few  hours  and  last  for  a  week  or  more,  perhaps 
leaving  a  pigmented  patch  for  months. 

E.  multiforme  toxicum  is  due  to  a  toxin  or  to  gastric  irritation.  The 
•chief  causes  are  dyspepsia,  constipation,  tainted  food,  auto-intoxication 
and  infectious  disease.  It  chiefly  affects  the  chest,  neck  and  face.  Septic 
■erythema  and  serum  disease  are  of  toxic  origin. 

Intertrigo  is  an  erythema  due  to  friction  between  two  moist  surfaces, 
especially  the  folds  of  the  groins,  between  the  genitals  and  thighs,  between 
the  buttocks  and  round  the  anus,  behind  the  ears  and  in  the  axillee.  It  is 
worst  in  the  "  bathing  drawers  area,"  and  is  often  called  a  "  napkin  rash." 
If  limited  to  the  buttocks  and  perineum,  it  may  be,  but  ought  not  to  be, 
mistaken  for  the  rash  of  congenital  syphilis  (p.  871).  At  first  there  is  a 
simple  erythema.  Warmth,  moisture  and  additional  irritation  lead  to 
"the  formation  of  small,  superficial  vesicles  or  denudation  of  the  skin  over  a 
larger  or  smaller  area,  producing  intertriginous  ulceration.     Thin  scabs 


1002  Chapter   L  XXIII. 

form  and,  under  suitable  treatment,  recovery  is  rapid.  The  ulceration  is- 
most  extensive  on  the  buttocks  because  of  the  faecal  irritation.  Malnutri- 
tion, combined  with  lack  of  cleanliness  and  failure  to  keep  the  parts  dry,. 
is  the  chief  cause.  Other  common  causes  are  the  use  of  diapers  which  have 
been  dried  but  not  washed,  or  washed  in  soda  and  water  but  not  thoroughly 
rinsed  out  in  pure  water  afterwards  ;  and  various  dusting  powders.  Over- 
feeding with  starchy  foods  renders  the  stools  acid  and  irritating.  The  rash 
is  much  more  limited  in  area  than  that  of  syphilis,  and  differs  from  eczema 
in  the  absence  of  weeping. 

In  its  treatment  it  is  important  to  prevent  chafing,  by  means  of  lint 
soaked  in  oil,  or  covered  with  zinc  ointment,  and  kept  between  the  opposing 
surfaces.  Before  vesiculation  or  ulceration  has  occurred  wash  with  warm 
boric  lotion,  dry  gently  and  thoroughly,  and  dust  on  a  powder  of  ac.  salicyl.3, 
starch  10,  talc  87  parts.  In  the  later  stages  rely  on  ointments  of  zinc,  boric 
acid,  zinc  and  vaseline,  or  more  stimulating  ones  of  resorcin  gr.  5  or 
ichthyol  gr.  10  ad  oz.  1.  Internally  give  rhubarb  and  soda,  grey  powder,, 
calomel  or  aromatic  chalk  powder,  according  to  the  state  of  the  digestive 
organs. 

E.  Multiforme. — In  its  simplest  form  this  consists  of  a  variable  patchy,, 
evanescent  efflorescence  (E.  jug  ax)  sometimes  papular  (E.  papulatum),. 
without  heat,  pain  or  swelling,  and  perhaps  itching.  An  exudative  variety 
is  sometimes  called  E.  marginatum,  circinatum,  iris,  gyratum  o'r  annulare.. 
It  comes  out  on  the  backs  of  the  hands  and  feet,  the  lower  arms  and  legs,, 
and  may  affect  the  mucous  membranes.  At  first  it  consists  of  small,. 
vivid,  light  red  spots.  These  become  dusky  and  fade  in  the  centre,  and 
enlarge  peripherally,  perhaps  coalescing.  Sometimes  there  are  smalL 
peripheral  vesicles  {herpes  iris  or  E.  vesiculosorum)  or  urticarial  spots.. 
They  fade  in  2-6  weeks  and  leave  some  pigmentation.  Occasionally  the 
rash  is  associated  with  slight  evening  fever,  pains  in  the  limbs,  articular 
swelling,  especially  in  knees  and  ankles,  and  renal  and  intestinal  haemorrhage.. 
Such  cases  are  closely  allied  to  purpura  haemorrhagica.  It  is  rarely  severe 
in  children.  Keep  the  child  in  bed,  apply  cooling  powders  and  ointments, 
warm  baths,  and  give  calomel  and  aspirin  or  salicylates  internally. 

Seborrhcea. — The  secretion  of  the  sebaceous  glands  is  often  excessive,, 
especially  on  the  heads  of  infants.  The  newborn  may  present  a  patch  ol 
seborrhcea  capitis. 

Seborrhcea  sicca,  pityriasis  simplex  capitis,  scurf  or  dry  scaly  sebor- 
rhcea, is  a  branny  desquamation  composed  of  dried  sebum.  It  occurs  in 
quite  young  infants,  is  very  common  about  puberty,  and  may  simulate 
tinea  tonsurans.  Wash  the  head  with  soft  soap  twice  a  week.  Apply- 
nightly  a  lotion  of  ac.  salicyl.  dr.  l,ol.  ricini  dr.  2,  ol.  rosae  m.  10,  sp.vin. 
rect.  ad  oz.  6;  or  ac.  salicyl.  gr.  10,  sulph.  praecip.  gr.  5-30,  ung.  rosae  oz.  L. 

Seborrhcsic  eczema  is  the  moist  and  crusted  type.  It  takes  the  form 
of  a  dirty  yellow  or  brownish  yellow  patch  of  dried,  greasy  secretion  on_ 


The  Skin.  1003 

the  scalp.  Small  patches  are  simple  and  uncomplicated.  Neglected  ones 
are  liable  to  spread  over  the  whole  scalp  and  set  up  an  eczematous  inflam- 
mation which  extends  to  the  face,  neck,  trunk  and  limbs.  The  nose, 
mouth  and  eyes  escape.  It  is  most  common  in  overfed,  constipated  babies 
and  may  clear  up  spontaneously  on  a  mixed  diet.  There  is  a  superficial 
catarrh,  exudation,  scabbing  and  not  much  itching.  The  redness  is  seen 
at  the  edges  of  the  patch,  being  hidden  by  the  dried  secretion  in  the  centre. 
A  well-defined  crescentic  red  edge  is  visible  at  the  margin  of  the  scalp 
in  extensive  cases. 

The  primary  local  patch  must  be  soaked  with  warm  oil  or  a  mixture 
of  ac.  salicyl.  2-5,  ol.  ric.  40,  ol.  oliv.  ad  100  parts  ;  or  poulticed  with  a 
borated  starch  poultice  (p.  77).  It  can  then  be  removed  by  washing  gently 
with  a  superfatted  soap  and  water.  The  process  must  be  repeated  as  soon 
as  the  scab  forms.  After  cleansing,  apply  precipitated  sulphur  gr.  5-30 
in  an  ounce  of  benzoated  lard  or  of  ung.  aq.  rosse  ;  or  zn.  oxid.  gr.  10, 
hydrarg.  ammon.  gr.  3,  lanoline  and  vaseline  aa  \  oz.  For  chronic  patches 
use  resorcin  gr.  5-10  or  ichthyol  gr.  15-30  in  an  ounce  of  a  simple  excipient 
or  of  ung.  ac.  borici.     Keep  the  head  cool,  and  uncovered  indoors. 

The  general  seborrhceic  eczema,  which  affects  the  whole  body  in  adults 
and  is  somewhat  like  a  syphilitic  roseola,  is  rare  in  children.  It  simulates 
rose  rash,  and  is  distinguished  by  the  presence  of  seborrhcea  capitis.  Its 
treatment  is  that  of  eczema. 

Eczema. — Eczema  is  a  simple  dermatitis  of  a  catarrhal  nature.  Its 
first  stage  of  erythematous  patches  may  be  absent.  In  the  second  stage 
vesicles  or  papulo-vesicles  form  and  burst,  discharging  a  clear,  yellow, 
viscid,  slightly  alkaline,  irritant,  serous  fluid.  The  discharge  stains  and 
stiffens  linen,  or  dries  and  forms  crusts  on  the  skin.  The  corneous  layer 
exfoliates  and  leaves  cracks  or  fissures.  Usually  there  is  much  itching,  and 
in  acute  cases  considerable  constitutional  disturbance.  The  secondary 
effects  are  due  to  itching,  scratching  and  infection.  Apparently  eczema  is 
often  a  localised  oedema  of  the  skin  with  the  formation  of  deep-seated 
vesicles  in  the  rete  mucosum,  non-microbic  and  therefore  due  to  a  toxic 
state  of  the  blood. 

Etiology. — Dryness  of  the  skin  and  excessive  sebum  are  predisposing 
causes.  It  is  as  absurd  to  rigidly  maintain  that  the  disease  is  purely 
constitutional  as  it  is  to  believe  it  invariably  a  local  affection  of  the  skin 
which  can  be  cured  by  local  measures  alone.  In  the  majority  of  cases 
both  factors  are  concerned  and  must  be  carefully  investigated.  There  is 
an  undoubted  hereditary  predisposition.  Many  infants  in  the  same  family, 
though  well  nursed  and  looked  after,  suffer.  In  some  of  these  families  there- 
is  an  arthritic  diathesis,  a  history  of  gout  or  allied  states,  and  there  is  little 
doubt  that  this  diathesis  exercises  some  influence,  possibly  through 
circulating  toxins.  In  others  there  is  a  history  of  neuroses,  hay  fever, 
asthma  or  rheumatism.     The  disease  is  rare  in  the  tuberculous. 


1004  Chapter  L  XX 1 1 1. 

In  many  cases  there  is  no  evidence  of  dietetic  error.  Overfeeding  and 
unsuitable  food  are  apt  to  disturb  normal  metabolism,  set  up  intestinal 
irritation  and  catarrh,  and  lead  to  the  production  of  toxins  or  by-products 
of  digestion.  The  disease  is  rare  in  marasmus  and  not  infrequent  in 
exceptionally  fat  babies.  Possibly  the  exciting  factor  is  some  peculiarity 
in  the  milk,  even  in  breast-milk,  or  the  excess  of  sodium  chloride  in  cows' 
milk.  More  often  it  is  the  excess  of  protein  or  fat  in  the  milk,  or  some 
error  in  the  maternal  diet.  These  breast-fed  sufferers  are  generally  over- 
bed, fat  and  anaemic.  Combined  with  the  overfeeding  is  deficient  elimina- 
tion. The  bowels  are  constipated,  the  renal  secretion  insufficient,  the  liver 
overloaded,  and  the  stools  white  and  offensive.  This  state  of  the  liver  and 
stools  is  most  common  in  infants  fed  on  proprietary  foods.  In  older 
children,  the  dietetic  cause,  if  any,  is  usually  an  excess  of  milk  and  carbo- 
hydrates. 

External  causes  are  predisposing  and  exciting.  Eczema  due  to 
■external  irritation  is  a  traumatic  eczema  and  unconnected  with  constitutional 
eczema.  Atmospheric  conditions  of  heat  and  cold,  east  and  north-east 
winds,  cause  "  chapping  "  of  the  face  and  hands,  a  "dry  eczema."  Hard 
water,  strong  and  caustic  soaps,  powders,  ointments,  sweat,  dirt,  irritant 
discharges  and  unsuitable  clothing  are  common  causes.  Fever  increases 
the  liability  by  the  suffusion  of  the  skin  which  it  induces. 

External  irritants  include  antiseptics,  arnica,  etc.,  those  of  certain 
plants  such  as  the  primula  obconica,  of  caterpillars,  and  of  the  various 
forms  of  trade  dermatitis. 

The  eater-pillar  rash  is  set  up  by  the  hairs  of  the  caterpillars  and  cocoons 
-of  various  moths,  notably  the  tiger  (woolly  bear  caterpillar) ,  silver-y,  golden-y 
vapourer,  gold-tail,  silver-tail,  brown-tail,  drinker  and  oak-egger  moths. 
The  poison  is  either  formic  acid,  or  a  substance  allied  to  cantharidin,  in 
the  hairs.  The  rash  is  a  dermatitis,  eczema,  impetigo  or  urticaria.  It 
often  begins  with  redness  and  itching,  and  develops  into  small  papules, 
vesicles  and  pustules  or  into  wheals.     Apply  an  alkaline  or  lead  lotion. 

No  definite  microbial  cause  of  eczema  has  been  found.  The  vesicle 
is  sterile  at  first.  Unna's  morococcus  is  a  variety  of  staphylococcus 
albus.  Microbial  infection  produces  secondary  pustular  dermatitis. 
Vaccination  is  sometimes  blamed,  for  the  fever  induced  may  stir  up  a 
•seborrhcea  into  an  acute  eczema.     Sometimes  it  has  a  beneficial  effect. 

Keflex  causes  are  of  little  importance.  Teething  receives  its  mead  of 
blame.  Facial  eczema  may  break  out  or  increase  in  severity  with  the 
eruption  of  a  tooth,  but  this  does  not  prove  reflex  action.  "Worms  are  more 
apt  to  cause  eczema  through  their  toxins  than  by  reflex  irritation. 

Symptoms. — In  dry  eczema  or  chapping  the  skin  presents  cracks 
and  a  moist  exudation  which  crusts  and  irritates.  On  the  cheeks  it  gives 
rise  to  marked  redness,  E.  rubrum,  and  is  chronic.  This  may  spread  to  the 
forehead,  ears  and  neck,  scalp  and  trunk.     The  skin  is  red  and  swollen. 


The  Skin.  1005 

Small  papules  form,  coalesce,  and  produce  a  moist  exuding  surface.  Itching 
of  the  face  and  head  is  severe,  and  leads  to  scratching  and  bleeding, 
secondary  infection  and  pustulation  ('pustular  eczema).  There  is  no  such 
disease  as  a  true  pustular  eczema.  It  is  a  pustular  dermatitis  from  local 
irritants  or  infection,  generally  on  the  scalp,  and  like  impetigo.  Crusts- 
form  and  on  removal  leave  an  inflamed  granular  surface,  discharging  serum 
and  sero-pus,  and  bleeding  readily.  Or  the  eczematous  process  may  not 
progress  beyond  the  stage  of  redness,  thickening  of  the  skin,  scaliness  and 
itching.  Kestlessness  and  insomnia  result  from  the  itching  and  dis- 
comfort.    Glands  may  enlarge  and  suppurate. 

Acute  eczema  is  more  common  in  males  than  females,  begins  in  the 
second  to  fourth  month,  is  as  frequent  in  the  breast-fed,  is  often  unassociated 
with  gastro-intestinal  irritation,  and  in  90  per  cent,  is  a  seborrhceic  eczema 
spreading  from  the  head.  Occasionally  it  is  secondary  to  dry,  scaly  eczema, 
to  some  parasitic  affection,  or  of  constitutional  origin.  The  exciting- 
cause  is  generallv  a  trivial  one,  acting  with  undue  virulence  because  of 
the  predisposition  in  the  skin  or  the  constitutional  state.  The  patient  is 
almost  invariably  a  fat  baby  with  blue  eyes  and  smooth,  delicate  skin. 

The  distribution  in  infants  varies.  In  the  first  stage  there  is  diffuse 
redness  and  roughness  of  the  cheeks  and  forehead.  It  may  be  limited  to 
these  regions,  to  the  malar  bones,  the  upper  lip,  chin  or  behind  the  ears. 
The  patches  show  minute  papulo-vesicles,  which  becomes  confluent  and 
spread,  with  cracking  and  oozing,  local  swelling,  heat  and  redness,  and  the 
formation  of  yellowish  crusts.  It  next  extends  over  the  scalp,  unless  it 
has  spread  from  there,  and  over  the  face,  but  avoids  the  skin  of  the  nose,  round 
the  eyes  and  the  mouth.  Crusting  is  very  marked.  Patches  appear  on  the 
forearms  and  calves,  and  sometimes  practically  all  over  the  body.  The 
general  appearance  and  symptoms  are  the  same  as  in  adults,  but  there  is 
greater  tendency  to  pustulation.  Large  scabs  form,  suppuration  extends 
underneath  them,  septic  absorption  ensues,  and  superficial  ulcers  are 
left  when  the  scabs  fall  off  or  are  removed. 

The  irritability  may  be  so  great  that  the  infant  is  worn  out  by  want  of 
sleep.  General  health  is  lowered  by  septic  absorption.  Itching  may  be 
unbearable  and  paroxysmal.  Glandular  suppuration  is  not  uncommon. 
Vomiting,  diarrhoea,  malnutrition,  bronchitis,  asthma  and  nephritis  are 
the  chief  complications.  Fever  and  convulsions  occur,  and  occasionally 
sudden  death,  "  eczema  death,''''  from  cardiac  failure  or  dyspnoea. 

Diagnosis. — Exclude  parasitic  causes  and  external  irritants.  Examine 
for  seborrhcea.  A  papular  rash  on  the  buttocks  may  be  mistaken  for 
congenital  syphilis.     Psoriasis  must  be  differentiated. 

Prognosis. — Recovery  depends  on  the  duration,  the  treatment  and 
a  careful  nurse.  It  usually  takes  months,  especially  if  there  are  digestive 
troubles.  Acute  infantile  eczema  is  very  liable  to  relapses.  It  rarely 
persists  after  the  first  year  and  practically  never  beyond  the  second  year. 


1006  Chapter  L XXIII. 

"Driving-in"  the  disease  is  harmless.  Death  may  be  unexpected,  from 
status  lymphaticus  or  from  weakness  of  the  cardiac  muscles,  the  result  of 
toxaemia  and  secondary  infection. 

Treatment. — Traumatic  eczema  is  curable  by  local  measures.  In  other 
varieties  constitutional  treatment  is  also  necessary.  Attend  to  the  diet, 
the  alimentary  tract,  and  to  eliminaton.  If  the  child  is  breast-fed,  diet  the 
mother  carefully  on  ordinary  lines  and  let  the  child  be  nursed  only  5  times 
in  24  hours,  giving  barley  water  beforehand,  if  it  is  desirable  to  reduce  the 
diet.  If  bottle-fed  on  cows'  milk,  reduce  the  percentage  of  protein.  If 
this  fails,  reduce  the  fat.  Milk  can  be  omitted  for  2-4  weeks,  if  the  child  is 
over  6  months  old.  If  the  child  is  overfed  on  carbohydrate  foods,  reduce  or 
omit  them  for  a  time.  Unsalted  milk  can  be  tried.  Curdle  1  quart  with 
rennet.  Wash  the  curd  several  times  with  water  and  pass  it  through  a 
sieve.  Replace  four-fifths  of  the  whey  by  barley  water  and  add  dr.  6-8 
of  sugar.  It  makes  a  creamy  soup.  For  older  children  reduce  the  amount 
of  milk  and  carbohydrates  ;  omit  meat  extracts,  broths,  tea  and  coffee, 
salt  foods,  and  possibly  eggs  ;  and  allow  raw  fruit  and  plenty  of  vegetables. 
In  fact  the  general  principle  of  diet  is  its  limitation  to  a  minimum  quantity 
of  the  simplest  foods. 

Give  alkaline  waters,  citrates  and  acetate  of  potash  for  the  kidneys  ; 
rhubarb  and  soda  if  the  stools  are  acid  and  fermented  ;  or  keep  the  bowels 
•open  with  calomel,  gr.  1-20  to  1-12  every  2  hours,  or  a  dose  of  grey  powder 
•every  3-5  days.  Vin.  antimon.  and  mag.  sulph.  are  useful  at  the  onset  of 
an  acute  case.  Salol,  /3-naphthol  and  benzo-naphthol  are  the  best 
intestinal  antiseptics.  Iron  tonics  and  ol.  mor.  are  needed  in  convalescence ; 
■arsenic  in  chronic  cases. 

The  underwear  must  be  of  silk,  fine  linen  or  cotton,  with  wool  over 
it.  The  child  must  be  kept  in  bed  in  acute  stages.  Fresh  air,  without 
undue  exposure,  and  sunshine  are  beneficial.  The  country  is  better  than 
the  seaside,  except  for  secondary  malnutrition  and  adenitis.  Soft  water 
is  necessary. 

Local  Treatment. — Protect  the  parts  from  exposure,  covering  the  face 
with  a  mask  of  lint,  making  holes  in  it  for  the  nose,  mouth  and  eyes.  Allay 
inflammation  and  dry  up  secretions  by  muslin  strips  soaked  in  calamine 
lotion  (p.  1001),  weak  alum  lotion,  or  resorcin  l-2percent.,  and  bandaged  on. 
To  relieve  itching  give  a  bath  of  bran,  starch  or  gelatine  and  water  ;  or  a 
lotion  of  borax  dr.  1-2,  or  creolin  dr.  1,  in  water  2  pints  ;  or  calamine  lotion, 
with  carbolic  acid  1-2  per  cent,  or  ichthyol  0*5-1  per  cent.  ;  or  apply 
lotio  nigra  freely  on  absorbent  wool  for  10-15  minutes  several  times  daily 
Powder  with  zn.  stearate.  Cleanse  with  carbolised  oil  1  per  cent.  Warm 
soft  water  must  be  used  for  washing  and  an  animal  fat  rubbed  in  after 
drying.  Neither  soap  nor  water  is  permissible  in  the  acute  vesicular  stage, 
for  it  removes  the  protective  exudation.  The  morning  bath  can  be  given 
in  mild  cases,  if  the  affected  parts  are  protected  by  ointment. 


The  Skin.  1007 

To  prevent  scratching  cut  the  nails  short,  put  on  gloves,  cover  the  parts 
with  dressings  and  bandages,  and  use  restraining  splints.  And  give 
internally  antimony  at  the  onset,  bicarbonates,  calomel,  chloral,  ichthyol, 
phenazone,  gelsemium  or  hypnotics. 

Crusts  are  removed  by  soaking  them  with  warm  olive  oil  for  12-24  hours, 
normal  saline,  weak  bicarbonate  solution,  carbolised  liquid  vaseline, 
boroglyceride  fomentations,  dr.  1  ad  1  pint,  bread  or  borated  starch  poultice. 
It  is  no  use  applying  ointments  during  the  oozing  stage  or  on  the  top  of 
■crusts. 

Infection  is  prevented  by  cleanliness,  protection  from  exposure,  the 
removal  of  scabs,  the  prevention  of  scratching,  and  the  use  of  creolin 
lotion  (dr.  |-1  ad  1  pint)  or  salicylic  acid  ointment.  In  extensive  cases 
■clean  with  weak  warm  gruel,  boroglyceride  lotion  or  a  creolin  bath. 
Subsequently  cleanse  with  warm  carbolised  oil  1  per  cent,  and  pledgets  of 
wool.  A  tar  bath  can  be  used  for  extensive  pustulation  or  impetigo  ; 
starch  poultices  and  creolin  lotion  for  less  severe  cases. 

To  dry  up  secretions  apply  dusting  powders  (p.  999).  They  are  easier 
±o  remove,  and  useful  for  keeping  opposed  surfaces  apart,  when  placed  in 
flat  muslin  bags.  They  must  not  be  dusted  on  the  scalp  because  of  the 
■difficulty  in  removal. 

For  protection  and  stimulation  of  the  surface  apply  on  lint,  fixed  on 
with  a  soft  bandage,  a  cream  or  paste  (p.  1000)  containing  zn.  oxide  ;  or 
the  zinc  cream  recommended  by  Malcolm  Morris,  consisting  of  lanoline 
•dr.  1-2,  ol.  olivae  oz.  1,  aq.  calcis  oz.  1,  zn.  oxid.  dr.  6-7,  a  thick  cream 
in  which  strips  of  muslin  or  old  linen  are  soaked.  Ichthyol  dr.  ^  can  be 
kidded,  if  desired.  Or  use  Lassar's  paste  with  ac.  salicyl.  gr.  10-20,  sulph. 
prsecip.  gr.  10-30,  or  with  calomel,  bismuth,  subnit.  or  resorcin  gr.  10-20 
ad  oz.  2. 

In  the  dry  scaling  stage  wash  with  creolin  lotion  and  apply  liq.  carb. 
-detergens  or  alcoholic  solution  of  coal  tar  dr.  J,  hydrarg.  amnion,  gr.  10, 
vaseline  oz.  1-2  ;  or  zn.  oxid.  1,  ung.  picis  liq.  2,  ung.  aq.  rosae  4  parts. 
'Ointments  of  tar,  sulphur,  salicylic  acid,  resorcin  or  mercury  are  now 
suitable.  Coal  tar  preparations  must  be  used  with  care,  and  strong 
antiseptics  avoided,  in  infancy.  If  it  is  desirable  to  omit  bandages,  use 
.a  zinc  gelatin  or  plaster  mull ;  or  Pick's  paste  (p.  1000)  with  zn.  oxide 
..gr.  40,  carbolic  acid  gr.  5,  or  tar  m.  10  per  ounce.  For  pustular  der- 
matitis ung.  hyd.  amm.  1,  lanoline  1,  vaseline  3-6  parts  is  a  suitable  appli- 
cation. 

Psoriasis. — A  family  history  of  the  disease  is  often  present  and  has 
been  traced  through  3  generations.  The  position  in  life  is  unimportant, 
the  general  health  excellent,  and  the  sex-incidence  about  equal.  Possibly 
a  gouty  or  rheumatic  heredity  has  some  influence.  Attacks  sometimes 
follow  vaccination  and  exanthemata.  The  age-incidence  is  roughly  50  per 
-cent,  under  15  years,  20  per  cent,  under  7  years,  and  5  per  cent,  under 


1008  Chapter  LXXIII. 

3  years  of  age.  A  few  eases  begin  in  the  first  year,  e.g.  at  5  and  38  days 
(Bille),  3  months  (Billard),  4  months  (Newmann).  It  is  most  common  in 
spring,  autumn,  winter  and  cold  weather.  Possibly  it  is  influenced  by  lack 
of  sun  and  light.     Attacks  may  occur  annually  or  at  frequent  intervals. 

It  often  begins  with  one  or  two  isolated  patches,  spreads  locally,  and 
finally  becomes  general  through  blood  infection  or  increasing  metabolic 
changes  in  the  system. 

According  to  the  size  of  the  patches  it  is  named  P.  punctata,  guttata? 
nummulata  or  diffusa.  These  are  merely  stages  in  its  development. 
During  involution  the  spots  clear  up  at  the  centre  and  leave  a  circinate 
or  gyrate  outline.  In  children  the  patches  are  small,  punctate,  guttate  or 
nummular,  round  or  oval,  showing  abrupt  transition  to  healthy  skin.  The 
scales  may  adhere  into  a  crust,  and  on  removal  leave  a  red  base.  The 
rash  is  widely  distributed,  not  limited  to  the  extensor  surfaces,  and  may 
even  involve  the  penis.  The  face  and  palmar  surfaces  of  the  hands  and 
feet  usually  escape.  On  the  whole  the  extensor  surfaces  and  dorsal  region 
are  most  involved,  and  the  rash  diminishes  peripherally.  The  scales  are 
small  and  easily  detached,  varying  in  colour  with  that  of  the  skin.  On 
the  scalp  it  is  difficult  to  distinguish  from  seborrhcea  sicca,  but  generally 
an  isolated  patch  can  be  found  which  is  covered  with  thick  white,  silvery, 
not  greasy,  scales.  Bleeding  spots  are  left  on  scraping  off  the  scales.  The 
nails  are  brittle  and  cracked  ;  not  thickened,  but  tilted  up  by  accumulated 
epidermis,  due  to  chronic  inflammation  of  the  nail  bed. 

Treatment. — Cure  every  patch,  not  merely  the  bulk  of  them,  for 
recrudescence  is  common.  Internal  remedies  seem  of  more  value  than 
local  ones  for  permanent  benefit.  The  best  drugs  are  rhubarb  and  soda,, 
alkalies  and  diuretics,  nitric  acid  after  food,  salicin  and  tonics  ;  and 
arsenic  in  chronic  stages.  A  cooling  lotion  or  ointment,  as  in  eczema,, 
may  be  needed  in  acute  stages. 

Give  an  alkaline  bath  of  sod.  carb.,  of  creolin  dr.  1  in  6  gallons,  or  a  warm 
bath  for  10-15  minutes  with  sulphur  or  soft  soap  ;  remove  scales  by 
scrubbing  ;  and  apply  to  each  spot  liq.  carbonis  detergens,  ung.  ac.  salicyl.,. 
or  an  ointment  of  ac.  salicyl.  gr.  10-20,  hyd.  ammon.  gr.  10,  creolin  dr.  1, 
vaseline  oz.  1,  to  which  may  be  added  chrysarobin  gr.  10,  sulph.  prsecip.. 
gr.  10,  soft  soap  dr.  1-2.  Ung.  picis  liq.  1,  vaseline  7  parts,  is  useful,  smelly 
and  dirty.  01.  cadeini  dr.  \-2,  vaseline  ad  oz.  1,  is  preferable.  Chrysarobin 
is  most  efficacious,  but  stains  everything  and  may  cause  severe  erythema 
or  acute  conjunctivitis.  It  makes  the  patches  white  and  the  sound  skin 
red.  White  precipitate  ointment  is  then  rubbed  in.  Chrysarobin  gr.  5-10, 
ac.  salicyl.  gr.  10  in  traumaticin  oz.  1,  can  be  painted  on  each  spot.  It 
forms  a  film  which  does  not  stain  when  dry.  Besorcin,  naphthol,  and 
other  tar  preparations  are  also  of  value.  For  the  head  use  sp.  saponis  alk., 
rubbed  in  at  night  and  washed  out  in  the  morning  ;  or  hyd.  amm.  gr.  10, 
soft   soap  and   vaseline   p. a.    oz.    1,  rubbed    in   nightly   after    washing ;. 


The  Skin.  1009 

or  ac.  salicyl.  5  per  cent,  in  ol.  ricini   and  ol.  olivse  p. a.,  to  remove  the 
scales. 

The  sulphur  baths  of  Harrogate,  Strathpeffer,  Aix-la-Chapelle  and 
Barege  in  the  Pyrenees,  and  the  arsenical  waters  of  La  Bourboule,  Levico 
and  Roncegno  in  the  Tyrol  are  more  suitable  for  chronic  cases  in  adults. 

Most  cases  in  children  are  curable  in  4-6  weeks.  Dietetic  treatment  is 
sometimes  needed.  Bulkley  (1908)  found  the  urine  abnormally  acid  and 
containing  a  double  quantity  of  urea.  He  states  that  meat  diet  accentuates 
the  rash,  and  prescribes  a  true  vegetarian  diet,  excluding  milk,  eggs  and 
fish.     Such  a  diet  is  unsuitable  and  unnecessary  in  childhood. 

Scleroderma  is  localised  or  generalised.  In  the  local  type  there  are 
patches  of  dull  or  glossy,  ivory  white,  hard  skin  ;  often  stiff,  thickened  and 
painful ;  sometimes  symmetrical,  though  no  two  patches  are  exactly  alike, 
and  called  herpetiform  morphcea.  It  disappears  in  time,  leaving  the  skin 
a  little  thin,  brown  and  shrivelled.  In  a  more  severe  type  the  cellular 
tissues,  muscle  and  bones  are  affected  and  arrested  in  their  growth,  e.g. 
facial  hemi-atrophy.  The  generalised  variety  is  a  type  of  Sclerema.  The 
skin  is  thick,  dry,  harsh,  immobile  and  parchment-like,  without  leueoderma 
or  pigmentation.  Its  natural  folds  are  obliterated,  the  facial  expression  is 
lost,  and  there  is  a  more  or  less  widespread,  "  hide  bound  "  appearance. 
It  may  be  associated  with  inflammation,  atrophy  and  contraction  of 
muscles.  Possibly  it  is  an  infection  of  the  subcutaneous  tissues  and 
muscles,  ending  in  sclerosis.  Its  course  is  progressive.  Some  patches  may 
recover  and  others  appear.  Persistent  massage  with  emollient  ointments 
is  beneficial. 

Corns  are  more  troublesome  in  adults  than  children,  except  in  the 
form  of  corneous  thickenings  of  the  heels  and  soles  from  unsuitable  boots. 
For  these  apply  salicylic  acid  gr.  30,  ext.  cann.  ind.  gr.  5,  collodion  oz.  1, 
nightly,  and  pare  off  the  thickened  skin.  A  lotion  of  soft  soap  oz.  2, 
methylated  spirit  oz.  3,  applied  on  lint,  will  prevent  the  corn  re-forming. 

Warts  are  often  multiple,  cause  little  or  no  discomfort,  and  may 
disappear  spontaneously.  They  are  most  numerous  on  the  hands,  fingers 
and  scalp.  Apparently  they  can  be  transmitted,  and  have  an  incubation 
period  of  1-8  months.  Disappearance  has  followed  the  taking  of  lime 
water,  oz.  1-4,  t.d.s.  Local  applications  include  wearing  gloves  dusted 
with  calomel  and  French  chalk  ;  saturated  caustic  soda  solution  daily  ; 
ac.  salicyl.  1,  ac.  lactici  1,  collodion  2  parts,  bis  die  ;  papain  dr.  1,  ac. 
hydrochl.  fort.  dr.  2,  bis  die  ;  glacial  acetic  acid  ;  chloral  hydrat.  gr.  15, 
ac.  acetic,  m.  15,  ac.  salicyl.  dr.  1,  ether  dr.  1,  collodion  dr.  4,  daily  ; 
sulphur  sublim.  2,  glycerine  5,  acetic  acid  1  part,  painted  on  several  times 
daily  ;  ol.  terebinth,  half-hourly  and  dried  in  before  the  fire  ;  the  galvano- 
cautery,  electrolysis,  X-rays,  re-vaccination  and  suggestion.  After  a 
single  application  of  X-rays  for  15-30  minutes,  the  wart  drops  off  in 
7-10  days,  leaving  smooth  healthy  skin,  with  no  scarring. 

3t 


1010  Chapter  L  XX I II. 

Molluscum  Contagiosum  is  due  to  the  metamorphosis  of  the  cells  of  the 
rete  Malpighii  into  keratin.  Probably  it  is  started  by  a  parasite  which 
sets  up  an  in-growing  epithelial  proliferation  of  the  duct  of  a  sebaceous 
gland.  It  may  become  inflamed.  Small,  waxy,  umbilicated  tumours,  like 
little  buttons,  are  found  in  variable  numbers  on  the  forehead,  face,  round 
the  eyelids,  and  sometimes  on  the  neck,  limbs,  genitals  and  round  the 
anus.  A  peculiar  cere  can  be  expressed,  on  making  a  small  incision.  The 
treatment  consists  of  curetting  after  expression  of  the  core.  Or  touch  the 
apex  of  each  tumour  with  a  drop  of  pure  carbolic  acid.  After  a  few 
applications  it  withers  and  falls  off. 

Lichen  Planus  is  a  rash  of  pinkish,  flat-topped,  shiny  papules,  which 
may  be  aggregated  into  pavement-like  plaques.  It  may  affect  the  mucous 
membranes.  It  especially  appears  on  the  extensor  surfaces  of  the  arms 
and  thighs.  The  palms  and  soles  are  usually  free.  Arsenic  or  biniodide  of 
mercury  should  be  given ;  and  antimony,  if  arsenic  exaggerates  the 
symptoms.     Lichen  spinulosus  consists  of  groups  of  spiny  papules. 

Alopecia. — General  thinning  of  the  hair  after  illness  is  treated  by  tonics 
and  rubbing  in  chloral  hydrat.  gr.  10,  ung.  hydrarg.  ox.  rub.  dr.  1-2,  lanolin 
ad  oz.  1.  True  alopecia  is  characterised  by  partial  or  complete  loss  of 
hair,  due  to  a  neurotrophic  or  toxic  affection  of  the  hair  papilla.  When 
universal  it  begins  in  patches,  which  are  asymmetrical  and  immune  frcm 
inflammatory  reaction.  No  parasitic  cause  has  been  found.  The  con- 
tagious cases  are  probably  varieties  of  ringworm.  The  bald  patches  are 
pale,  bloodless,  smooth,  shining  and  circumscribed.  Short  hair  stumps  at 
the  edges  are  thick  and  pigmented  at  the  free  end,. thin  and  pale  at  the 
attached  end,  like  "  notes  of  exclamation."  The  hair  root  is  atrophied, 
but  the  hair  is  more  adherent  than  in  ringworm.  The  course  is  very 
slow.  The  prognosis  is  better  than  in  adults.  The  longer  the  growth  of 
new  hair  is  delayed,  the  worse  is  the  prognosis.  Fine  downy  hairs  grow  and 
become  gradually  stronger  and  darker.     Eelapses  are  not  uncommon. 

Tonics  and  intestinal  antiseptics  may  do  good.  The  main  treatment  is 
local  irritation  by  massage,  faradism  and  drugs,  e.g.  ol.  cinnamon.  1,  ol. 
olivse  4  parts  ;  ol.  sinap.  dr.  1,  ol.  ric.  dr.  2,  sp.  rosmarini  ad  oz.  4  ;  liq. 
amm.  fort.,  chloroform,  ol.  sesam.  aa.  dr.  2-4,  ol.  limon.  dr.  \,  sp.  rosmarini 
ad  oz.  4  ;  bals.  Peru,  the  tinctures  of  capsicum,  iodine,  veratria  and 
cantharides,  pure  carbolic  acid,  ung.  chrysarobin  0-5-10  per  cent.,  ung.  hyd. 
ox.  rub.,  etc.,  in  sufficient  strength  to  produce  mild  inflammatory 
reaction. 

Sudamina. — The  rash  consists  of  multiple,  minute,  transparent  vesicles, 
or  minute  pustules,  due  to  the  accumulation  of  sweat  in  glands  whose 
ducts  are  blocked  by  dirt  or  epithelial  cells.  It  is  the  result  of  profuse 
sweating.  There  may  be  a  general  erythematous  base  or  intervening 
minute  red  papules.  On  the  palms,  soles  and  sides  of  the  fingers  it  appears 
as  minute,  whitish,  itching  papulo- vesicles.     The  rash  often  itches  and  is 


The  Skin.  1011 

followed   by   slight   desquamation.      Apply   vinegar   and   water,    dusting 
powder,  and  the  measures  used  for  intertrigo. 

Strophulus,  red  gum  or  milaria  rubra,  is  an  eruption  of  scattered  red 
papules,  due  to  inflammation  of  sweat  glands  by  retained  secretion.  The 
name,  strophulus,  is  occasionally  given  to  inflamed  sudamina  and  to 
lichen  urticatus.  Sometimes  tiny  vesicles  are  formed  and  the  rash  is 
analogous  to  prickly  heat.  Probably  there  are  two  kinds  of  "  red  gum," 
one  due  to  inflammation  of  the  sweat  glands  and  the  other  to  disturbance 
of  function  of  the  sebaceous  glands.  Frequently  there  is  a  good  deal  of 
■erythema  and  the  spots  resemble  insect  bites.  They  are  distributed  in 
irregular  groups,  appear  on  the  face,  are  often  abundant  on  the  front  of  the 
forearms,  just  above  the  wrist,  and  are  absent  from  the  hands.  They  dis- 
appear spontaneously.  Some  of  them  are  hard,  with  a  "  shotty  "  centre, 
like  abortive  pustules.  The  rash  bears  no  relation  to  the  state  of  health 
of  the  child,  the  diet  or  the  clothing.    No  special  treatment  is  needed. 

Acne. —  Comedones  or  "  black-heads  "  are  not  due  to  mere  plugging  of  the 
•ducts  of  sebaceous  glands  with  dirt  and  sebum.  Each  one  consists  of 
•concentric  layers  of  horny  cells,  enclosing  a  mass  of  the  micro-bacilli  of 
acne,  which  find  in  the  oily  sebum  a  suitable  soil.  This  horny  plug  sets  up 
irritation  and,  as  the  result  of  staphylococcal  infection,  gives  rise  to  the 
papules  or  papulo-pustules  of  acne.  Hence  acne  consists  of  three  stages, 
viz.  greasy  skin,  comedones,  and  folliculitis  from  secondary  infection. 

Grouped  comedones  are  common  in  infants  and  children,  especially 
on  the  forehead,  cheeks  and  chest.  Sometimes  they  are  due  to  the  applica- 
tion of  camphorated  oil,  Russian  tallow,  etc.,  and  consequent  blockage  of 
the  ducts. 

Acne  is  common  about  puberty,  rare  in  younger  children.  Single 
spots  can  be  touched  with  liquefied  carbolic  acid,  or  incised  and  washed  out 
with  carbolic  acid  20  per  cent.  For  multiple  acne  bathe  well  with  hot 
water  and  apply  a  good  lather  of  ichthyol  10  per  cent,  soap,  night  and 
morning,  during  the  inflammatory  stage.  Then  rub  in  nightly  an  ointment 
of  sulphur  preecip.  gr.  15,  hyd.  amm.  gr.  5,  hyd.  sulphid.  rub.  gr.  5,  vaseline 
ad  oz.  1. 

Prevention  consists  in  keeping  the  skin  free  from  excessive  sebum, 
squeezing  out  comedones  unless  inflamed,  and  rubbing  in  lysoform  soap 
lather  nightly  with  a  shaving  brush.  Lotions  are  often  preferable  to 
ointments,  e.g.  sulphur,  prsecip.,  glycerin.,  ether  aa  dr.  2,  sp.  vin.  rect.  dr.  i, 
aq.  rosae  ad  oz.  10,  mopped  on  freely  at  night  and  allowed  to  dry  on. 
Give  a  morning  saline  aperient,  regulate  the  diet,  and  prohibit  alcohol. 
Internally  give  the  sulphates  of  Fe.  and  Mg.,  and  tonics ;  and  yeast,  ceridin, 
or  calcium  sulphide  if  there  is  suppuration.  Disinfect  the  skin,  and  try 
vaccine  in  severe  cases. 

Furunculosis. — A  boil  runs  the  same  course  as  in  adults.  Small 
•ones,  containing  yellow  or  greenish-yellow  pus,  appear  in  great  numbers 


1012  Chapter  L  XX I II. 

on  the  scalp,  buttocks,  thighs  and  shoulders  of  marasmic  infants,  sometimes- 
in  successive  crops  for  months,  and  occasionally  in  the  well-nourished. 
They  are  due  to  infection  of  the  skin  by  the  staphylococcus  aureus,  and  may 
become  gangrenous  or  set  up  pyaemia.  Sulphur  baths,  ointments  and 
pastes  are  the  best  remedies. 

Prescribe  yeast,  the  ferment  of  beer  or  grapes ;  calcium  sulphide,, 
hypophosphites,  ferri-ichthyol,  arsenic,  iron,  ol.  mor.,  or  quinine.  Feed 
well  and  attend  to  the  digestive  tract.  Inject  locally,  to  induce  abortion,, 
tr.  iodi  or  pure  carbolic  acid,  m.  1-3.  To  relieve  pain  and  encourage 
suppuration,  apply  boric  acid  fomentations  or  starch  poultices.  Rub  an 
antiseptic  ointment  into  the  unaffected  skin.  Spontaneous  rupture  leaves- 
the  least  scar.  In  unimportant  places  incise  and  apply  antiseptics.  A 
satisfactory  method  of  treatment  is  the  application  of  glyc.  ac.  carbol.  on 
wool,  covered  by  guttapercha  tissue.  As  the  boil  points  the  epithelium  is- 
reflected  and  a  little  of  the  glycerine  injected.  The  slough  separates  in 
2-3  days.  Or  paint  the  boil,  except  the  apex  and  the  surrounding  skin, 
with  collodion,  flexile  2  and  non-flexile  3  parts,  covering  the  whole  with 
absorbent  antiseptic  wool.  As  the  collodion  contracts  it  squeezes  out  the 
core.     A  preliminary  small  incision  may  be  required. 

Impetigo  Contagiosa. — Pustular  dermatitis  may  occur  in  the  new- 
born and  cause  sepsis.  Impetigo  is  a  local  form,  usually  due  to  staphylo- 
coccal infection.  It  chiefly  affects  the  face,  head  and  hands,  and  is  spread 
by  scratching.  It  is  contagious.  Staphylococci  have  been  grown  in  puro 
culture  from  unopened  bullae  and  have  experimentally  produced  the 
disease ;  so,  too,  streptococci.  The  rash  begins  with  erythematous 
spots,  which  become  vesicles.  These  soon  contain  sero-pus  or  pus,  and  have 
a  slightly  red  areola.  The  pustules  rupture  and  discharge,  and  thick 
yellowish  scabs  are  formed,  leaving  a  moist  red  surface  on  removal.  The 
sores  may  become  circinate  through  healing  centrally  and  spreading 
peripherally.  Wash  with  a  weak  antiseptic  lotion.  Open  vesicles  and 
clean  the  skin.  Remove  crusts  after  softening  them.  Apply  sulphur  or 
white  precipitate  ointment,  or  a  sulphur  lotion.    Give  ol.  mor.  and  iron. 

Echthyma  is  closely  allied  to  impetigo,  but  the  base  is  infiltrated  and 
leaves  a  pigmented  scar.  It  is  most  common  on  the  nates  and  lower  limbs, 
rare  on  the  trunk,  and  is  secondary  to  scratch  infection.  In  the  gangrenous- 
form,  like  gangrenous  varicella,  deeply  cut  ulcers  are  formed,  with  a  black 
slough  at  the  base.     The  treatment  is  the  same  as  in  impetigo. 

Pemphigus. — This  is  a  bullous  eruption,  occurring  sporadically  or 
epidemically,  and  like  pemphigus  neonatorum  (p.  142)  in  its  pathology.  It 
comes  out  suddenly  and  rapidly  all  over  the  body  and  limbs,  but  is  rare  on 
the  palms  and  soles.  It  begins  on  the  extremities,  trunk,  buttocks,  or 
perhaps  on  the  eyelids.  Though  somewhat  allied  to  herpes  the  rash  has  no 
definite  nerve  distribution.  At  first  the  bullae  are  like  those  of  simple  scalds. 
Later  they  show  a  narrow  red  areola,  due  to  inflammation.    They  vary  in. 


The  Skin.  1013 

size  from  a  pin  head  to  a  crown  piece.  Usually  they  are  not  very  numerous, 
sometimes  only  a  few,  but  occasionally  almost  the  whole  body  is  covered 
and  they  may  coalesce.  Their  contents  are  clear  or  cloudy  serum,  which 
may  become  purulent.  They  are  absorbed,  or  the  bullse  burst  in  1-3  days 
and  leave  a  raw  surface  which  soon  becomes  thinly  scabbed.  After  the 
scab  falls  off  some  discolouration  is  left.  The  rash  may  affect  the  mucous 
membrane,  causing  swelling  of  the  gums  and  intense  congestion  of  the 
buccal  mucosa.  Bulla?  in  the  small  and  large  intestine  give  rise  to  abdominal 
pain  and  diarrhoea.     Eosinophilia  is  generally  present. 

In  mild  cases  there  are  no  symptoms.  In  severe  ones,  sometimes  fatal, 
there  is  high  fever,  restlessness,  anorexia,  vomiting,  rigor  or  chilliness, 
offensive  urine  and  albuminuria.  Even  apyrexial  cases  may  prove  fatal. 
The  rash  lasts  from  2-7  or  more  weeks  ;  may  appear  in  crops  ;  may  be 
recurrent,  or  chronic  with  exacerbations  ;  and  may  be  followed  by  com- 
plete desquamation,  leaving  the  cuticle  red  and  weeping.     Death  is  rare. 

Protect  the  parts  from  injury  and  sepsis,  by  means  of  antiseptic 
dusting  powders  and  lotions.  Prick  the  vesicles.  Relieve  pain.  Give 
bran  and  oak  bark  baths.     Arsenic  is  the  most  useful  drug. 

Herpes. — Syn.  :  Herpetic  fever —  Herpes  zoster — Shingles — Labial  herpes 
— Zona  ophthalmicus. — This  is  a  general  disease  with  a  local  manifestation 
rather  than  a  simple  skin  affection.  It  is  divisible  into  a  : — (1)  Specific 
or  infective  variety,  an  acute  specific  infectious  disease  ;  (2)  Toxsemic 
type,  of  digestive  or  febrile  origin  ;  (3)  Secondary  variety.  The  most 
probable  explanation  is  that  the  rash  is  due  to  neuritis  and  that  the  neuritis 
depends  on  many  causes.  Barensprung  (1861)  found  a  lesion  in  the 
posterior  root  ganglion,  and  ascribed  it  to  irritation  of  the  spinal  or 
Gasserian  ganglia,  and  occasionally  to  peripheral  nerve  irritation.  Head 
and  Campbell  (1900)  discovered  an  acute  inflammatory  condition  of  the 
ganglia  in  acute  cases,  and  secondary  degenerative  changes,  not  demon- 
strable before  the  eleventh  day,  in  the  posterior  nerve  roots  and  peripheral 
nerves.  Changes  take  place  in  the  spinal  cord,  similar  to  those  following 
section  of  the  posterior  root.  The  area  of  the  rash  corresponds  with  that 
of  the  affected  posterior  root  ganglion.  Complete  recovery,  or  sclerosis  and 
persistent  pain,  may  ensue. 

Primary  herpes  is  the  result  of  an  infection  of  the  posterior  root 
ganglia  which  irritates  the  nerves  and  causes  the  rash.  Secondary  herpes 
is  due  to  these  ganglia  being  implicated  by  injury,  disease,  or  drugs  such  as 
arsenic. 

The  specific  variety  is  in  many  respects  analogous  to  acute  poliomyelitis, 
except  that  the  poison  attacks  the  sensory  and  not  the  motor  parts  of  the 
nervous  system.  There  is  a  distinct  prodromal  period.  The  rash  comes 
out  on  the  third  or  fourth  day,  sometimes  within  a  few  hours,  and  is  not 
always  localised.  It  occurs  in  epidemics,  chiefly  in  spring  and  autumn. 
In  true  herpes  zoster  second  attacks  are  infrequent.     Relapses  occur  in 


1014  Chapter  L XXI II. 

about  1  per  cent.  On  the  other  hand  there  are  cases  which  are  markedly 
recurrent  and  probably  non-specific.  Thus,  in  4  girls  I  have  known 
frequent  recurrence  on  the  lips  or  cheek.  Ophthalmic  zona  has  recurred 
3-4  times  a  year  from  childhood  (Matignon). 

Symptoms  of  Shingles. — After  a  variable  period  of  malaise,  digestive 
disturbance,  chilliness  or  rigors,  and  fever,  a  pain  develops  along  certain 
nerve  paths  or  metameric  areas.  It  is  often  severe,  burning,  itching, 
stabbing  or  neuralgic,  and  may  be  ascribed  to  pleurisy  or  pneumonia.  The 
lymph  nodes  are  enlarged,  sometimes  before  the  eruption.  In  1-5  days  the 
rash  comes  out  along  the  course  of  a  cutaneous  nerve.  At  first  it  is  papular, 
but  the  papules  quickly  develop  into  clear  vesicles,  of  the  size  of  a  pin  head 
to  a  split  pea.  Each  vesicle  is  surrounded  by  a  red  areola  and  these  areolae 
may  coalesce.  The  rash  is  more  or  less  continuous,  large  groups  of  vesicles 
being  linked  together  by  smaller  ones  or  single  vesicles.  Their  contents 
are  sterile,  become  sero-purulent,  and  soon  dry  up,  leaving  scabs  in  1-2  days. 
The  pain  usually  disappears  with  the  eruption  of  the  rash.  Fever  subsides 
quickly  and  recovery  is  rapid.  Fever  may  persist  for  6  days.  The  blood 
shows  leucopenia,  a  reduction  of  polymorphs  to  an  average  of  45  per  cent.  ; 
and  moderate  eosinophilia,  6-8  per  cent.  The  complications  are  slight 
adenitis,  extensive  ulceration  and  gangrenous  dermatitis. 

Labial  herpes  is  common  in  digestive  disturbance,  pneumonia  and 
cerebrospinal  fever.  In  children  I  have  seen  herpetic  eruptions  on  prac- 
tically every  part  of  the  body,  except  perhaps  the  palms  and  soles.  They 
are  less  frequent  on  the  shoulders  and  limbs  than  in  adults.  Occasionally 
it  attacks  the  mucous  membrane  of  the  mouth,  pharynx,  larynx,  nose  or 
genitals.  It  is  rare  under  4  years  of  age.  The  sex-incidence  is  twice  as 
great  in  females.  Shingles  is  rarely  bilateral  and  is  limited  by  the  middle 
line  of  the  body,  but  not  rigidly,  for  the  nerve  filaments  sometimes  encroach 
over  the  border.     Fever  and  gastric  symptoms  are  the  common  signs. 

French  dermatologists  have  described  "  isolated  vesicles  disseminated 
over  the  body  in  herpes  zoster."  Aberrant  vesicles  of  this  type  have- 
been  noted  by  English  observers.  They  are  about  the  size  of  a  hemp 
seed,  with  a  red  areola,  like  varicella. 

Treatment. — Keep  the  child  in  bed  until  the  fever  has  subsided.  Give 
a  calomel  purge,  mild  febrifuge  and  light  diet.  Paint  the  rash  with 
collodion,  or  dust  on  equal  parts  of  calomel,  zinc  oxide  and  starch,  and  put 
on  a  pad  of  absorbent  wool  to  protect  it  from  injury  and  prevent  rupture 
of  the  vesicles.  Treat  secondary  ulceration  and  gangrene  on  ordinary 
surgical  principles.  Give  hypophosphites,  arsenic  and  cod-liver  oil  in 
convalescence. 

Tuberculosis  of  the  Skin.— The  bacillus  has  been  found  in  lupus 
vulgaris,  lichen  scrofulosorum,  scrofuloderma  or  tuberculous  gummata,. 
and  acute  miliary  tuberculosis  of  the  skin,  a  rare  eruption  of  acneiform 
papules.     Lupus  vulgaris  may  occur  after  measles  in  a  nodular  form  on  the 


The  Skin.  1015 

face,  trunk  and  limbs.  Lichen  scrofulosorum  consists  of  an  insignificant 
eruption  of  very  small,  pink,  follicular  papules  in  circinate  patches  on  the 
abdomen  and  limbs.  It  lasts  for  months,  but  may  finally  disappear  and 
leave  pigmented  scars.  Tuberculous  gummata  are  small  deep-seated 
abscesses,  which  sometimes  burst  spontaneously,  and  are  an  advanced 
stage  of  Acne  Scrofulosorum.  This  consists  of  one  or  more  papules,  up 
to  a  pea  in  size,  at  first  subcutaneous,  and  later  dusky  red  or  purplish  and 
involving  the  skin.  They  often  break  down,  forming  small  punched  out 
ulcers  which  heal  and  leave  a  circular  scar.  They  are  generally  situated 
on  the  limbs,  run  an  indolent  course,  and  may  slowly  disappear.  The 
bacillus  is  said  not  to  have  been  discovered  in  these  nodules.  Scrapings 
from  one,  taken  from  a  well-nourished  boy,  produced  tuberculosis  in 
guinea  pigs.  Many  of  these  children  are  fat  and  appear  healthy.  One  such 
child  under  my  care  died  from  tuberculous  meningitis,  and  caseous  nodules 
were  present  in  the  brain. 

Erythema  Induratum  vel  Scrofulosorum  (Bazin's  disease)  is  apparently 
a  later  stage  of  the  last  variety.  Deep-seated,  painless,  dusky  or  bluish 
plaques  and  nodules  are  found  in  the  legs,  generally  the  calves,  of  delicate 
girls  who  stand  a  great  deal.  They  are  apt  to  ulcerate.  Scrapings  have 
produced  inoculation-tuberculosis  in  guinea  pigs.  The  treatment  is 
essentially  that  of  tuberculosis  and  that  appropriate  for  the  nodules  and 
ulcers,  if  any.  Gummatous  broken  down  nodules  should  be  curetted  and 
swabbed  with  pure  carbolic  acid. 


PARASITIC     SKIN    AFFECTIONS. 

Ringworm — Tinea     Tonsurans — Favus — Insect     Bites— Harvest     Bugs — 
Pediculosis — Scabies —  Creeping  Larvce. 

Tinea,  or  ringworm,  has  been  known  for  centuries.  Gruby,  of  Paris 
(1843),  first  ascribed  tinea  tonsurans  to  a  cryptogamic  fungus  which  he 
named  the  microsporon  Audouini,  after  Audouin  who  had  recently  described 
such  a  fungus  in  silkworm  disease.  Malmstein,  of  Stockholm  (1844), 
discovered  a  similar  fungus  and  called  it  the  trichophyton  tonsurans. 
Sabouraud  has  made  extensive  and  valuable  researches,  and  has  described 
(1908)  11  varieties  of  fungus.  By  far  the  most  common  is  the  microsporon. 
It  is  present  in  60-65  per  cent,  of  the  scalp  cases  in  Paris,  and  in  90-95  per 
cent,  of  those  in  London  and  Edinburgh.  The  remainder  are  due  to  a 
large  spored  fungus  in  the  form  of  threads,  trichophyton  mcgalosporon 
endothrix  and  ectothrix.  The  ectothrix  variety,  in  which  the  fungus 
lies  outside  the  hair,  between  the  dermic  portion  of  the  shaft  and  the  hair 
follicle,  is  the  most  curable.     The  species  conveyed  from  the  horse  is  very 


1016  Chapter  L  XXI 1 1. 

liable  to  set  up  suppurative  lesions.  Kingworm  of  the  body  is  almost 
always  due  to  a  trichophyton. 

Etiology. — The  botanical  character  and  origin  of  the  fungus  are 
uncertain.  Probably  trichophytons  exist  saprophytically.  The  ectothrix 
is  generally  communicated  by  domestic  birds  or  animals,  and  the  microsporon 
from  another  child,  horse,  cat  or  dog.  Ringworm  is  transmitted  by  direct 
contagion  or  through  the  medium  of  caps,  brushes,  etc.  Both  sexes  are 
equally  liable.  Body  ringworm  may  occur  at  any  age.  Scalp  ringworm, 
due  to  the  microsporon,  is  peculiar  to  children  and  does  not  persist  in 
adults.     Fair-haired  are  more  susceptible  than  dark-haired  children. 

Pathology. — In  the  common  type  the  fungus  grows  first  in  the  epithe- 
lium, forming  small  greyish  scaly  patches.  It  gradually  invests  the  hair 
with  a  white  or  greyish  mosaic  sheath  of  spores,  while  the  mycelia  invade 
its  substance.  The  hairs  extend  2-3  mm.  beyond  the  orifices  of  the  follicles, 
and  are  finer  and  longer  than  in  the  trichophyton  infections.  In  the 
endothrix  variety  they  are  broken  off  short,  level  with  the  scalp,  "  black- 
spot  "  ringworm,  and  show  no  trace  of  a  sheath.  The  fungus  is  within  the 
hair,  the  spores  are  arranged  in  chains,  and  the  patch  is  free  from  scales. 
In  the  ectothrix  type  the  hair  and  epidermis  are  affected,  and  the  dermic 
portion  of  the  hair  has  a  sheath.  The  fungus  is  really  an  endo-ectothrix 
for  it  invades  the  shaft,  erodes  it  from  within,  and  causes  the  hair  to  break 
off  close  to  the  mouth  of  the  follicle.  The  microsporon  erodes  the  shaft 
from  outside  and  the  hair  breaks  off  a  short  distance  from  the  surface. 
In  cultures  on  agar  maltose  6  out  of  the  11  varieties  parasitic  on  man  and 
animals  (Sabouraud)  are  small-spored,  like  the  microsporon,  and  form 
large  white  powdery  growths  ;  4  are  large-spored  and  form  large  white 
downy  cultures  ;  and  the  microsporon  audouini  forms  disc-shaped,  downy 
or  woolly  growths. 

Mode  of  Examination. — Extract  a  hair  from  the  edge  of  the  patch  by 
gentle  traction  in  its  long  axis,  so  as  to  get  as  much  as  possible  of  the  bulb. 
Put  it  in  warm  liq.  potassae  for  |  minute,  transfer  it  to  fresh  water  and  then 
to  glycerine,  and  examine  under  a  ^-|  in.  objective.  For  staining,  soak  it 
in  ether  for  5  minutes  to  dissolve  out  the  fat ;  stain  in  a  dye  of  gentian 
violet  5  per  cent,  in  alcohol,  70  vol.  strength,  for  5-60  minutes,  with  gentle 
heat ;  decolourise  with  Gram-iodine  solution,  clear  with  anilin  oil,  wash  in 
xylol  and  mount  in  xylol  balsam.  The  spores  are  stained  blue.  For  red 
staining  use  carbol-fuchsin,  2  per  cent.  The  microsporon  stains  the  most 
readily. 

Tinea  Tonsurans  is  extremely  prevalent,  almost  peculiar  to  children, 
and  entails  exclusion  from  school  or  education  in  special  schools.  It  is 
most  common  at  5-10  years  of  age,  may  occur  in  the  first  year  of  life, 
decreases  in  frequency  after  the  tenth  year,  and  virtually  ceases  at  puberty. 
Boys  are  more  often  infected  than  girls,  through  interchange  of  caps. 
The  incubation  period  is  about  a  fortnight. 


Parasitic  Shin   Affections.  1017 

It  starts  round  a  hair  follicle  as  a  small  papule  which  spreads  and  forms 
a  round  or  oval,  slightly  raised,  scaly  patch,  dirty  grey  or  yellowish  to 
reddish  brown  in  colour.  A  microsporon  patch  is  round,  sharply  defined, 
a,nd  has  a  narrow  red  areola.  It  is  studded  with  short,  broken,  atrophied 
hairs  of  a  dirty  white  appearance,  because  of  their  mycelial  sheaths.  They 
project  as  cone-like  knobs,  causing  a  goose-skin  aspect  of  the  patch.  The 
hairs  are  loose  and  can  be  pulled  out  without  pain,  and  are  thickened  from 
infiltration  with  fungus. 

The  short  stumpy  hairs  have  been  described  as  like  "bent  fingers"  or 
"stubble  in  a  cornfield."  They  are  irregular  in  growth  and  direction,  and 
taper  off  at  the  free  ends  or  finish  off  abruptly.  In  the  megalosporon  type 
the  stumps  of  the  hairs  are  broken  off  at  a  level  with  the  skin  and  look 
like  black  dots. 

Sometimes  the  fungus  is  disseminated  in  numerous  isolated  patches 
all  over  the  scalp,  or  there  may  be  a  general  scaliness  liable  to  be  mistaken 
for  pityriasis  or  seborrhoea.  In  another  variety,  tinea  decalvans,  the  hairs 
fall  out  and  leave  smooth  patches  like  those  of  alopecia,  but  broken  hairs 
are  found  at  the  edges  and  many  of  the  follicles  are  indicated  by  black 
•dots.  An  impetiginous  form  exhibits  scabs  and  crusts,  through  which 
broken  hairs  often  project.  In  Jcerion  the  patch  is  inflamed,  raised,  boggy 
and  fluctuating,  and  exudes  pus.  It  is  the  result  of  too  active  treatment, 
inoculation  with  pus  cocci,  a  specially  virulent  ectothrix  infection,  or  an 
attempt  at  cure  by  nature.  The  follicles  are  filled  with  broken  hairs  or  pus, 
and  occasionally  a  subcutaneous  abscess  forms,  but  there  is  no  sloughing. 
Permanent  baldness  may  ensue.  Kerion,  impetigo  and  inflammatory 
patches  like  boils  are  the  only  complications. 

Course. — In  the  young  it  spreads  rapidly  and  may  involve  the  whole 
scalp  in  a  week  or  two.  The  disseminated  type  is  persistent,  because  small 
patches  are  apt  to  escape  cure.  In  chronic  cases  the  orifices  of  the  follicles 
are  blocked  and  it  is  difficult  to  reach  the  enclosed  fungus.  Baldness  is 
rare,  except  as  the  result  of  treatment  or  kerion.  The  latter  works  its  own 
•cure,  for  the  purulent  inflammation  destroys  the  fungus.  The  older  the 
child,  the  more  quickly  is  it  curable.  Untreated  cases  recover  after 
puberty.  The  microsporon  variety  is  the  most  intractable  and  may  persist 
for  3-6  months.  Tinea  decalvans  is  curable  in  a  few  weeks.  Chronic 
thickening  and  the  effects  of  injudicious  treatment  prolong  every  case. 

Tinea  Circinata. — This  occurs  at  any  age  and  in  either  sex.  It  is 
most  common  in  young  children.  It  is  due  to  the  trichophyton,  occasion- 
ally the  microsporon.  The  fungus  grows  centrifugally,  the  mycelial 
threads  spreading  and  causing  erythema  which  fades  at  the  centre  as  it 
•extends  peripherally,  forming  the  characteristic  ring-like  patches  on  the 
skin.  As  the  erythema  fades  the  patches  become  scaly.  After  remaining 
stationary  for  a  time  they  gradually  die  away.  Sometimes  there  are 
patches  but  no  rings  ;  occasionally  concentric  or  incomplete  rings.     Itching 


1018  Chapter  L XXIII. 

may  be  present  and  lead  to  scratching  and  pyogenic  infection.  The  rash 
is  most  common  on  the  neck  and  face,  hands  and  forearms,  and  the  trunk. 
It  tends  to  recovery  but  may  persist  for  months,  if  untreated. 

Onychomycosis  or  ringworm  of  the  nails. — The  fungus,  generally  an 
ectothrix,  invades  the  nail  and  sets  up  inflammation.  The  nail  becomes 
thickened,  dull,  uneven  and  brittle.  Exfoliation  occurs  and  under  the 
free  border  is  seen  a  mass  of  disintegrated  nail  structure.  Microscopical 
examination  is  necessary  to  distinguish  it  from  favus  and  psoriasis. 

Ringworm  of  the  palms  and  soles  begins  with  vesicles  and  blisters  which 
rupture  and  leave  a  bare  pink  surface.  This  becomes  dry  and  scaly, 
spreads  at  the  edges,  and  has  a  thickened  border.  The  fungus  is  found 
in  the  fluid  and  scales.     There  is  much  itching. 

Treatment. — Attend  to  the  general  health  for  it  is  often  poor.  Note 
the  age  of  the  patient,  coarseness  of  the  hair,  and  the  extent,  distribution 
and  clinical  characters  of  the  disease.  It  is  difficult  or  impossible  to 
destroy  the  parasite  in  situ.  Consequently  epilation  or  depilation  is 
desirable.  Epilation  is  only  suitable  for  small  patches,  and  is  even  then 
unsatisfactory  for  many  hairs  break  off. 

Depilation  is  best  carried  out  by  means  of  X-rays.  This  method  of 
treatment  is  undoubtedly  the  best,  provided  it  is  carried  out  by  an  expert.. 
There  is  no  danger  of  injury  to  the  brain.  In  skilled  hands  the  risks  of 
dermatitis  and  permanent  baldness  are  very  small.  The  treatment  must 
not  be  applied  if  the  scalp  is  inflamed,  especially  if  inflamed  by  iodine. 
Subsequent  irritation,  before  the  hairs  drop  out,  leads  to  scratching  of  the 
scalp,  pus  infection,  impetigo  and  folliculitis.  The  rays  are  not  parasiticidal, . 
but  the  fungus  falls  out  with  the  hairs. 

The  hair  is  cut  short,  and  the  affected  areas  marked  out  with  a  blue 
pencil.  Unaffected  areas  are  protected  by  lead  sheeting.  Or  the  rays  are 
concentrated  by  means  of  lead-glass  cylinders,  of  suitable  size,  on  the 
affected  patch  at  a  distance  of  15  cm.  from  the  source  of  the  rays.  The  dose 
is  measured  by  means  of  colour  changes  in  pastilles  devised  by  Sabouraud, 
placed  8  cm.  from  the  source  of  the  rays.  It  is  better  to  give  one  full 
exposure  than  several  milder  ones  for  the  risk  of  over-dosage  is  less,  seeing 
that  the  effects  cannot  be  measured  for  some  time.  The  hair  falls  out  in 
14-21  days,  grows  again  in  6-8  weeks,  and  is  fully  grown  in  another  3  months. 
Apply  a  weak  white  precipitate  ointment  to  prevent  infection  by  the 
falling  hairs.  Usually  there  is  a  little  erythema  a  week  after  the  exposure. 
The  prolonged  period  of  partial  or  complete  baldness  is  a  disadvantage. 
For  extensive  cases  it  is  necessary  to  depilate  the  whole  head,  dividing  it 
into  4-5  areas  for  separate  exposure.  Depilated  patches  become  quite 
smooth.  Diseased  stumps,  which  have  escaped,  in  the  margins  of  patches 
may  be  treated  by  croton-oil  needling.  A  needle  coated  with  a  film  of  the  oil 
is  gently  inserted  into  the  follicle,  taking  care  not  to  pierce  the  skin.  The 
hair  can  then  be  pulled  out  or  is  shed  from  pustular  folliculitis. 


Parasitic  Skin    Affections.  1019 

Depilation  by  inflammatory  treatment  results  in  kerion.  It  causes- 
discomfort,  often  pain  ;  is  unsightly  and  even  alarming  ;  and  is  difficult 
to  regulate  in  extent.  Croton  oil,  Coster's  paste  (iodine  dr.  2,  ol.  cadeini 
oz.  1),  liq.  epispasticus,  pure  carbolic  acid,  chrysarobin,  formalin,  tur- 
pentine, hyd.  iod.  rub.,  etc.,  are  used. 

The  croton  oil  method  is  the  best,  and  is  suitable  for  small  patches. 
Cut  the  hair  short  for  \  in.  round  and  rub  carbolised  vaseline  into  this  area. 
Hub  one  drop  of  croton  oil  into  the  patch  with  a  camel's  hair  brush  and  put 
on  a  linseed  poultice  in  3  hours,  covered  with  oiled  silk.  Eemove  the 
poultice  next  morning,  wash  with  warm  water,  prick  the  yellow  blisters, 
and  paint  and  poultice  as  before.  Repeat  this  daily  until  kerion  is  set  up. 
Then  apply  boroglyceride  lotion  to  reduce  the  inflammation,  and  extract 
all  the  stumps.  A  red  bald  patch  is  left  and  downy  hair  grows  in  6-8  weeks. 
Or  an  ointment  of  croton  oil  dr.  l,lanoline  ad  oz.  l,can  be  rubbed  in  daily, 
until  the  requisite  amount  of  inflammation  is  set  up  and  all  the  hairs  have 
been  epilated.     Allow  no  scabbing. 

A  single  application  of  blistering  fluid  cures  some  cases.  In  chronic 
ones  it  must  be  applied  weekly,  diluted  with  glycerine  if  blistering  is  to  be 
avoided. 

A  simple  method. — Cut  the  hair  quite  short  for  |  in.  round  a  patch  or 
shave  the  whole  head  every  2  weeks.  Rub  in  turpentine  and  then  wash 
with  soft  soap  or  sp.  saponis  alk.  to  remove  all  sebum  and  epithelial  debris. 
Repeat  the  soft  soap  washing  every  2  or  3  nights.  Mark  out  affected 
areas,  and  rub  carbolised  lanoline  or  glycerine  (1  in  8)  into  the  rest  of  the 
scalp.  Keep  on  a  linen  head  covering  by  day  and  night.  A  lotion  of  ac. 
salicyl.  gr.  5-10  in  ether  or  chloroform  dissolves  out  fat,  dehydrates  the 
tissues,  loosens  hairs  and  attacks  the  fungus.  It  must  be  brushed  in 
nightly. 

Mild  measures,  such  as  just  described,  may  cure  recent  cases  and 
those  due  to  the  megalosporon.  Other  remedies  of  this  type  are  a  saturated 
solution  of  Na.  CI.,  or  vaseline  and  Na.  CI.  pa.  ;  sod.  hyposulphit.  dr.  1-2, 
vaseline  oz.  2  ;  and  saturated  solution  of  boric  acid  in  methylated  spirit 
or  ether,  applied  for  15  minutes  daily. 

More  severe  remedies  include  : — (1)  Hyd.  perchlor.  gr.  10,  acetic  acid 
oz.  2,  glacial  acetic  oz.  1,  applied  daily  for  2-3  days  ;  (2)  Carbolic  acid  1, 
balsam  of  Peru  1,  petroleum  10,  glycerine  10  parts,  every  1-3  days  ;  (3)  Pure 
carbolic  and  iodine,  aa  dr.  1,  collodion  oz.  2,  painted  on  once  or  weekly  ; 

(4)  Ac.  carbol.  dr.  1,  ac.  salicyl.  dr.  1,  vaseline  oz.  1,  rubbed  in  m.  et  n.  ; 

(5)  Chrysarobin  gr.  10-60  ad  adip.  benzoat.  oz.  1,  alone  or  with  ac.  salicyl. 
gr.  10-20,  or  hydrarg.  amm.  gr.  10-20,  and  a  little  ichthyol  to  reduce  the 
inflammation;  (6)  Copper  oleate  gr.  30  in  ung.hydarg. oleatis,  20  per  cent., 
oz.  1  ;  (7)  Formalin,  10  per  cent,  solution,  applied  on  2-3  successive  days, 
and  followed  by  boric  fomentations.  It  is  often  painful  and  may  cause 
useless  eczematous  inflammation  or  much  oedema.    (8)  Decolourised  iodine, 


1020  Chapter  LXXIII. 

made  by  adding  calomel  to  the  tincture  and  decanting  the  clear  fluid, 
applied  by  camel's  hair  brush  ;  (9)  Mercurial  ointments,  unsuitable  for 
very  young  children  or  those  with  delicate  skins  ;  (10)  Sulphur  praecip. 
dr.  1,  ac.  carbol.  gr.  10-30,  ol.  olivae  and  lanoline  aa  oz.  \  ;  sulph.  praecip. 
dr.  1,  hyd.  amm.  gr.  20-30,  ac.  salicyl.  gr.  5-15,  ol.  olivae  and  lanoline  ad  oz.  1 ; 
(11)  Naphthalin  20  per  cent,  solution  ;  (12)  Liq.  ammon.  5,  ess.  terebinth, 
25,  camphorated  alcohol  125  parts  (Hallopeau),  rubbed  in  daily  after 
washing  with  soft  soap,  and  followed  by  inunction  of  iodated  vaseline, 
1  per  cent. 

Successful  treatment  depends  more  on  the  care  and  thoroughness  with 
which  it  is  carried  out  than  the  actual  parasiticide  used.  Drugs  do  not 
penetrate  sufficiently  deeply  to  kill  the  fungus,  so  epilation  or  depilation  is 
essential,  followed  by  the  use  of  ointments  which  prevent  superficial  spread. 

Ringworm  of  the  skin  is  easily  cured  by  painting  with  tr.  iodi,  alone  or 
with  the  addition  of  30  per  cent,  acetic  acid  or  5  parts  of  alcohol ;  or  with 
Coster's  paste.  An  ointment  of  hydrarg.  amm.,  gr.  3  ad  oz.  1,  is  suitable 
for  young  children.  The  signs  of  cure  are  the  absence  of  broken  hairs  and  of 
fungus  on  microscopical  examination.  Make  a  weekly  examination  for  a 
month. 

Favus  is  almost  invariably  due  to  the  achorion  Schonleinii.  It  is 
sometimes  transmitted  from  mice,  cats  and  dogs.  Fortunately  it  is  rare 
in  this  country,  and  chiefly  seen  among  aliens  in  the  East  end  of  London. 
It  begins  round  the  hair  follicle  as  a  yellow  deposit  or  plaque,  which 
gradually  increases  in  size  until  it  is  convex.  The  colour  slowly  changes  to 
grey  or  dust-like.  The  odour  is  that  of  mice.  The  hair  atrophies  and 
drops  out.  Favus  is  chiefly  limited  to  the  head  but  may  affect  the  nails. 
It  is  treated  by  X-rays,  epilation,  daily  washing  with  a  disinfectant,  and 
the  application  of  a  mercurial  or  pyrogallic  ointment. 

Insect  Bites. — Midges,  gnats,  mosquitoes  and  other  insects  cause  a 
local  itching  swelling,  very  like  urticaria  and  occasionally  resembling 
erythema .  nodosum.  Sometimes  the  swelling  is  as  great  as  in  angio- 
neurotic oedema.  The  bite  of  a  fly  may  prove  fatal  by  conveying  infection 
and  setting  up  pyaemia.  Wasp  stings  are  usually  trifling,  but  may  produce 
drowsiness,  urticaria,  swelling  of  eyelids  and  lips,  and  croupy  breathing, 
with  perhaps  nausea  and  vomiting.  A  single  sting  has  proved  fatal  in  25 
minutes.  Bee  stings  are  more  severe  and  convey  3  poisons,  convulsive, 
stupefying  and  inflammatory.  The  local  effects  are  redness,  swelling  and 
■itching.  Constitutional  symptoms  are  nausea,  vomiting,  pallor,  giddiness, 
prostration  and  general  urticaria.     Alcohol  and  ammonia  must  be  given. 

Fleas  rarely  attack  the  face.  Extensive  bites  may  cause  fever,  up  to 
103°  F.,  restlessness,  insomnia,  and  general  malnutrition.  Erythematous 
wheals,  and  even  bullae,  may  be  produced. 

Bugs  constantly  attack  the  face  and  hairless  scalp.  They  may  cause 
ill-defined,  dusky,  oedematous  blotches,  and  neither  wheals  nor  irritation. 


Parasitic  Skin   Affections.  1021 

The  puncture  often  cannot  be  seen  without  a  lens,  and  may  bleed  at  times. 
According  to  Hutchinson  urticaria  pigmentosa  is  due  to  this  cause. 

Preventive  treatment  consists  in  keeping  off  or  catching  the  insects. 
Sulphur  internally,  sulpur  soap  or  chinosol  in  the  bath,  and  the  application 
to  exposed  parts  of  tr.  pyrethri,  musk,  carbolic  acid,  or  the  oils  of  lavender, 
cloves,  citronella,  cinnamon  and  eucalyptus  may  keep  them  off.  Suitable 
preventives  for  fleas  and  bugs  are  powdered  cloves  dusted  on  the  bed- 
clothes, essence  of  thyme,  and  pledgets  of  absorbent  wool  sprinkled  with 
50  per  cent.  Jeyes  fluid  and  wrapped  up  in  the  night  garments  during  the 
day. 

For  relief  of  the  irritation  apply  Eau  de  Cologne  or  vinegar  and  water, 
a  raw  onion,  lead  lotion,  strong  ammonia,  carbolic  acid  5-10  per  cent., 
menthol  1  part  in  4  of  olive  oil  or  spirit,  or  ichthyol  collodion. 

Harvest  Bugs  (leptus  autumnale  or  bHe  rouge)  produce  the  harvest 
rash,  erythema  autumnale  or  prurigo  du  Rouget,  in  the  months  of  July  to 
September.  They  are  minute,  almost  spherical  insects,  with  6  legs  and 
sharp  mandibles,  red  or  yellowish  red  in  colour,  somewhat  like  cayenne 
pepper,  and  extremely  active.  A  lens  is  required  in  order  to  see  them. 
They  chiefly  attack  the  legs  and  ankles  of  children  in  hay  and  cornfields, 
about  French  beans  and  in  chalky  places.  Burrowing  into  and  burying 
themselves  in  the  epidermis,  or  in  a  hair  follicle,  they  give  rise  to  intolerable 
local  itching.  A  papule  or  wheal  is  formed  and  runs  its  course  in  about  a 
week.  If  the  head  only  penetrates  the  epidermis,  the  abdomen  swells 
until  visible  as  a  bright  red  dot.  Sometimes  there  is  a  general  urticaria. 
The  itching  causes  insomnia  and  scratching,  which  leads  to  impetigo, 
pustules,  ulceration,  and  haemorrhage  into  and  round  the  papules,  producing 
a  purplish  zone. 

The  preventive  measures  suitable  in  the  case  of  other  biting  insects 
should  be  adopted  for  children  who  play  about  in  infected  fields.  Give  a 
creolin  bath  at  bedtime  to  destroy  the  parasite  ;  or  apply  balsam  of  Peru 
or  benzene,  followed  by  a  warm  bath.  Use  the  ordinary  remedies  for  the 
relief  of  insect  bites,  and  an  ointment  of  sulphur,  carbolic  acid,  picis  liq. 
or  hyd.  subchlor. 

Scabies,  due  to  the  acarus  scabiei,  is  acquired  by  direct  contact  with  a 
pre-existing  case  or  infected  garments.  The  parasites  invade  the  tender, 
protected  parts  of  the  skin,  between  the  fingers  and  toes,  the  axillae,  genitals 
and  buttocks.  The  feet  of  infants  are  often  affected  because  they  play 
with  them.  The  male  acarus  lives  on  the  surface,  while  the  female  burrows 
into  the  horny  layer  of  the  skin.  She  gives  rise  to  great  irritation,  and  a 
papulo-vesicular  or  pustular  rash,  especially  on  the  hands  and  fingers. 
Pustulation  is  common  in  children.  The  pustules  vary  in  size  and  may 
coalesce.  On  the  trunk  and  buttocks  the  rash  is  very  like  lichen  urticatus. 
It  may  be  confined  to  the  lumbar  region.  The  burrows  are  white  or  black, 
according  to  the  degree  of  cleanliness.     They  may  be  visible  with  a  lens 


1022  Chapter  L  XX I II. 

between  and  on  the  sides  of  the  fingers  and  toes,  and  on  the  sides  of  the 
feet,  but  they  are  often  invisible  or  indistinct,  being  easily  destroyed  by 
scratching  and  vesiculation.  On  scratching  away  the  epidermis  at  the 
distal  end  of  a  burrow,  with  a  needle  on  a  holder,  the  parasite  clings  to 
the  needle  and  can  be  examined  in  liq.  potassse. 

At  first  there  may  be  merely  itching,  chiefly  at  night,  and  perhaps 
patches  of  transitory  erythema.  The  scratching  and  itching  soon  induce  a 
polymorphic  eruption.  A  limited  number  of  small  itching  vesicles  in 
characteristic  places,  with  surrounding  healthy  skin,  is  not  uncommon  and 
is  significant,  though  burrows  may  not  be  visible.  These  are  the  true 
acarian  vesicles,  chronologically  the  first  sign.  The  face  and  scalp  are 
never  attacked,  except  in  infants.  Scabies,  caught  from  dogs,  gives  rise  to 
a  papulo-vesicular  rash  and  no  typical  burrows.  Impetigo,  ecthyma, 
lymphangitis,  adenitis  and  albuminuria  are  complications.  Dermatitis 
may  be  due  to  treatment.  Untreated  cases  vary  in  duration  and  severity, 
according  to  the  state  of  health,  hygienic  surroundings  and  cleanliness, 
but  do  not  get  well  spontaneously. 

Treatment. — Destroy  the  parasite,  prevent  re-infection,  and  cure  the 
rash.  Boil  or  stove  all  linen,  gloves  and  bedclothes.  Give  a  hot  bath, 
using  soft  soap  and  a  nail  brush,  and  then  rub  in  sulphur  ointment,  or 
balsam  of  Peru  1  part  in  5  of  olive  oil.  The  balsam  should  be  painted  over 
Uae  skin  and  rubbed  in  gently.  Sulphur  ointment  is  too  strong  for  infants. 
It  must  not  be  rubbed  in  as  it  is  apt  to  set  up  dermatitis.  Tr.  benzoini  may 
be  rubbed  in  twice  daily  and  followed  by  a  bath  in  2  days'  time.  Liq. 
calcis  sulphurata  is  strong  enough  for  mild  cases.  Sulphur  baths  are 
rarely  needed.  Both  storax  and  balsam  of  Peru  have  been  followed  by 
albuminuria  ;  and  a  fatal  case  of  acute  nephritis  in  a  boy,  aged  15,  has 
occurred  after  the  use  of  the  balsam,  so  it  is  advisable  to  examine  the 
urine  previously.  There  is  no  risk,  if  it  is  only  applied  for  6-8  hours  and  a 
hot  bath  then  given.  Another  suitable  ointment  is  ^-naphthol,  5-10  per 
cent.  ;  it  neither  stains  nor  smells  unpleasant,  and  does  not  aggravate 
secondary  rashes.  After  2-4  days  of  the  use  of  ointments  give  a  bath  and 
apply  zinc  oil,  or  ac.  salicyl.  gr.  5,  ol.  ric.  40,  ol.  olivae  ad  100  parts,  for  the 
dermatitis. 

Pediculosis  vel  Phtheiriasis  {the  lousy  diathesis). — Pediculi  are  true 
insecta.  They  suck  blood  by  means  of  a  haustellum  or  proboscis,  an 
elongation  of  the  oesophagus,  and  do  not  bite.  The  male  is  smaller  than 
the  female.  The  nits  are  attached  by  cement  substance  to  the  hairs,  and 
have  an  operculum  or  lid,  and  cannot  be  brushed  off.  Multiplication  is  very 
rapid.  P.  Capitis  has  a  triangular  head.  P.  Vestimentorum  is  the  largest, 
and  has  a  more  oval  head  and  narrower  thorax.  P.  Pubis  is  the  broadest 
and  has  a  crab-like  body  ;  and  the  thorax  is  not  differentiated  from  the 
abdominal  segment  as  it  is  in  the  other  varieties.  It  is  rare  but  may  affect 
the  eyelashes,  and  is  then  readily  destroyed  by  ung.  hyd.  oxid.  flav. 


Parasitic  Skin    Affections.  1023 

The  body  louse  is  found  where  the  clothes  are  tight.  It  causes  reflex 
shivery  movements,  and  pigmentation  and  scarring  due  to  scratching. 
Nits  are  found  on  the  short  hairs.  Give  a  sulphur  or  carbolic  acid  bath, 
and  rub  ung.  staphysagrise  into  neck  bands,  etc.  Alkaline  baths  relieve 
irritation. 

The  head  louse  is  far  the  most  common.  It  produces  no  immediate 
effects,  but  the  scratching  and  irritation  lead  to  secondary  infection, 
suppurative  and  ulcerative  affections  of  the  scalp,  and  secondary  adenitis. 
The  vermin  must  be  destroyed  and  the  nits  removed.  Local  applications 
must  be  free  from  danger,  non-injurious  to  the  hair  or  scalp,  destructive 
of  nits,  certain  and  rapid  in  action,  and  inexpensive.  Soak  the  head  with 
•oil  of  sassafras  and  cover  it  with  a  calico  cap  for  8-12  hours.  Comb  with 
a  fine  comb  and  shampoo  well.  This  destroys  both  vermin  and  nits,  and 
a  pint  bottle,  price  3s.  6d.,  is  enough  for  30  children.  Other  suitable 
methods  are  hot  carbolic  lotion,  1  in  40,  acetic  acid,  and  vinegar,  alone 
or  with  0-5  per  cent.  hyd.  perchlor.  Petroleum,  paraffin  and  naphtha 
5  per  cent,  are  dangerous  in  the  presence  of  a  light.  Acetic  acid  dissolves 
the  cement  and  the  nits  can  then  be  combed  off.  Greasy  applications, 
•e.g.  hyd.  amm.  gr.  10,  ol.  olivae  m.  10,  lard  oz.  1,  kill  the  parasite  by  blocking 
up  the  air  passages.  An  elegant  and  quick  method  is  to  use  1-1 J  pints  of 
methylated  or  rectified  spirit,  pouring  it  from  a  jug  slowly  from  behind, 
with  the  hair  thrown  forward  and  the  head  over  a  basin.  Then  comb 
with  a  wide  toothed  comb  or  brush  well.  One  application  is  sufficient. 
The  hair  is  then  washed  with  a  little  milk  and  exposed  to  sun,  to  restore  its 
lustre.  The  spirit  causes  smarting  if  the  skin  is  inflamed  or  broken,  is 
expensive,  and  must  not  be  used  near  a  naked  light.  Equal  parts  of 
xylol  and  spirit  or  ether,  rubbed  in  with  a  mop  of  absorbent  wool,  is  rapid 
and  efficacious.     The  nits  can  be  easily  combed  off. 

Creeping  Larvae. — Syn.  :  Hyponoderma. — A  creeping  eruption  of  the 
skin  has  been  described  and  named  myiasis  linearis  or  larva  migrans,  but 
no  larva  or  parasite  has  been  discovered.  It  occurs  chiefly  in  Russia  and 
Arabia.  Lee  (1870)  reported  a  case  in  a  girl,  aged  3  years,  the  eruption 
beginning  below  the  ankle  and  travelling  up  the  thigh  and  on  to  the 
abdomen.  In  a  girl,  4  years  old  (Van  Harlingen,  1902),  the  eruption  began 
on  the  foot  as  a  line  of  small  vesicles  with  a  peculiar  beaded  look,  the 
vesicles  containing  black  granules  ;  and  in  a  boy,  5  years  old,  it  began  on 
the  sole  and  extended  on  to  the  dorsum  as  a  serpiginous  bright  red  rash, 
painful  and  itchy,  and  feeling  like  whipcord  under  the  skin.  Crocker  has 
noted  7  inches  progress  in  one  day.  Thus,  its  main  characters  are  the 
progress,  serpiginous  aspect,  and  sometimes  itching.  It  should  be  treated 
by  tar  ointment,  electrolysis,  or  incision  and  curettage  at  the  end  of  the 
track  of  the  eruption. 


INDEX. 


Abdominal  cysts,  356. 

distension,  87. 

muscular  defect,   798. 

symptoms,  249. 

tumours,  356. 
Abiotrophy,  621. 
Abscess,  v.  special  regions. 
Acephaly,  106,  627. 
Acetonaemia,   149. 
Acetonuria,  149. 
Acholia,  147. 
Acholuric  jaundice,  136. 
Achondroplasia,  192. 
Achylia  gastrica,  256. 
Acid  Intoxication,  149,  153,  166. 
Acidasmia,  149. 
Acidosis,  149. 
Aciduria,  149. 
Acne,  1011. 

scrofulosorum,  1015. 
Acquired  characters,  18. 
Acrobatic  rickets,  178,  187. 
Acrocyanosis,  459. 
Acromegaly,  202. 
Acute  rickets,  164. 
Acute  yellow  atrophy,  361. 
Addison's  disease,  212. 
Adenitis,  519. 

tuberculous,  520. 

treatment,  523. 
Adenoid  facies,  240-1,  370. 

growths,  239,  373. 

tissues  of  pharynx,  230. 
Adolescence,  3,  609. 
Adolescert  rickets,  189. 
Adrenal  glands,  210. 

haemorrhage  into,  130,  104. 

in  diphtheria,  890. 

insufficiency  of,  212. 

tumours,  211. 
Agenesis  corticalis,  672,  628,  681. 
Agonal  convulsions,   737. 

intussusception,  322. 
Air  passages,  foreign  bodies  in,  394. 
Albinism,  18,  550. 
Albuminuria,  551. 

functional,  552. 

in  diphtheria,  891. 

in  nephritis  (q.v. ) 

in  the  newborn,  552. 

nomenclature  of,  552. 

tests  for,  551. 
Albumosuria,  551. 
Alcohol,  83. 

and  heredity,  20. 
Alexia,  791. 
Alimentary  canal,  cysts  of,  357. 

tumours  of,  357. 


Alkaptonuria,  549,  550. 
Alopecia,   1010. 
Alveolar  defects,  216. 
Amastia,  597. 
Amaurosis,  975,  986. 

acute  cerebral,  655. 

fleeting,  655. 

in  pertussis,  965. 

post-eclamptic,  741. 
Amaurotic  family  idiocy,  681. 
Amblyopia,  986. 
Ambulatory  epilepsy,  744. 
Amenorrhcea,  609. 
Ammonia  excretion,  151. 
Amniotic  navel,  120. 
Amyloid  liver,  367. 
Amyoplasia  congenita,  733. 
Amyotonia  congenita,  733. 
Anaemia,  509. 

ganglionare,  515. 

infantum  pseudo-leukaemica,  512. 

lymphatica,  515. 

pernicious,  510. 

progressive,  515. 

rheumatic,  827. 

splenica,  514. 

splenica  infantum,  512. 

treatment  of,  518. 
Anaesthesia,  93. 

deaths  from,  95. 

poisoning,  155. 
Anal  fissure,  336. 

spasm,  336. 
Anaphylaxis,  904. 
Anarthna,  790. 
Anchylostoma,  315. 
Anencephaly,  627. 
Aneurysm,  456. 

miliary,  690. 
Angina  Ludovici,  887,  888. 

pneumococcal,  232. 
•  Vincent's  232. 
Angular  curvature,  713. 
Anidrosis,  724. 
Ano-rectal  prolapse,  337. 
Anorexia,  250. 
Anosteoplasia,  194. 
Antiseptics,  intestinal,  300,  920. 
Antitoxin,  in  diphtheria,  898. 

rashes,  900. 
Antrum,  empyema  of,  377. 
Anuria,  561. 
Anus,  diseases  of,  333.  336. 

development  of,  334. 

fissure  of,  336. 

malformations  of,  334. 

prolapse  of,  336. 
Aorta  and  aortic  orifice,  474. 

3  u 


1026 


Index. 


Aortic  disease,  490. 

Aortitis,  456. 

Aphasia,  790. 

Aphthse  in  newborns,  217. 

Aphthous  stomatitis,  218. 

Aplasia,  periosteal,  195. 

Apoplexy,   632. 

neonatorum,  116. 
suprarenal,  130. 
Appendicitis,  340. 
Appendix,  and  hernia,  331. 

intussusception  of,  322. 
Appetite.  250. 
Arsenic,  82,  841. 
Arterial  system,  congenital  stenosis 

of,  474. 
Arterio-sclerosis,  456. 
Arteritis,  124,  455. 
Arthritis,  813. 

deformans,  819. 
gonococcal,  814. 
pneumococcal,  813. 
rheumatoid,  819. 
septic,  815. 
syphilitic,  817. 
tuberculous,  815. 
Arthrogryposis,  749. 
Artificial  feeding,  52. 
Ascaris  lumbricoides,  313. 
Ascites,  348. 
Asphyxia,  local,  454. 

neonatorum,   115. 
Ass's  milk,  62. 
Astasia-Abasia,  779. 
Asthma,  400,  402. 
Asymmetry  of  head,  109. 
Atavism,  17. 
Ataxia,  cerebellar,  683. 
hereditary,  715. 
in  diphtheria,  894. 
Atelectasis,  117. 

acquired,  393. 
Ateleiosis,   199. 
Atheroma,  456. 
Athetosis,  673,  674. 

familial,  680. 
Athrepsia,   170. 
Athyroidism,  205. 
Atonia  congenita,  733. 
Atresia  of  anus,  334 
of  intestine,  317. 
of  oesophagus,  246. 
Atrophic  cirrhosis,  364. 
Atrophy,  infantile,  170,  171,  173. 
idiopathic  muscular,  730. 
lipomatous  muscular,  729. 
muscular,  725-733  (q.v.). 
peroneal,  727. 

progressive  neuro-muscular,  727. 
spinal  neuritic,  727. 
Auricles  of  heart,  462,  464. 
Auscultation,  6. 


Babinski's  sign,  615. 
Bacilluria,  568. 
Backwardness,  9,  780. 
Bacteriology  of  milk,  56. 


Bacteriuria,  568. 

Bad  habits  in  idiocy,  782. 

Balanitis,  593. 

Balloon  belly,  309. 

Ballooning  of  abdomen,  707,  798. 

Banti's  disease,  515. 

Barlow's  disease,  165. 

Baths,  72. 

Bazin's  disease,  1015. 

Beading  of  ribs,  181,  185,  193. 

Bednar's  aphtha?,  217. 

Bee  stings,  1020. 

Belladonna,  969. 

Bell's  palsy,  723. 

Belly  affection,  147. 

Biett's  bands,  144. 

Bile  ducts,  malformations,  135. 

obliteration  of,  135. 
Bile  pigment  in  stools,  273. 
Biliary  calculus,  134. 
cirrhosis,  362,  363. 
concretions,  134. 
Bilious  attacks,  278. 
Birth  palsy,  cerebral,  672. 
peripheral,  719. 
spinal,  722. 
Bladder,  calculus,  569. 
diverticulum,  567. 
inversion,  567. 
malformations,  567. 
nerve  supply,  563. 
tuberculosis,  568. 
tumour,  570. 
Bleeding,  77. 
Blenorrhcea,  981. 
Blepharitis,  ciliary,  976. 
Blepharospasm,  755. 
Blindness,  v.  Amaurosis. 
Blood,  503. 

characters  of,  507. 
disorders  of,  532. 
examination  of,  503. 
reaction  of,  505. 
Blood  cells,  origin  of,  506. 
Blood  pressure,  450. 
spectra,  557. 
vessels,  diseases  of,  455. 
Body  rocking,  760. 
Boiling  of  milk,  57. 
Boric  acid  in  milk,  49. 
Bottle  feeding,  52. 
Brachycephaly,  628. 
Brachydactyly,  19,  107. 
Bradycardia,  450. 
Brain,  at  birth,  612. 

concussion  of,  687. 
fever,  423. 
Branchial  fistula,  209. 

vascular  arches,  464. 
Breast,  affections  of,  39. 

care  of,  27. 
Breast  feeding,  35. 

contra-indications,  38. 
Breathing  exercises,  242. " 
Brittle  bones,  195. 
Bromides,  82. 
Bromoform  poisoning,  969. 
Bronchiectasis,  427. 
Bronchiolectasis,  428. 


Index. 


1027 


Bronchitis,  406. 

acute,  406. 

capillary,  40;). 

chronic,  409 

fibrinous,  407. 

membranous,  407. 

plastic,  407. 
Broncho-pneumonia,  409. 

tuberculous,  857. 
Brudzinski's  reflex,  616. 
Buccal  spots,  945. 
Bugs,  1020. 
Buhl's  disease,  126. 
Bulbar  crises  in  diphtheria,  895. 
Bulbar  palsy,  698. 

infantile  progressive,  681. 
Bulimia,  250. 
Bull  neck,  931. 
Buphthalmos,  982. 
Butter  milk,  63. 


Cacao  oil,  1000. 
Calamine  lotion,  1001. 
Calculus,  v.  Stone. 
Calf  knee,  187. 
Calmette's  reaction,  860. 
Calorie  values  of  foods,  35. 
Cancrum  oris,  220. 
Cane  sugar  as  a  food,  33. 
Caput  Medusae,  457. 
Caput  succedaneum,  109. 
Carbohydrate  fever,  279. 
Carbohydrate  foods,  64. 

effects  of,  32. 
Cardiac  strain,  signs  of,  494. 
Caries  of  spine,  713. 

of  teeth,  224. 
•Carpopedal  spasm,  749,  752. 
Casein  foods,  61. 
Caseinogen,  43. 
Catalepsy,  ocular,  665. 
Cataract,  982. 
Caterpillar  rash,  1004. 
Cavity  in  lungs,  signs  of,  857. 
Cephal-hsematoma,  109. 
•Cephal-hydrocele,  111,  112. 
■Cerebellar  aplasia,  628. 

ataxia,  683. 

degenerations,  671. 

diplegia,  683. 

gait,  716. 

reel,  716. 

tumours,  693. 
Cerebral  abscess,  694. 

degenerations,  671. 
infantile,  680. 

development,  612. 
arrested,  681. 

diplegia,  672. 

embolism,  689. 

infantile  palsy,  697. 

malformations,  627. 

paralysis,  in  pertussis,  965. 

sclerosis,  diffused,  680. 

spastic  paralysis,  672. 

tumours,  689. 
•Cerebrospinal  fluid,  617-619. 
■Cerebrospinal  meningitis,  647. 


Chapping  of  skin,  1004. 
Chemistry  of  lactation,  29. 
Chest,  examination  of,  5,  6,  389. 

pigeon-breasted,  389. 

rachitic,  181,  185. 

small,  389. 
Chicken  pox,  951. 
Chilblains,  453. 
Child  crowing,  751. 
Childhood,  2. 

Chin  cough,  v.  Pertussis,  961. 
Chloral,  83. 

Chloroform  poisoning,  155. 
Chloroma,  517. 
Chlorosis,  510. 

Choleraic  diarrhoea,  289,  282. 
Chondrodystrophy  foetalis,  192. 
Chorea,  831. 

cordis,  838. 

and  rheumatism,  832,  828. 

electrica,  755. 

familial,  680. 

hemichorea,  674. 

knee  jerks  in,  837. 

mollis,  837. 

paralytica,  835,  837. 

relapses  in,  840. 

rheumatica,  832,  828. 
Choroid,  affections  of,  984. 
Choroid  tubercles,  665. 
Choroiditis,  metastatic,  653. 
Choroido-retinitis,  879. 
Chvostek's  sign,  617. 
Circulation,  foetal,  465. 

functional  disorders  of,  453. 
Circumcision,  592. 
Cirrhosis  of  liver,  362-365. 
Cleft  palate,  214. 
Cleido -cranial  dysostosis,   194. 
Clitoris,  599. 
Clubbing  of  fingers,  477. 
Club-foot,  805. 
Coal  tar  products,  82. 
Co-arctation  of  aorta,  474. 
Cod-liver  oil,  81. 
Cceliac  disease,  147. 
Coincidence  of  diseases,  925. 
Colic,   275. 

reflex,  276. 
Cold  baths,  73. 

fomentations,  74. 

pack,  74. 
Colitis,  285,  286,  289-293. 

chronic,  292. 

tuberculous,  293. 

ulcerative,  292. 
Collapse,  91,  87. 

of  lung,  5. 

acquired,  393. 
Colles's  Law,  866,  867. 
Colhmaria,  373. 
Coloboma,  976. 
Colon,  dilatation  of,  307. 

inflammation  of,  285-293. 

malformations  of,  318. 

stenosis  of,  318. 

ulceration  of,  286. 
Colostrum,  26,  41. 
Colour  blindness,  18. 


1028 


Index. 


Coloured  urine,  550. 
Comedones,  1011. 
Concato's  disease,  432. 
Concussion  of  brain,  687. 
Condensed  milk,  61. 
Condylomata,  873. 
Conjunctival  reaction,  860. 
Conjunctivitis,  977-980. 

follicular,  980. 

phlyctenular,  979. 

purulent,  137. 
Consanguinity,  19. 
Constipation,  303-310. 
Contractures  of  cerebral  origin,  673. 

hysterical,  779. 

Volkmann's  722. 
Convulsions,  735. 

treatment  of,  745. 

varieties  of,  737. 
Cornea,  affections  of,  983. 

family  degeneration  of,  984. 
Corns,  1009. 
Cor  triloculare,  461. 
Coryza,  371. 

paroxysmal,  400. 

vasomotor,  400. 
Cough,  barking,  392. 

hysterical,  392. 

nocturnal,  391. 

paroxysmal,  966. 

physiological,  391. 

reflex,  391,  987. 

spasmodic  night,  391. 
Counter-irritation,  77. 
Cow,  management  of,  48. 
Cow-pox,  953. 
Cow's  milk,  46. 

and  human  milk,  49. 
Coxa  valga,  810. 

vara,  810. 
Cranial  depressions,  111. 

defects,  106. 

sutures,  abnormal,  624. 
Craniectomy,  630. 
Craniotabes,  184,  875. 
Cream,  47. 

Creams  for  the  skin,  1000. 
Crede's  method,  138. 
Creeping  larvse  in  skin,  1023. 
Creosote,  80. 
Cretinism,  204. 
Cross-legged  gait,  676. 
Croton-oil  needling,  1018. 
Croup,  varieties  of,  380,  751. 

varicellar,  953. 
Cryptorchism,  594. 
Cupping,  77. 
Curds  in  stools,  272. 
Cutaneous  therapy,  84. 
Cutis  marmorata,  950. 

Cyanosis  in  congenital  heart  disease,  476. 
Cyclical  albuminuria,  552. 
Cyclical  vomiting,  158. 
Cyclops,  628. 
Cystic  disease,  of  liver,  363. 

of  lungs,  428. 

of  kidneys,  572. 
Cystinuria,  550. 
Cystitis,  568. 


Cysts,  in  abdomen,  356. 

in  colon,  357. 
Cyto-diagnosis,  cerebrospinal,  618„ 

pleural,  434. 


Dacryo-adenitis,  981. 

-cystitis,  981. 
Dactylitis,  874. 
Day-blindness,  984. 
Day-dreaming,  773. 
Day-terror,  771. 
Dead  fingers,  454. 
Deafness,  988. 

in  syphilis,  879. 
Deaf-mutism,  792. 
Death,  sudden,  102. 

and  the  thymus,  529. 

after  antitoxin,  900. 

from  overlaying,  102. 

in  diphtheria,  891,  898. 
Definitions,  2. 
Deformities,  106. 
Degeneration,  stigmata  of,  781. 
Delayed  aneesthetic  poisoning,  55_ 

chloroform  poisoning,  55. 
Delirium,  788. 
Dementia  praecox,  788. 
Dental  caries,  224. 
Dentition,  222. 

disorders  of,  224. 

management  of,  226. 

in  rickets,  185. 
Dermatographism,  532. 
Dermatotherapy,  999. 
Deterioration,  physical,  170. 
Development,  7. 
Dextrocardia,  466. 
Diabetes,  162. 

insipdus,  562. 
Diaphragmatic  hernia,  113. 
Diaphysitis,  807. 
Diarrhoea,  chronic,  295. 

infective,  287. 

reflex,  276. 

simple,  286. 

symptomatic,  281. 

treatment  of,  296. 
Diarrhceal  affections,  281-302- 

nomenclature  of,  282. 
Diastasis  recti,  120,  187. 

in  myelocystocele,  626. 
Diazo-reaction,  549. 

in  measles,  946,  947. 

in  typhoid,  914. 
Diet  after  weaning,  66. 

artificial,   54. 

in  illness,  70. 

in  school  life,  69. 
Dilatation  of  colon,  307. 

of  heart,  481. 

of  stomach,  248. 
Diphtheria,  884. 

antitoxin  in,  898. 

ataxia  in,  894. 

aural,  889. 

avian,  885. 

bacteriology,  884. 

bulbar  crises  in,  895- 


Index. 


1029 


Diphtheria — 

complications  of,  892. 

conjunctival,  889. 

cutaneous,  889. 

diagnosis  of,  895. 

etiology  of,  887. 

faucial,  symptoms  of,  887. 

hemorrhagic,  890. 

heart  in,  890. 

hypertoxic,  890. 

infection,  mode  of,  885. 

kidneys  in,  891. 

laryngeal,  888,  896. 

latent,  890. 

nasal,  889. 

oral,  890. 

paralysis  in,  893. 

pathology  of,  886. 

pharyngeal,  888. 

prognosis  of,  897. 

quarantine  in,  904. 

relapses  in,  898. 

sensory  disturbances  in,  895. 

stomatitis  in,  890. 

toxaemia  in,  890. 

treatment  of,  898. 

vomiting  in,  897. 
Diphtheritic  paralysis,  893,  896. 

prognosis  of,  898. 

treatment  of,  904. 
Diplegia,  athtotic,  673. 

cerebellar,  683. 

cerebral,  672. 
Dirt  eating,  250. 
Disinfection,  924. 

of  excreta,  918. 
Disseminated  sclerosis,  718. 
Diverticulum  tumour,  121. 
Dobell's  solution,  373. 
Dolichocephaly,  628. 
Dolor  capitis,  761. 
Dosage,  78. 
Double  head,  624. 
Dried  milk,  61. 
Drug  treatment,  78. 
Ductus  arteriosus,  469. 
Dumb  chorea,  837. 
Duodenal  malformations,  317. 

ulcer,  260. 
Duodenitis,  359. 
Dwarfs,  198. 
Dyspepsia,  254. 

gastric,  254,  256. 

intestinal  274,  277,  256. 
Dysuria,  561. 


Earache,  991. 

Ear,  and  hearing,  987. 

congenital  abnormalities,  9S9. 

cough,  987. 

examination  of,  998. 

foreign  bodies  in,  990. 

furunculosis  of,  991. 

impacted  wax  in,  991. 

insects  in,  990. 

syphilitic  affections  of,  879. 

tuberculosis  of,  995. 


Echthyma,  1012. 
Eclampsia,  735. 

nutans,  757,  759. 

rotans,  757. 
Ectopia  cordis,  466. 

testis,  594. 

vesica;,  567. 
Ectromelus,  106. 
Eczema,  1003. 

auris,  990. 

death,  1005. 

palmare,  143. 

traumatic,  1004. 
Electrical  currents,  619. 

in  exam,  of  nervous  system,  619. 
Electrical  reactions,  620. 
Electro-therapeutics,  620. 
Elephantiasis,  congenital,  459. 
Embolism,  cerebral,  689. 
Emphysema,  398. 

subcutaneous,  399. 
Empyema,  abdominal,  350. 

pleural,  438. 

treatment  of,  443. 
Encephalitis,  697. 

focal,  700. 
Encephalocele,  624. 
Enchondroma,  807. 
Endocarditis,  484. 

infective,  485. 

pneumococcal,  486. 

rheumatic,  827. 

tuberculous,  487. 
Enema  rash,  88. 
Enemata,  87,  88. 
Energy- Quotient,  35. 
Enfance,  premiere,  2. 

seconde,  2. 
Enlarged  tonsils,  235. 
Enophthalmos,  724. 
Enteralgia,  275,  250. 
Enteric  fever,  v.  Typhoid,  911. 
Enteritis,  tuberculous,  293. 
Entero-colitis,  289. 
Entu'esis,  563. 

uretica,  563. 
Eosinophilia,  505. 
Ependymitis,  632,  633,  878. 
Epidermolysis  bullosa,  142. 
Epilepsy,  742. 

Jacksonian,  744. 
Epiphysis,  separation  of,  810. 
Epiphysitis,  807. 

syphilitic,  818. 
Epispadias,  591. 
Epistaxis,  375. 

in  diphtheria,  890,  892. 
Epithelial  pearls,  218. 
Erb's  juvenile  atrophy,  732. 

sign,  617. 

upper  arm  palsy,  719. 
Erysipelas,  127. 

of  fauces,  232. 
Erythema,  1001. 

auris,  990. 

autumnale,  1021. 

calorum,  1001. 

exudativum  multiforme,  540,   1002 

induratum,  1015. 


1030 


Index. 


Erythema — 

infectiosum,  950. 

multiforme,  1002. 
toxicum,  1001. 

neonatorum,  1001. 

nodosum,  535. 

pernio,  453. 

scrofulosorum,  1015. 

septicum,  1001. 
Erythrocytes,  504. 
Eustachian  tube,  987. 
Examination  of  children,  3. 
Excreta,  disinfection  of,  918. 
Exfoliative  dermatitis,  142. 
Exomphalos,  119. 
Exophthalmos,  724. 
Exophthalmic  goitre,  207. 
Exostosis,  807. 
Eyeball,  982. 

Eyelids,  affections  of,  976. 
Eyes,  affections  of,  975. 

examination  of,  975. 

syphilis  of,  879. 


Facial  atrophy,  732,  726. 

palsy,  723. 

spasmodic,  673. 

phenomenon,  617. 

spasm,  756. 
Facies  Hippocratica,  4. 
Facio-scapulo -humeral  atrophy,  732. 
Faecal  incontinence,  335. 
Faeces,  271. 
Fainting,  452. 
Fallopian  tubes,  604. 
False     membrane     on     tonsillotomy 

wounds,  233. 
Fat  diarrhoea,  32,  152. 

dyspepsia,  32. 

effects  of,  32,  151. 

rickets,  183. 
Fats,  for  skin,  999. 
Fatty  liver,  367. 

after  anaesthesia,  155. 
Favus,  1020. 
Feeblemindedness,  780. 
Femoral  hernia,  331. 
Fever,  88. 

reduction  of,  87,  90. 
Fifth  disease,  950. 
Fissure  of  anus,  336. 
Fistula,  hypogastric,  121. 

in  ano,  339. 

recto-vaginal,  604. 

umbilical,  120. 
Flat-foot,  806. 

Flatulence,  treatment  of,  87. 
Fleas,  1020. 
Foetal  circulation,  465. 

rickets,  190. 
Folie  de  doubte,  757. 

periodique,  788. 
Follicular  colitis,  291. 

pharyngitis,  238. 

tonsillitis,  231. 
Fontanelle,  9. 
Food  fever,  154,  270. 

poisoning,  284. 


Foramen  ovale,  patent,  463,  467. 
Foreign  bodies  in  air  passages,  394. 

in  nose,  374. 

in  oesophagus,  247. 
Formalin  in  milk,  49. 
Fourth  disease,  937. 
Fragillitas  ossium,  195. 
Friedreich's  disease,  715. 
Frost-bite,  453. 
Functional  familial  disorders,  684. 

neuroses,  non-spasmodic,  761. 

neuroses,  spasmodic,  735. 
Furunculosis,  1011. 


Gagging,  773. 
Galactogogues,  44. 
Gall  bladder,  defects  of,  134. 
Gall  stones,  134. 
Gangrene,  454-5. 

of  lung,  395. 

of  mouth,  220. 

of  tonsil,  234. 

of  vulva,  560. 
Gangrenous  dermatitis,  952,  956. 
Gastralgia,  250. 
Gastric  contents,  249,  266. 

digestion,  253. 

dyspepsia,  254,  256. 

fever,  278. 

spasm,  262. 

ulcer,  258. 
Gastritis,  256. 

membranous,  257. 
Gastro-duodenitis,  359. 
General  paralysis,  682. 
Genital  system,  591,  599. 

malformations  in  female,  599. 
in  male,  591. 
Genu  recurvatum,  187. 
Geographical  tongue,  217. 
German  measles,  941. 
Giant  swelling,  458. 
Giants,  202. 
Gigantism,  202. 
Gingivitis,  167. 
Glands,  518. 

mediastinal,  520. 

mesenteric,  522. 

thoracic,  520. 
Glandular  enlargement,  519. 

fever,  523. 
Glass  pox,  951. 
Glaucoma,  congenital,  982. 
Glioma  of  brain,  689. 

of  eye,  985. 
Glossitis  areata,  217. 
Glottic  oedema,  384. 

spasm,  751. 
Glycosuria,  162. 
Glycuronic  acid,  549. 
Goat's  milk,  62. 
Goitre,  acquired,  204. 

congenital,  203. 

exophthalmic,  207. 
Gonococcal  peritonitis,  350. 
Gonococcus,  602. 
Gonorrhoea  in  female,  600. 
Goyraud's  accident,  813. 


Index. 


1031 


Granular  kidneys,  581. 

lids,  980. 
Granuloma,   121. 
Great  toe  reflex,  615. 
Green  stools,  273. 
Grocco's  triangle,  437. 
Growing  pains,  826. 
Growth,  7,  11. 

anomalies  of,  198. 
Gum  rash,  1011. 
Gummata,  cutaneous,  873. 

in  brain,  690. 

tuberculous,  1015. 
Gynaecomastia,  598. 
Gyrospasm,  757. 


Habit  chorea,  755. 

spasm,  755. 

vomiting,  251. 
Haematemesis  neonatorum,  128. 

in  gastric  ulcer,  258. 
Haematocolpos,  603. 
Haematoma,  109. 

of  dura  mater,  670. 
Hsemato salpinx,  603,  604. 
Haematuria,  556,  560. 

idiopathic,  560. 

tests  for,  557. 
Haemoglobin,  percentage  of,  504,  508. 
Hsemoglobinuria,  558. 

paroxysmal,  558. 
Haemophilia,  543. 
Haemoptysis,  392. 
Haemorrhage  from  the  cord,  122. 
Hemorrhagic  disease,  127. 
Haemorrhoids,  339. 
Hair  balls,  257. 
Hanot's  cirrhosis,  362. 
Hare-lip,  214. 
Harrison's  sulcus,  181,  186. 
Harvest  bugs,  1021. 
Haut  mal,  743. 
Hay  fever,  400. 
Headache,  761. 

paroxysmal  recurrent,  764. 
Head  banging,  759. 

burying,  759. 

deformity  of,  8. 

measurements,  8. 

nodding,  757. 

rolling,  759. 

shaking,  757. 
Hearing,  988. 

acquirement  of,  773. 

examination  of  998. 
Heart,  abnormalities  of,  467. 

at  birth,  448. 

bilocular,  467. 

degeneration  of,  482. 

development  of,  461. 

developmental  errors  of,  467. 

dilatation  of,  481. 

examination  of,  448. 

functional  disorders  of,  451. 

functional  murmurs  of,  450. 

in  diphtheria,  890. 


Heart — 

in  rheumatism,  826,  825. 

in  syphilis,  875. 

malposition  of,  466. 

overstrain  of,  480. 

reptilian,  467. 

sounds  of,  449. 

trilocular,  467,  461. 

valvular  disease  of,  488. 
congenital,  470. 
Heart-disease,  acquired,  480. 

congenital,  461,  465-479. 
in  mongols,  785. 
pathogenesis  of,  465. 

prognosis  of,  490. 

treatment  of,  493. 
Heat,  effects  on  milk,  57,  58. 

local  applications  of,  76. 
Hebephrenia,  789. 
Height,  11. 
Hemeralopia,  984. 
Hemi-ataxia,  674,  694. 

-atrophy,  facial,  1009. 

-chorea,  674. 

-crania,  763. 

-hypertrophy,  202. 
Hemiplegia,  673. 

post-natal,  677. 
Henoch's  purpura,  541. 
Hepatic  cirrhosis,  362-4. 

congenital,  135. 
Hepatic  inadequacy,  161. 
Hepatoptosis,  359. 
Heredity,  13. 
Hermaphroditism,  591. 
Hernia,  327-331. 

and  appendix,  331. 

and  phimosis,  328. 

of  appendix,  329. 

congenital  umbilical,   119. 

diaphragmatic,  113. 

femoral,  331. 

inguinal,  327,  330. 

Littre's,  329. 

umbilical,  120. 

umbilical,  congenital,  119. 
Herpes,  1013. 

of  vulva,  599. 
Herpetic  fever,  1013. 
Hip,  affections  of,  810. 

congenital  dislocation  of,  811. 

tuberculous,  815. 
Hirschsprung's  disease,  307. 
Hodgkin's  disease,  525. 
Hoffmann's  bacillus,  884. 
Holding-breath,  753. 

spasms,  751. 
Hot-air  bath,  73. 
Hot  bath,  73. 

compress,  73. 

fomentation,  73. 
Human  milk,  40. 
Humanised  milk,  60. 
Hutchinson's  teeth,  223. 
Hutinel's  theory,  574. 
Hydatid  in  liver,  367. 
Hydatids,  312. 
Hydranencephalus,  632. 
Hydrocele,  328,  597. 


1032 


Index. 


Hydrocephalus,  630-638. 

concealed,  636. 

ex  vacuo,  631. 

in  syphilis,  878. 
Hydrocolpos,  603. 
Hydromicrocephalus,  632. 
Hydronephrosis,  572-3. 
Hydrotherapy,  70. 
Hydrothorax,  432. 
Hygroma,  208-9. 
Hyperacusis,  681. 
Hyperidrosis,  724. 
Hyperostosis  cranii,  623. 
Hyperpyrexia,  89,  827. 
Hypertonicity,  9. 
Hypertrophic  cirrhosis  of  liver,  362. 

rhinitis,  373. 

stenosis  of  pylorus,  262. 
Hypertrophy,  of  limbs,  202. 

of  pylorus,  262. 

pseudo-muscular,  720. 
Hypnotics,  83. 
Hypodermics,  84. 
Hyponoderma,  1023. 
Hypoplasia,  arterial,  474. 
Hypospadias,  591. 
Hypostatic  congestion,  393. 
Hypotonia,  9. 

congenita,  733. 
Hysteria,  777. 

at  puberty,  610. 


Ice  bag,  74. 

Ichthyosis,  143. 

Icterus  embryonum,  133. 

gravis,  360. 

neonatorum,  133. 
Idiocy,  780. 

amaurotic,  681. 

by  deprivation,  781. 

Mongolian,  783. 
Idioglossia,  793. 
Idiots  savants,  775. 
Ileo-colitis,  289. 
Imbecility,  780. 

acquired,  788. 
Immunity,  24. 
Imperforate  anus,  334. 
Imperial  drink,  79. 
Impetigo  auris,  990. 

contagiosa,  1012. 
Inanition,    173. 

fever,  89. 
Incontinence  of  faeces,  335. 

of  urine,  561,  563. 
Indicanuria,  548,  154. 
Indigestion,  intestinal,  277. 

gastric,  256. 
Infantilism,  198. 
Infection,  923. 

prevention  of,  924. 
Infective  diarrhoea,  287. 

endocarditis,  485. 

fevers,  923. 
Influenza,  906. 
Inguinal  hernia,  327. 
Injury  at  birth,  106,  108. 


Insanity,  788. 

adolescent,  788. 

moral,  786. 
\    Insect  bites,  1020. 
Insomnia,  765. 
Intertrigo,  1001. 
Intestinal  antiseptics,  300,  920. 

atresia,  317. 

digestion,  271-280. 

dyspepsia,  256,  274,  277. 

fermentation,  273. 

malformations,  317. 

obstruction,  317. 

parasites,  311. 

stenosis,  317. 
Intracranial  haemorrhage,  687. 

tumours,  689. 
Intraspinal  haemorrhage,  688. 

tumours,  719. 
Intrathoracic  tumours,  396. 
Intra-uterine  death,  100. 

factors,  21. 

putrefaction,  100. 

rickets,  190. 
Intubation,  902. 
Intussusception,  319. 
Inward  convulsions,  737,  751,  104. 
Iodine,  80. 

Iris,  affections  of,  984. 
Iritis,  syphilitic,  879. 
Iron,  81,  518. 

in  foods,  34,  33. 

lemonade,  81. 
Irrigations,  nasal,  373. 

rectal,  87. 
Ischaemic  myositis,  722. 

paralysis,  722. 
Ischio-rectal  abscess,  339. 
Isolation,  924. 
Isthmus  stenosis  of  aorta,  474. 


Jacksonian  epilepsy,  744,  699. 
Jaundice,  catarrhal,  359. 

familial,  136. 

infectious,  360. 

in  newborns,  133. 

malignant,  361. 

obstructive,  359. 

pyaemic,  136. 

syphilitic,  136. 
Jaws,  deformity  of,  214,  370. 
Joint  diseases,  813. 
Jousset's  method,  434. 
Juvenile  atrophy,  Erb's,  732. 


Kalmucks,  783. 
Katatonia,  789. 
Kephir,  62. 

Keratitis,  interstitial,  879. 
Keratomalacia,  983. 
Keratosis  palmaris,  143. 
Kernig's  sign,  616. 
Kidneys,  571. 

absence  of,  571. 

atrophy  of,  571. 

cystic,  572. 


Index. 


1033 


Kidneys — 

development  of,  573. 

disease  of,  574. 

treatment,  584. 

displaced,  572. 

granular,  581. 

large  white,  580. 

malformations  of,  571. 

movable,  572. 

supernumerary,  571. 

tuberculous,  588. 

tumours  of,  589. 
Koplik's  spots,  945. 
Koumiss,  62. 
Kreatinin,  549,  149. 


Laboratory  methods  of  feeding,  51. 
Labyrinthitis,  996. 

and  deafness,  792. 
Lachrymal  apparatus,  981. 
Lact-albumin,  43. 
Lactation,  29. 

Lactic  acid  and  rickets,  182. 
Lactobacilline  milk,  63. 
Lactosuria,  549. 

Laennec's  suffocative  catarrh,  104. 
Lalling,  793. 

La  maladie  de  Woillez,  412,  420. 
Landry's  paralysis,  685. 
Lard,  1000. 
Laryngeal  spasm,  catarrhal,  380. 

in  newborn,  387. 
Laryngeal  stridor,  385. 

congenital,  385. 
Laryngismus  stridulus,  751. 
Laryngitis,  catarrhal,  381. 

chronic,  384. 

membranous,  383. 

spasmodic,  380. 

stridulosa,  380. 

syphilitic,  384. 

tardive,  in  measles,  948. 

tuberculous,  384. 
Laryngo spasm,  751. 
Larynx,  affections  of,  379. 

examination  of,  379. 

foreign  bodies  in,  394. 

papilloma,  387. 

post-diphtheritic  stenosis,   904. 

stenosis  of,  904,  876. 

symmetrical  nodules  in,  387. 
Lassar's  paste,  1000. 

zinc  oil,  1000. 
Late  rickets,  189. 
Lateral  curvature  of  spine,  802. 
Lavage,  252. 
Length,  growth  in,  11. 
Lens,  affections  of,  982. 
Leptomeningitis,  647. 
Leucocytes,  varieties  of,  504. 
Leucocytosis,  508. 
Leucopenia,  508. 
Leukaemia,  515. 

Leyden's  hereditary  atrophy,  727. 
Lichen  pilaris,  143. 

planus,  1010. 

scrofulosorum,  1015. 


Lichen — 

spinulosus,  1010. 

urticatus,  532-3. 
Lientery,  276,  282. 
Lime  and  rickets,  182. 

salts  in  foods,  34. 
Lipomatous  muscular  atrophy,  729. 
Lip-tie,  217. 
Lisping,  793. 
Lithsamia,  148,  277. 
Lithuria,  148. 
Little's  disease,  672. 
Littre's  hernia,  329. 
Liver,  affections  of,  358,  157. 

abscess  of,  366. 

congenital  cirrhosis  of,  135. 

congestion  of,  366-7. 

inadequacy  of,  161. 

in  acidosis,  152. 

in  rickets,  188. 

syphilis  of,  877. 

tumours  of,  367. 
Lobster  claw,  107. 
Lotions  for  skin,  1001. 
Louis's  law,  854. 
Lubricants  for  skin,  1000. 
Lungs,  diseases  of,  390-431. 

abscess  of,  396. 

acute  congestion  of,  412,  420. 

and  respiration,  390. 

gangrene  of,  395. 

tumours  of,  396. 
Lumbar  puncture,  617. 
Lymph,  disorders  of,  532. 
Lymph  glands,  518. 
Lymphadenoma,  525. 
Lymphaemia,  515,  516. 
Lymphangitis  of  navel,  123. 
Lymphatic  anaemia,  515. 
Lymphatism,  528-9. 
Lymphocythaemia,  515. 
Lymphoid  structures,  503. 
Lymphosarcoma,  525. 


Macrocephalus,  628. 
Macro  cheilia,  216. 
Microglossia,  217. 
Macrogyria,  628. 
Macrostoma,  216. 
Maggots,  v.  Myiasis,  316. 
Main  en  griffe,  728. 

en  trident,  785. 
Malformations,  17. 
Malignant  purpuric  fever,  647. 
Malnutrition,  170,  173. 
Malted  foods,  65. 
Mammae,  597. 

abscess  of,  598. 

at  puberty,  599. 

in  newborns,  598. 

maternal,  care  of,  27. 
Mania,  788. 
Manustupration,  605. 
Marasmus,  170,  174. 
Marmorek's  serum,  862. 
Marrow  lymph  glands,  518. 
Marrow,  structure  of,  506. 


1034 


Index. 


in  constipation,  305. 
Mastitis,  598. 

in  mother,  39. 
Mastoid  caries,  996. 
Mastoiditis,  996. 
Masturbation,  605. 
Maternal  impressions,  22. 
Matzoon,  62. 
Measles,  943. 

blood  in,  944. 

German,  941. 

mortality  from,  949. 

prevention  of,  950. 

relapses  in,  949. 

varieties  of,  947. 
Meat  foods,  65. 
Meckel's  diverticulum,  121,  122. 

hernia  of,  329. 

obstruction  due  to,  317. 
Meconium,  271. 

bacteriology  of,  284. 
Median  nerve  reflex,  616. 
Mediastinal  glands,  520. 
Mediastino-pericarditis,  500. 
Megalerythema  epidemicum,  950. 
Meibomian  cyst,  977. 
Melsena  neonatorum,  128. 
Membranous  colitis,  291-3. 

gastritis,  257. 

laryngitis,  383. 

rhinitis,  375. 

tonsillitis,  232,  887 
Mendelian  theory,  15. 
Mendel's  reflex,  615. 
Meningismus,  633. 

in  typhoid,  916. 
Meningitis,  643-670. 

acute,  644. 

basilar,  653. 

caseating,  663. 

cerebrospinal,  647. 

chronic  basilar,  653. 

in  mumps,  973. 

in  pertussis,  965. 

in  typhoid,  916. 

post-basal,  653. 

purulent,  644. 

septic,  644. 

serous,  632. 

suppurative,  644. 

syphilitic,  669,  878. 

tuberculous,  660. 

typhoidal,  916. 
Meningitis,  age-incidence,  643. 

classification,  644. 

diagnosis  of,  657. 

exudate  in,  645. 

prognosis  of,  657. 

treatment  of,  658. 
Meningocele,  624. 

spinal,  626. 
Meningo-encephalocele,  624. 

-myelocele,  625. 
Menstrual  psychoses,  789. 
Menstruation,  and  nursing,  44. 

delayed,  609. 

disorders  of,  608-9. 

fcetal,  608. 

precocious,  609. 


Mental  deficiency,  780. 

disorders,  symptoms  of,  789. 
Mercury,  81. 
Merycism,  251. 
Mesenteric  cysts,  356. 

glands,  522. 
Mesocardia,  466. 
Metabolic  disorders,  147. 
Meunier's  sign,  944. 
Microcephalus,  628. 

Microdactyly,  in  myositis  ossificans,  800„ 
Micrognathia,  216. 
Microgyria,  628. 
Microphthalmos,  982. 
Microstoma,  216. 
Micturition,  561. 
Migraine,  763. 

ophthalmic,  764. 
Migrainous  gastric  neurosis,  158. 
Milaria  rubra,  1011. 
Miliary  tuberculosis,  855. 
Milk,  bacteriology  of,  56. 

condensed,  61. 

dried,  61. 

effect  of  attenuants  on,  58. 
of  heat  on,  57,  58. 

examination  of,  41. 

of  cow,  46. 

of  ass,  62. 

of  goat,  62. 

of  woman,  40. 

mixtures  of,  50  54. 

peptonised,  60. 

unsalted,  1006. 
Mitral  regurgitation,  488,  470. 

stenosis,  489,  470. 
Mollities  ossium,  195. 
Molluscum  contagiosum,  1010. 
Mongolian  idiocy,  783. 
Monoplegia,  673. 
Moral  insanity,  786. 
Morbilli,  943. 
Morbus  cseruleus,  476. 

maculosus,  537. 
Morphcea,  1009. 
Mortality,  100. 
Morton's  fluid,  626. 
Morvan's  disease,  641. 
Mother,  in  pregnancy,  26. 
Motor  functions,  615. 

examination  of,  615. 
Mouth,  care  of,  213. 
Mucous  disease,  277. 
Mumps,  v.  Parotitis  specifics,  97 1, 
Muscles,  absence  of,  798. 

deficiency  of,  798. 

inflammation  of,  799. 
Muscular  atrophy,  725-733. 

congenital,  733. 

facial,  732. 

facio-scapulo-humeral,    732. 

idiopathic,  730. 

juvenile  type  of  Erb,  732. 

Leyden's  hereditary,  727. 

lipomatous,  729. 

peroneal,  727. 

progressive,  of  infants,  732. 

pseudo-muscular,  729. 

Werdnig-Hoffmann's  type,  727. 


Index. 


1035- 


Musculo -spiral  palsy,  722. 
Mussel  poisoning,  533. 
Mustard  pack,  baths,  etc.,  75. 
Myatonia  congenita,  733. 
Myelsemia,  515-6. 
Myelitis,  713. 

from  pressure,  713. 
Myelocele,  625. 
Myelocystocele,  625. 
Myelocystomeningocele,  626. 
Myelocytes,  505. 
Myelocythsemia,  515. 
Myelomeningocele,  625. 
Myiasis,  316. 

aural,  990. 

cutaneous,  1023. 

intestinal,  316. 

nasal,  374. 
Myocarditis,  482. 

rheumatic,  827. 
Myocardium,  480. 

in  diphtheria,  487. 

in  tuberculosis,  487. 
Myoclonus,  754. 
Myogenic  theory,  463. 
Myokymia,  754. 
Myomalacia  cordis,  482. 
Myopathy,  v.  Muscular  atrophy,  725. 
Myositis,  799. 

ischsemic,  722. 

ossificans,   799. 
Myotonia  congenita,  685. 
Myotonia  of  newborns,  616. 
Myxcedema,  205. 

congenital,  204. 


Nails,  in  scarlatina,  936. 

in  syphilis,  873. 

psoriasis  of,  1008. 

ringworm  of,  1018. 
Nasal  catarrh,  371. 

discharges,  371. 

lotions,  373. 

obstruction,  369. 

polypus,  374. 

stenosis,  369. 

syringing,  373. 
Naso-pharynx,  examination  of,  241. 
Navel,  care  of,  119. 

amniotic,  120. 

skin,  120. 
Nephritis,  574. 

acute,  576. 

chronic  interstitial,  581. 

chronic  parenchymatous,  580. 

diphtheritic,  579. 

eye  symptoms  in,  582. 

gastro-intestinal,  575. 

influenzal,  579. 

in  infancy,  575. 

in  newborns,  575. 

primary,  579. 

scarlatinal,  576. 

septic,  579. 

syphilitic,  877. 

treatment  of,  584. 


uraemia  in,  582. 


Nervous  diseases,  classification,  621. 
Nervous  system,  at  birth,  612. 

examination  of,  613. 

malformations  of,  623. 
Neurasthenia,  775,  277. 
Neuroses,  spasmodic  functional,  735. 

non-spasmodic,  761. 
Neurotic  children,  772. 
Newborn,  the,  2. 
Night  blindness,  984. 

-mare,  767. 

sweats,  767. 

terror,  768. 
Nipples,  affections  of,  39. 

care  of,  27. 
N-excretion,  151. 
Nitrogenous  foods,  65. 
Nocturnal  epilepsy,  743. 
Nodal  fever,  535. 

rhythm,  463. 
Nodding  spasm,  757. 
Noma,  220. 

vulvae,  566. 
Nose,  369. 

congenital  anomalies,  369. 

foreign  bodies  in,  374. 

maggots  in,  374. 

obstruction  of,  369. 

syphilis  of,  871,  875. 

tuberculosis  of,  375. 
Nuclear  atrophy,  628. 
Nursing,  70. 
Nutmeg  liver,  366. 
Nyctalopia,  984. 
Nystagmus,  760. 

in  head  nodding,  758. 


Obesity,  200. 

local,  of  Landouzy,  708. 
Obstetrical  paralysis,  719. 
Ocular  catalepsy,  665,  667. 

palsy,  982. 
Oculo-motor  palsy,  724,  982. 

periodic,  764. 
Odontalgia,  227. 
Oedema,  457. 

acute  general,  575. 

angioneurotic,  458. 

essential,  574. 

glottidis,  384. 

hereditary,  459. 

idiopathic,  574. 

infantile,  574. 

neonatorum,  146. 

renal,  584. 

treatment  of,  584. 
Oesophagus,  245. 

foreign  bodies  in,  247. 
Oils,  for  skin,  999. 
Ointments,  1000. 
Oligocardia,  450. 
Oliguria,  561. 
Omental  tumours,  357. 
Omphalitis,  123. 
Onanism,  605. 
Onychia,  syphilitic,  873. 
Onychomycosis,   1018. 


1036 


Index. 


Ophthalmia  neonatorum,  1 37. 

phlyctenular,  979. 

v.  conjunctivitis,  977. 
Ophthalmic  reaction,  860. 
Ophthalmic  migraine,  764. 
Ophthalmoplegia,  698. 

Braziliana,  983. 

congenital,  982. 

familial,  680. 

periodic,  764. 

progressive,  680. 
Opisthotonos,  cervical,  of  infants,  653. 
Opium,  83. 

Oppenheimer's  sign,  616. 
Opsonins,  91. 
Optic  nerve,  986. 

neuritis,  in  cerebral  tumour,  691. 
in  oxycephalus,  623. 
in  meningitis,  646,  652,  656. 
in  tuberculous  meningitis,  665. 
Orbital  periostitis,  377. 
Orchitis,  596. 

in  mumps,  973.  • 

Os  revelateur,  874. 
Osteitis,  807. 

of  upper  jaw,  377. 
Osteo-arthritis,  819. 

-arthropathy,  821. 

-dystrophy  foetalis,  194. 

-genesis  imperfecta,  195. 

-malacia,  195. 

-myelitis,  807. 
of  spine,  809. 
of  upper  jaw,  377. 

-psathyrosis,   195. 
Otitis  media,  991,  879. 

treatment  of,  996. 

varieties  of,  994. 
Otorrhoea,  995,  997. 
Ovarian  pedicle,  torsion  of,  605. 
Ovaries,  604. 

inflammation  of,  in  mumps,  973. 
Overgrowth  at  puberty,  609. 
Overlaying,  102. 
Overstrain  of  heart,  480. 
Oxaluria,  559. 
Oxycephalus,   623. 
Oxyuris  vermicularis,  314. 


Pachymeningitis,  670. 

syphilitic,  878. 
Packs,  74. 

Painful  pronation  of  childhood,  812. 
Palate,  in  idiots,  781. 
Palpation,  5. 
Pancreatic  cysts,  356. 
Pancreatitis,  273,  973. 
Panophthalmitis,  in  meningitis,  653. 
Paracentesis  of  chest,  443. 

of  ear,  997. 

of  pericardium,  499. 
Paralysis,  acute  atrophic,  701. 

agitans,  718. 

Bell's,  723. 

birth,  672,  719. 

cerebral,  672,  697. 

classification  of,  673. 

crural,  722. 


Paralysis — 

diphtheritic,  893. 

Erb's,  719. 

essential,  of  children,  701. 

facial,  723,  673. 

facio-scapulo -humeral,   732. 

general,  682. 

hereditary  spastic  spinal,  718. 

hysterical,  779. 

infantile  atrophic,  701. 
cerebral,  697. 

in  pertussis,  965. 

intermittent  spinal,  684. 

in  the  morning,  705. 

in  the  newborn,  719. 

ischsemic,  722. 

Landry's  685. 

obstetrical,  719. 

oculo-motor,  724. 

periodic,  684. 

peroneal,  722. 

pressure,  722. 

pseudo-hypertrophic,  729. 

radial,  722. 

spasmodic  spinal,  672. 

spastic  spinal,  718. 

spinal  infantile,  701. 

teething,  702. 

upper  arm,  719. 
Paralytic  chorea,  837. 
Paralytic  idiocy  in  hydrocephalus,  637. 
Paramyoclonus  multiplex,  754. 
Paranoia,  789. 
Paraphimosis,  593. 
Paraplegia,  infantile  spasmodic,   672. 

spastic,  713. 
Parasites,  cutaneous,  1015-1025. 

intestinal,  311,  316. 
Parasyphilis,  869. 
Parathyroids,  208. 
Paratyphoid  fever,  920. 
Paravertebral  triangle,  437. 
Paronychia,  syphilitic,  873. 
Parotid  swelling,  228. 
Parotitis,  secondary,  228. 

specific,  971. 
Paroxysmal  screaming,  771. 

sneezing,  400. 
Parrot's  nodes,  874. 
Pasteurisation  of  milk,  57. 

test  for,  58. 
Patent  ductus  arteriosus,  469. 

foramen  ovale,  467. 

septum  ventriculorum,  467. 
Pavor  diurnus,  771. 

nocturnus,  768. 
Pediculosis,  1022. 
Poliosis  rheumatica,  538. 
Pemphigus,  1012. 

congenital,  142. 

neonatorum,   142. 

syphilitic,  872. 
Penis,  affections  of,  591-4. 
Pentosuria,  549. 
Peptonised  milk,  60. 
Peptonuria,  551. 
Percussion,  5. 
Pericarditis,  494. 

latent,  495. 


Index. 


1037 


Pericarditis — 

obliterative,  500. 
pneumococcal,  495. 
purulent,  495,  497. 
rheumatic,  827. 
Pericardium,  adherent,  501. 

tuberculosis  of,  487. 
Periodic  paralysis,  684,  764. 
Periosteal  aplasia,  195. 

cachexia,  164. 
Periostitis,  acute,  807. 
hsemorrhagic,  164. 
syphilitic,  874. 
Peritoneum,  affections  of,  348. 
Peritonitis,  acute,  348. 
chronic,  352. 
fulminating,  344. 
gonococcal,  350. 
perforative,  344. 
pneumococcal,  350. 
tuberculous,  352. 
Peritonsillar  abscess,  233. 
Perleche,  218. 
Pernicious  anaemia,  510. 
Peroneal  atrophy,  727. 
Pertussis,  961. 

morbid  anatomy,  967. 
Petit  mal,  744. 
Pharmacotherapy,  78. 
Pharyngeal  abscess,  238,  243. 

affections,  238. 
Phenomenon  of  the  fist,  616. 
Phimosis,  592. 

and  hernia,  328. 
Phlebitis,  of  the  cord,  124. 
in  systemic  veins,  457. 
Phlyctenule,  979. 
Phobias,  777. 
Phosphaturia,  549. 

in  Henoch's  purpura,  540. 
Phosphorus  in  foods,  34. 
Photophobia,  975. 
Phrenics,  phenomenon  of,  617. 
Phtheiriasis,  1022. 
Phthisis,  acute,  857. 
chronic,  858. 
galloping,  857. 
Physical  deterioration,  170. 
Physico-therapy,  76. 
Physiology  of  lactation,  29. 
Pica,  250. 

Pigeon-breast,  186,  389. 
Pigmentation,  congenital,  146. 
in  Addison's  disease,  212. 
in  albuminuria,  555. 
Piles,  339. 

Pirquet's  reaction,  860. 
Pituitary  function,  202,  210. 
Pityriasis  capitis,  1002. 
Plantar  reflex,  615. 
Pleura,  432. 
Pleural  effusion,  436. 
Pleurisy,  432. 
Pleuro-pneumonia,  424. 
Pneumococcal  angina,  232. 
fever,  419,  424. 
infection  of  lungs,  419. 
peritonitis,  350. 
pharyngitis,  238. 


Pneumonia,  419. 

abortive,  424. 

ante-natal,  419. 

catarrhal,  409. 

cerebral,  423. 

chronic,  427. 

croupous,  419. 

disseminated  patchy,  409. 

eclamptic,  423. 

fibrinous,  419. 

gastro -intestinal,  424. 

in  the  newborn,  419. 

lobular,  409. 

nephritic,  424. 

pleuro-,  424. 

tuberculous,  858. 

white,  876. 
Pneumothorax,  447. 
Polioencephalitis,  697. 
Poliomyelitis,  697,  701. 

anterior,  701. 
Pclitzerisation,  989. 
Polyadenitis,  febrile,  523. 

tuberculous,  520. 
Polycythemia,  476. 
Polydactyly,  107. 
Polymastia,  597. 
Polymyositis,  799. 
Polyneuritis,  724,  896. 
Polyorrhomenitis,  432. 
Polypus,  nasal,  374. 

rectal,  337. 

umbilical,  121. 
Polyserositis,  432,  500. 
Polythelia,  598. 
Polyuria,  561. 
Porencephalus,  632,  638. 
Post-adenoid  abscess,  238,  243. 
Post-basic  meningitis,  653. 
Post-nasal  catarrh,  238,  371. 
Pot-belly,  181,  187. 
Pott's  disease,  713. 
Poultices,  76. 
Powders  for  skin,  999. 
Precocious  menstruation,  609. 

puberty,  200,  211. 
Precocity,  200. 

intellectual,  774. 

mental,  774. 
Preconceptional  factors,  19. 
Pregnancy,  during  lactation,  38. 
Premature  infants,  96. 
Prepuce,  591. 
Preservatives  in  milk,  49. 
Pressure  paralysis,  722. 

paraplegia,  713. 
Priapism,  592. 
Proctitis,  338. 
Procursive  epilepsy,  744. 
Profeta's  law,  866. 
Progeria,  201. 
Prolapsus  ani,  337. 

recti,  337. 
Proprietary  foods,  63. 
Prostate,  tumours  of,  595. 
Proteins,  effects  of,  31. 

in  milk,  50. 
Protozoa,  316. 
Prurigo,  532,  534. 


1038 


Index. 


Prurigo,  varicelliforme,  953. 
Pseudo-glioma,  653,  656. 

-hypertrophic  paralysis,  729. 

-muscular  hypertrophy,  729. 

-renal  dropsy,  575. 

-tetanus,  750. 
Psoriasis,  1007. 
Psychasthenia,  776. 
Psychoses,  menstrual,  789. 
Ptosis,  congenital,  982. 
Puberty,  609. 

disorders  of,  610. 

precocious,  200,  211. 
Pug  nose,  871. 
Pulled  elbow,  813. 
Pulmonary  artery,  471. 

osteo-arthropathy,  821. 

regurgitation,  473. 

stenosis,  471. 
Pulse,  2,  449. 

variations  in,  450. 
Pulsus  paradoxus,  497,  501. 
Purin  bodies  in  urine,  547. 
Purpura,  537. 

abdominalis,  540. 

fulminans,  539. 

hsemorrhagico ,  538. 

Henoch's  540. 

rheumatica,  538. 

simplex,  538. 

symptomatic,  538. 
Pyaemia  neonatorum,  122,  125. 
Pysemic  jaundice,  136. 
Pyelitis,  585. 
Pyelo-nephritis,  585. 
Pylorus,  261-270. 

spasm  of,  261. 

stenosis  of,  262. 

hypertrophic  stenosis  of,  262. 
Pyrocatechin,  549. 


Quinine,  80. 
Quinsy,  233. 


Rachitis,  v.  Rickets,  178. 
Radial  palsy,  722. 
Rage,  attacks  of,  776. 
Ranula,  228. 
Raynaud's  disease,  454. 
Reaction  of  degeneration,  620. 
Recrudescent  rickets,  189. 
Rectal  feeding,  86. 

spasm,  336. 

therapy,  85. 
Rectum,  diseases  of,  333. 

malformations  of,  333. 

polypus  of,  337. 

prolapse  of,  337. 

spasm  of,  336. 
Recurrent  vomiting,  158. 
Red  gum,  1011. 
Reflex  action,  615. 

tests  for,  616. 
Reflex  colic,  276. 

cough,  391,  987. 

diarrhoea,  276. 

vomiting,  252. 


Refractive  errors,  986. 
Regurgitation,  250. 
Renal  calculus,  587. 

epistaxis,  560. 

tuberculosis,  588. 

tumours,  589. 
Respiration,  5,  390. 
Respiratory  system,  389. 
Retention  of  urine,  561. 
Retina,  cyanosis  of,  477. 
Retinitis  pigmentosa,  985. 
Retino-choroiditis,  985. 
Retro-oesophageal  abscess,  245. 

-pharyngeal  abscess,  243. 
Reversion,  17. 
Rhagades,  870. 
Rheumatic  chorea,  831. 

fever,  823. 

gout,  819. 

nodules,  825,  828. 
Rheumatism  and  chorea,  832,  828. 
Rheumatoid  arthritis,  819. 
Rhinitis,  371-5. 

diphtheritic,  889. 

vasomotor,  400. 
Rickets,  178. 

acrobatic,  187. 

acute,  164. 

adolescent,  189. 

haemorrhagic,  164. 

intra-uterine,  190. 

late,  189. 

recrudescent,  189. 

scurvy,  164. 

teething  in,  185. 
Rigor  mortis  in  the  still-born,  100. 
Ringworm,  v.  Tinea,  1015. 
Roseola,  epidemic,  941. 
Rose  rash,  941. 
Rotheln,  941. 
Roundworms,  313. 
Rubella,  941. 
Rubeola,  943. 
Rumination,  251. 


Sacral  tumours,  626. 
Sacro-coccygeal   cysts,   dimples,   and 

sinuses,  627. 
Saddle  nose,  871. 
St.  Vitus's  Dance,  831. 
Salaam  fits,  759. 
Salicyl  compounds,  80. 
Salicylates,  poisoning  by,  842. 
Salicylic  acid  in  milk,  49. 
Salivary  glands,  228. 
Salivation,  229. 

in  pertussis,  963. 
Salts  in  milk,  33. 
Salve  muslins,  1001. 

stick,  1001. 
Scabies,  1021. 
Scapula,  elevation  of,  805. 
Scarlatina  anginosa,  931. 

hsemorrhagica,  932. 

inoculation,  932. 

maligna,  932. 

septica,  931. 

simplex,  930. 


Index. 


1039 


Scarlatina — 

surgical,  932. 

toxic,  932. 
Scarlatina,  925. 

bacteriology  of,  926. 

blood  in,  933. 

desquamation,  930. 

infectivity  of,  927. 

incubation  of,  928. 

infection,  mode  of,  926. 
duration  of,  928. 

nephritis  in,  576. 

quarantine  in,  928. 

rash,  919. 

relapses,  938. 

rheumatism,  935. 

second  attacks,  938. 

tongue,  933. 

varieties,  930. 
Schafer's  reflex,  616. 
Schonlein's  disease,  538. 
School  life,  766. 
Scissor-legs,  811. 
Sclerema,  1009. 

adiposum,  146. 

neonatorum,  145. 
Scleroderma,   1009. 
Scleroedema,  145. 
Sclerosis,  cerebral,  671. 
diffused,  680. 

disseminated,  718. 

multiple,  718. 

myopathic,  718. 
Scoliosis,  802. 

Screaming,  paroxysmal,  771. 
Scurvy,  164. 
Sea  bathing,  76. 
Seborrhcea,  1002. 
Senility,  201. 

Sensory  disturbances,  614. 
Sepsis  neonatorum,  122. 
Septum  of  bulb,  defects  of,  468. 
Septum  ventriculorum,  patent,  461,  467. 
Serositis,  multiple,  432. 
Serous  apoplexy,  632. 

meningitis,  632. 
Serum  disease,  900. 
Shingles,  1013. 
Sialo-adenitis,  228. 
Silver  nitrate  injections,  88. 
Sinusitis,  antral,  377. 

frontal,  377. 
Situs  inversus,  466. 
Skin  diseases,  999. 

parasitic,  1015. 

therapeutics,  999. 
Skin,  navel,  120. 
Sleep,  764. 

at  school,  766. 
Sleepiness,  765. 
Small  pox,  958. 
Sneezing,  400. 
Snuffles,  374. 

in  syphilis,  871. 
Soaps,  72. 

Sodium  citrate  in  milk,  59. 
Somnambulism,  767. 
Somniloquence,  768. 
Spasm,  habit,  755. 


Spasm — 

mimic,  755. 

nodding,  757. 
Spasmodic,  functional  neuroses,   735. 

paraplegia,  672. 

spinal  paralysis,  672. 

tabes  dorsalis,  672. 
Spasmophilia,  735. 
Spasmus  nutans,  757. 
Spastic  paraplegia,  672. 

rigidity  of  limbs,  672. 

spinal  paralysis,  718. 
Special  features  of  disease,  6. 
Specific  fevers,  923. 
Speech,  acquirement  of,   789. 

defects  of,  789. 

in  chorea,  837. 
Spermatic  cord,  torsion  of,  595. 
Spina  bifida,  625. 
Spinal  cord,  at  birth,  612. 

affections  of  713. 

tumours  of,  719. 
Spinal  paralysis,  infantile,  701. 

intermittent,  684. 
Spine,  angular  curvature,  713. 

lateral  curvature,  802. 

osteomyelitis  of,  809. 

rachitic  curvature,  186. 
Spirochseta  pallida,  864. 
Spleen,  511. 

in  rickets,  188. 

in  syphilis,  875. 
Splenic  anaemia,  512,  514. 

pseudo-leukaemica,  512. 
Spleno-lymph  glands,  518. 
Spleno -medullary  leukaemia,  515. 
Splenomegaly,  familial,  514. 
Split-hand  and  foot,  107. 
Sports,  19. 
Spotted  fever,  647. 
Sprengel's  deformity,  805. 
Sputum,  393. 

collection  of,  860. 
Squint,  982. 
Stammering,  793. 
Starch  digestion,  63. 
Status  eclampticus,  740. 

epilepticus,  747. 

lymphaticus,  528. 

thymicus,  528. 
Stereotypia  in  idiocy,  782. 
Sterilisation  of  milk,  57. 
Sterno -mastoid  tumour,  112. 
Stiff-neck  fever,  647. 
Stigmata,  of  degeneration,  781. 

of  hysteria,  778. 
Stimulants,  83. 
Stomach,  248-260. 

diphtheria  of,  890. 

size  of,  52. 
Stomatitis,  varieties  of,  217-219. 

erythemato-pultaceous,  945. 
Stone  in  bladder,  569. 

kidney,  587. 

single  kidney,  571. 

ureter,  570. 

urethra,  561. 
Stools,  271. 

abnormalities  of,  272. 


1040 


Index. 


Stools — 

disinfection  of,  918. 

examination  of,  274. 
in  diarrhoea,  287. 
Strise  patellares,  936. 
Stridor,  congenital  laryngeal,  385. 
Strophulus,  532,  1011. 
Stuttering,  793. 
Stye,  977. 

Sub-diaphragmatic  abscess,  352. 
Sub-lingual  fibroma,  217. 

ulcer,  217. 

in  pertussis,  964. 
Sub-navel  abscess,  124. 
Sub-periosteal  abscess,  807. 
Sub-phrenic  abscess,  352. 
Subsidiary  methods  of  feeding,  59. 
Sucking  pads,  214. 
Suckling,  mode  of,  36. 
Sudamina,  1010. 
Sudden  death,  102. 
Sugar  in  urine,  549. 
Suicide,  788. 
Supernumerary  auricles,  989. 

mammae,  597. 

nipples,  598. 
Suprarenal  apoplexy,  130. 

glands,  210. 

haemorrhage,  130,  104. 
Sutures,  abnormal,  624. 
Sweating,  724. 
Swooning,  452. 
Sympathetic  nerves,  724. 
Syncope,  452,  103. 

local,  454. 
Syndactyly,  107. 
Synovitis,  813. 
Syphilis,  acquired,  864. 

at  birth,  870. 

coincident,  864. 

conceptional,  865. 

congenital,  865. 

contagiousress  of,  867. 

course,  880. 

diagnosis,  880. 

foetal,  869. 

in  nurse,  867. 

in  third  generation,  868. 

late  congenital,  880. 

pathology,  869. 

prognosis,  880. 

symptoms,  869. 

transmission  from  father,  23,  865. 
from  mother,  866. 

treatment,  881. 
Syphilitic  anaemia,  875. 

arthritis,  817. 

cirrhosis,  365. 

dactylitis,  874. 

epiphysitis,   818. 

jaundice,  136. 

keratitis,  879. 

meningitis,  878. 

myocarditis,  875. 

nephritis,  877. 

onychia,  873. 

orchitis,  596. 

periostitis,  874. 

rashes,  871. 


Syphilitic — 

spleen,  875. 

teeth,  876. 

wig,  873. 
Syringomyelia,  640. 
Syringo-myelocele,  625. 


Tabes  dorsalis,  718. 

spasmodic,  672. 

hereditary,  715. 

mesenterica,  512. 
Tachycardia,  451. 
Taeniae,  311. 
Talipes,  805. 
Talking  in  sleep,  768. 
Tapeworms,  311. 
Tarsal  cysts,  977. 
Taste,  tests  for,  783. 
Tears,  981. 

bloody,  981. 
Teeth,  222. 

and  nutrition,  226. 

care  of,  227. 

caries  of,  224. 

-grinding,  768. 

in  syphilis,  876. 

in  rickets,  185. 

milk,  223. 

permanent,  225. 
Teething,  v.  Dentition,  222. 

paralysis,  702. 
Temper,  attacks  of,  776. 
Temperature,  7. 
Testes,  diseases  of,  594-596. 

undescended,  594. 
Tetanilla,  747. 
Tetanus,  130. 
Tetany,  747. 
Therapeutics,  70. 
Thigh  friction,  605. 
Thin  rickets,  183. 
Third  nerve,  recurrent  palsy,  764. 
Thirst  fever,  89. 
Thomson's  disease,  685. 
Thoracic  glands,  520. 
Thorax,  389. 
Thread  ulcer,  902. 
Threadworms,  314. 
Throat,  examination  of,  6. 
Thrombosis,  cerebral,  688. 

in  diphtheria,  891. 

venous,  457. 
Thrush,  218. 
Thymic  asthma,  529. 
Thymus  gland,  526. 
Thyroid  gland,  203. 

inflammation  of,  204. 

insufficiency  of ,  199,  202. 
Thyro-glossal  cyst,  208. 

fistula,  208. 
Tic,  co-ordinated,  755. 

convulsive,  756. 

psychical,  756. 

simple,  755. 
Timiditv,  773. 
Tinea,  1015. 

circinata,  1017. 

of  nails,  1018. 


Index. 


1041 


Tinea — 

tarsi,  976. 

tonsurans,  1016. 
Tongue,  216. 

geographical,  217. 

raspberry,  217. 

strawberry,  933. 
Tongue-tie,  217. 
Tonsil,  affections  of,  230. 

of  Gerlach,  230. 

of  Luschka,  230. 
Tonsillar  cyst,  232. 
Tonsillotomy,  236,  233. 
Tonsils,  enlarged,  235. 

enucleation  of,  236. 

inflammation  of,  230-236. 

tuberculosis  of,  237. 
Toothache,  227. 
Tornwaldt's  bursa,  239. 
Torticollis,  801. 
Tower  skull,  623. 
Trachea,  393. 
Tracheo -bronchitis,  406. 
Tracheotomy,  903. 
Trachoma,  980. 
Transfusion,  85. 
Transmission  of  disease,  22. 

of  peculiarities,  17. 
Traumaticin,  1001. 
Tremors,  674. 
Trephining,  value  of,  630. 
Treponema  pallidum,  864. 
Trichinosis,  316,  799. 
Trichocephalus  dispar,  315. 
Trichotillomania,  258. 
Tricuspid  regurgitation,  490. 

stenosis,  489,  471. 
Trilocular  heart,  467. 
Trismus,  130. 
Trophic  disturbances,  617. 
Trophcedema,  459. 
Trousseau's  phenomenon,  616. 
Tuberculin  tests,  861. 

treatment  by,  92,  861. 
Tuberculosis,  844. 

age-incidence,  852. 

bacillus  of,  845. 

blood  in,  855. 

differences  in  adults,  854. 

feeding  experiments,  848. 

infection,  cause  of  general,  852. 
mode  of,  846. 
by  air,  850. 

by  alimentary  tract,  849,  851. 
by  milk,  847. 
by  tonsils,  850. 

local  lesion  in,  849. 

mortality  from,  852. 

post  mortem  evidence,  851. 

sociological  factors,  847. 

symptoms,  854,  855,  857,  859. 

tests  for,  860. 

treatment  of,  861. 

varieties  of,  853,  856. 
Tuberculosis,  844. 

ante-natal,  22. 

congenital,  844. 

foetal,  844. 

of  bladder,  568. 


Tuberculosis — 

of  brain,  660. 

of  breasts  in  mother,  39. 

of  colon,  293. 

of  ear,  995. 

of  eyelids,  980. 

of  glands,  519. 

of  heart,  487. 

of  intestine,  293. 
primary,  851. 

of  joints,  815. 

of  kidney,  588. 

of  liver,  365. 

of  lungs,  857,  858. 

of  nose,  375. 

of  penis,  594. 

of  peritoneum,  351-352. 

of  skin,  1014. 

of  testis,  596. 

of  tonsils,  237. 

general,  855. 

miliary,  855. 

pneumonic,  857,  858. 
Tumours,  cerebellar,  693. 

cerebral,  689. 

of  the  cord,  719. 

of  alimentary  tract,  357. 

of  bladder,  570. 

of  lungs,  396. 

of  kidneys,  589. 

intracranial,  689. 
Tylosis,  976. 
Tympanites,  274. 
Typhoid  fever,  911. 

blood  in,  914. 

haemorrhage  in,  915. 

perforation  in ,  915. 

relapses  in,  917. 

renal,  914. 

treatment  of,  918. 

Widal's  test  in,  914. 


Ulcera  pterygoidea,  217. 
Ulcerative  colitis,  292,  286. 

stomatitis,  219. 

tonsillitis,  231. 
Umbilical  cord,  8,  119. 

abnormalities  of,  119. 

at  birth,  119. 

infections  of,  123. 
Umbilical  eczema,  122. 

fistula,  120. 

gangrene,  124. 

haemorrhage,  122. 

hernia,  120. 

polypus,  121. 

ulcer,  124. 
Upper  arm  palsy,  719. 
Urachal  cyst,  356. 
Uraemia,  582. 

treatment  of,  585. 
Urea,  547. 
Ureter,  abnormal  opening  of,  563. 

dilatation  of,  572. 

malformations  of,  572. 
Urethra,  defects  of,  592. 

in  female,  599. 
Urethritis,  594,  599. 


3  x 


1042 


Index. 


Uric  acid,  548. 

Uricaeidaamia,  v.  Lithsemia,  148. 

Urine,  546. 

abnormal  constituents  of,  549. 

collection  of,  546. 

coloured,  550. 

disinfection  of,  918. 

incontinence  of,  561,  563. 

in  diphtheria,  891. 

in  nephritis,  574. 

normal  constituents  of,  547. 

quantity  of,  546. 

variations  in,  561. 

retention  of,  561. 
Urobilin,  547. 

Urobilinogen,  547,  148,  273. 
Urticaria,  532. 

giant,  458. 

pigmentosa,  535. 

renal,  575. 

tuberosa,  458. 
Uterus,  604. 

in  the  male,  591. 
Uvula,  222. 


Vaccination,  953. 
Vaccines,  91. 
Vaccinia,  953. 

generalised,  957. 

latent,  956. 

pemphigoides,  956. 

secondary,  957. 
Vagina,  599. 

tumours  of,  603. 
Valsalva's  method  of  inflation,  989. 
Valvular  heart  disease,  488. 

congenital,  470. 
Variations  in  offspring,  19. 
Varicella,  951. 

gangrenosa,  952. 
Variola,  958. 
Varioloid,  958. 
Veins,  abnormalities  of,  465. 

diseases  of,  457. 
Venous  pulsation,  462. 
Vernix  caseosa,  8. 
Vertigo,  691. 
Vincent's  angina,  232. 


Volkmann's  contracture,  722. 
Volvulus,  319. 
Vomiting,  250,  251. 

bilious,    cyclical,    fitful,    lithaemic, 
periodic,  recurrent,  158. 
Von  Jaksch's  disease,  512. 
Von  Pirquet's  reaction,  860. 
Vulva,  599. 

abscess  of,  604. 

herpes  of,  599. 

noma  of,  560. 
Vulvo-vaginitis,  600. 

gonorrhoea!,  601. 


Wakefulness,  765. 

Waldeyer's  lymphatic  ring,  230. 

Walking,  9. 

Warts,  1009. 

Wasp  stings,  1020. 

Weaning,  52. 

Webbed  fingers,  107. 

Weight,  10. 

Weil's  disease,  360. 

Werdnig-Hoffmann's  palsy,  727. 

Werlhoff's  disease,  537,  538. 

Wet  nurses,  26. 

Whey,  59. 

White  stools,  273. 

White  wine  whey,  60. 

Whooping  cough,  v.  Pertussis,  961. 

Widal's  test,  914. 

Winckel's  disease,  126. 

Winged  scapula,  707. 

Witches  milk,  598. 

Woillez,  la  maladie  de,  420. 

Word-blindness,  791. 

Word-deafness,  791. 

Worm  fever,  314. 

Wry  neck,  801. 

Wunderkinder,  775. 


Xerodermia,  143. 
Youth,  period  of,  2. 
Zona,  1013. 


LONDON : 

SHAW   &   SONS,    FETTER    LANE,    FLEET  STREET,    E.C. 

1910. 


^&*JZS~  "f  /sT/Zsr/tS  <* ""  <^/r.< 


/t/r*. 


